Clinicians largely use the 6MWT to measure the response of patients with moderate to severe heart or lung disease to medical interventions, such as surgery.⁴ They may also use it to predict morbidity and mortality and assess functional status.

The test evaluates the general response of the patient’s various bodily systems during this exercise, including the pulmonary and cardiovascular systems, systemic circulation, peripheral circulation, blood, neuromuscular units, and muscle metabolism. While researchers have found some correlation with cardiopulmonary testing, it is considered a complement to more formal testing.²

Patients don’t need exercise equipment or advanced training to complete the 6MWT. They need only to walk on a hard, flat surface for six minutes. The test particularly helps clinicians assess how patients might function during daily activities, which don’t usually call for maximal exercise capacity. Patients walk at their own pace during the test, resting as needed. 

Morbidity & Mortality Associations

The 6 Minute Walk Test may help predict morbidity and mortality for a variety of conditions. Researchers have found a significant difference in mortality rates based on the distance people walk during the 6MWT. A study of 102 healthy participants aged 20 to 50 years, who performed the 6MWT, listed the mean distance walked as 614 meters and the average distance as 593 meters for women and 638 meters for men.⁵

A study of 43 people with stable New York Heart Association functional II or III heart failure reported a mortality rate of 7% for people who walked more than 300 meters during the 6MWT and 79% for people who walked 300 meters or less, with significantly increased death risk for the second group.⁶

Adversely, a COPD study of nearly 15,000 patients reported that more than half of patients who walked less than 350 meters died within a 12-month period, while more than half of the patients who walked at least 350 meters survived.² Additional studies have reported that those with lower 6MWT and left ventricular ejection fraction of up to 0.30 have an increased risk of death.

An increased risk of hospitalization and mortality was found in people with chronic respiratory disease and a low 6MWT.² For patients with COPD and low 6MWT, an increased risk of death, hospitalization, or COPD exacerbations, were seen.^7,8  

6 Minute Walk Test Contraindications

Due to an increased risk for arrhythmias or cardiovascular collapse during the 6MWT, the test is contraindicated in patients with certain cardiovascular conditions. Conditions include patients who have unstable angina and/or myocardial infarction during the month previous to the test, resting heart rates of more than 120, or blood pressure of more than 180/100 mm Hg.

Patients with stable exertional angina may undergo the 6MWT after taking their antianginal drugs, with readily available rescue nitrate medication.⁹

6MWT Guidelines

The European Respiratory Society (ERS) and American Thoracic Society (ATS) established technical standards for field walking tests in 2014. They recommend that tests are performed along a course of at least 100 feet (roughly 30 meters). Preferably, this course is quiet, located within a physiotherapy gym or dedicated exercise testing room, and set at a comfortable temperature (with air conditioning available if needed).³

Further, patients should have rapid access to emergency medicine, including a crash cart, oxygen, sublingual nitroglycerine to treat chest pain, and Albuterol to relieve symptoms of asthma and COPD during the 6MWT. There should also be a telephone or other means of calling for help in the case of emergencies.³

Patients should wear comfortable clothing and appropriate shoes for walking, use their usual walking aids if any, and take their regular medications before the 6MWT. Those who are on long-term oxygen therapy should receive oxygen at their standard flow rate or as directed by a physician or a protocol.

Patients are not allowed to exercise vigorously within two hours of beginning the test or take a shortened version of the test or warm up before the test. Any respiratory function tests scheduled for the same day as the 6 Minute Walk Test should take place first, and the patient should take at least a 15-minute rest in a chair near the start of the 6MWT before beginning this test.

Finally, any subsequent 6MWT should occur close to the same time of day to minimize variations that may happen throughout the day. Patients should undergo at least two of these tests to help show if there are any changes over time.³

While the ERS/ATS guidelines assume the 6MWT will be done under medical supervision, a 2021 study of 110 patients scheduled for heart or vascular surgery reported that tests performed with smartphones or smart watches were as reliable as in-clinic tests. The investigators noted that digital tests allow physicians to continuously and objectively assess how patients function in the real world, evaluate capacity before performing any operations, and see how patients respond to therapy. Digital tests may also help provide more meaningful telemedicine encounters.¹⁰

References

1. Troosters T, Gosselink R, Decramer M. Six minute walking distance in healthy elderly subjects. Eur Respir J. 1999;14(2):270-4. doi:10.1034/j.1399-3003.1999.14b06.x

2. Harada ND, Chiu V, Stewart AL. Mobility-related function in older adults: assessment with a 6-minute walk test. Arch Phys Med Rehabil. 1999; 80(7):837-41. doi:10.1016/s0003-9993(99)90236-8

3. Fulk G, Echternach J, Nof L, O’Sullivan S. Clinometric properties of the six-minute walk test in individuals undergoing rehabilitation post stroke. Physiother Theory Pract. 2008;24(3):195-204. doi:10.1080/09593980701588284

4. O’Keeffe ST, Lye M, Donnellan C, Carmichael DN. Reproducibility and responsiveness of quality of life assessment and six minute walk test in elderly heart failure patients. Heart. 1998;80(4):377-82. doi:10.1136/hrt.80.4.377

5. Chetta A, Zanini A, Pisi G, et al. Reference values for the 6-min walk test in healthy subjects 20-50 years old. Respir Med. 2006;100(9):1573-8. doi:10.1016/j.rmed.2006.01.001

6. King SJ, Wessel J, Bhambhani Y, Sholter D, Maksymowych W. The effects of exercise and education, individually or combined, in women with fibromyalgia. J Rheumatol. 2002;29(12):2620-7. 

7. Focht BC, Rejeski WJ, Ambrosius WT, Katula JA, Messier SP. Exercise, self-efficacy, and mobility performance in overweight and obese older adults with knee osteoarthritis. Arthritis Rheum. 2005;53(5):659-65. doi:10.1002/art.21466

8. ATS Committee on Proficiency Standards for Clinical Pulmonary Function Laboratories. ATS statement: guidelines for the six-minute walk test. Am J Respir Crit Care Med. 2002;166(1):111-7. doi:10.1164/ajrccm.166.1.at1102. Erratum in: Am J Respir Crit Care Med. 2016;193(10):1185. doi:10.1164/rccm.19310erratum

9. Hajiro T, Nishimura K, Tsukino M, Ikeda A, Koyama H, Izumi T. Analysis of clinical methods used to evaluate dyspnea in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 1998;158(4):1185-9. doi:10.1164/ajrccm.158.4.9802091

10. Mak J, Rens N, Savage D, et al. Reliability and repeatability of a smartphone-based 6-min walk test as a patient-centred outcome measure. Eur Heart J. 2021;2(1):77-87. doi:10.1093/ehjdh/ztab018

The post 6 Minute Walk Test appeared first on The Cardiology Advisor.

This article will review ACE inhibitor class and utilization and examine the mechanism by which they reduce morbidity and mortality of patients with these chronic conditions.

ACE Inhibitor Classes Review

ACE Inhibitors Mechanism of Action

ACE is part of the renin-angiotensin-aldosterone system (RAAS) and converts angiotensin I to angiotensin II. The RAAS involves the brain, kidneys, lungs, and systemic vasculature and plays a role in cardiovascular, adrenal, and renal function through blood pressure regulation and electrolyte/fluid balance.^2,3 There are three main players in the RAAS: renin, angiotensin II, and aldosterone.

In the kidneys, renin is released into the bloodstream from juxtaglomerular cells in response to a decrease in blood pressure or sodium in the distal convoluted tubule or by beta-activation.³ Renin cleaves angiotensinogen, which is produced in the liver, to angiotensin I, an inactive precursor to angiotensin II.³ ACE, found in vascular endothelium of the kidneys and lungs, is responsible for catalyzing the conversion of angiotensin I to angiotensin II.³ Angiotensin II, a potent vasoconstrictor, then binds to and activates angiotensin type I and II receptors.³

Angiotensin II causes coronary and renal vasoconstriction, stimulates sodium reabsorption, and the release of aldosterone and antidiuretic hormone.¹ Angiotensin II plays a role in cardiac remodeling by increasing left ventricular mass, as well as myocyte and vessel wall hypertrophy.¹

Aldosterone, the third major player in the RAAS, increases sodium reabsorption thereby increasing water reabsorption and potassium excretion at the distal tubule and collecting duct of nephron.³

When angiotensin II binds to angiotensin type I and II receptors in the brain, it stimulates thirst and the release of the antidiuretic hormone vasopressin that increases water reabsorption in the kidney.³ Angiotensin II also decreases the sensitivity of the baroreceptor reflex preventing it from responding appropriately when blood pressure increases.³

ACE inhibitors affect the RAAS by competitively blocking the activity of ACE. Thus, ACE inhibitors prevent the conversion of angiotensin I to angiotensin II. This decrease in angiotensin II leads to a reduction in blood pressure, aldosterone secretion, and a subsequent decrease of sodium and water retention.² Angiotensin converting enzyme inhibitors are also responsible for increasing cardiac output and index and decreasing proteinuria.¹ A decrease in the left ventricular mass has been observed when ACE inhibitors are used which help prevent cardiac remodeling.¹

In addition, angiotensin converting enzyme inhibitors contribute to an increase in bradykinin, a vasodilator, by inhibiting its degradation. As a result, bradykinin increases the levels of nitric oxide leading to vasodilation and a further decrease in blood pressure.²

ACE Inhibitors Pharmacokinetics

Angiotensin converting enzyme inhibitors are widely available in oral formulations as a single product or as combination therapy. Currently, there are ten FDA-approved ACE inhibitors on the market: benazepril, captopril, enalapril, fosinopril, lisinopril, moexipril, perindopril, quinapril, ramipril, and trandolapril. Notably, enalapril is the only one with an IV formulation available. Pharmacokinetics for each ACE inhibitor varies by formulation.

In general, oral ACE inhibitors have an onset of 1 to 2 hours and lasts approximately 24 hours allowing for once daily dosing with the exception of captopril. Captopril has an onset of 15 minutes and lasts 4 to 6 hours, requiring 2 to 3 times per day dosing. Enalaprilat, the IV formulation of enalapril, has an onset of 15 minutes and lasts 6 hours.

Most angiotensin converting enzyme inhibitors are prodrugs, requiring hepatic conversion to an active metabolite. Captopril and lisinopril are not prodrugs, and thus are administered to patients with severe hepatic impairment. With the exception of fosinipril, ACE inhibitors require dose adjustment in patients with renal impairment or insufficiency.²

ACE Inhibitors Precautions & Warnings

ACE Inhibitors and Acute Kidney Injury

ACE inhibitors can cause acute renal injury, resulting in transient increases in blood urea nitrogen and serum creatinine. This increase in serum creatinine generally occurs within two weeks of starting an ACE inhibitor. Patients on diuretics, diagnosed with renal artery stenosis, or pre-existing renal impairment are at a greater risk of developing acute renal injury. As a result, in this patient population, an increase in serum creatinine is often observed immediately after starting an ACE inhibitor.^2,4 Nonetheless, renal function improves when angiotensin converting enzyme inhibition is reduced or discontinued.²

Do ACE Inhibitors Cause Hyperkalemia?

ACE inhibitors can cause hyperkalemia when used in conjunction with potassium sparing medications such as trimethoprim/sulfamethoxazole or potassium supplements, and in patients with chronic kidney disease or diabetes.⁴

Hypotension

Symptomatic hypotension leading to possible syncopal events can occur in patients that are volume depleted, hyponatremic, and on diuretics or other antihypertensive medications.^1,5 Hypotension is usually seen at initiation angiotensin converting enzyme inhibition or during dose titrations.⁵ The underlying cause should be corrected prior to restarting an ACE inhibitor.¹

Hematologic Effects

Neutropenia has been reported in patients with kidney impairment. Patients with kidney impairment and a collagen vascular disease are at a much greater risk of developing neutropenia.¹ A complete blood count (CBC) with differential test should be conducted at the beginning of treatment and periodically thereafter.⁶

ACE Inhibitors and Aortic Stenosis

Patients with aortic stenosis or hypertrophic cardiomyopathy with outflow tract obstruction can experience severe hypotension.^1,6 This is thought to be due to the reduction in afterload associated with angiotensin converting enzyme inhibitors.^1,6

ACE Inhibitors Indications

Although there isn’t enough evidence to support the use of some ACE inhibitors to treat certain conditions, they are generally used on or off labeled for the following indications:^1,6

• Heart failure
• Hypertension (adults)
• Stable coronary artery disease
• MI with left ventricular dysfunction
• ST-elevation myocardial infarction
• Proteinuria in chronic kidney disease

*Enalapril is only FDA approved for use in hypertension.

ACE Inhibitors Side Effects

ACE inhibitor-induced angioedema is a serious adverse event that occurs in 0.1 to 0.2% of patients.¹ This condition usually develops within hours to a week after starting ACE inhibitors but can also occur later during treatment course.^1,2 Black patients have a higher incidence of angioedema compared to other races, and the incidence of ACE inhibitor-induced angioedema is higher in women compared to men.²

A dry, non-productive cough is the most commonly reported adverse event that occurs in 5-20% of patients, with an onset anywhere from 1 to 6 months after the initiation of therapy.¹ If the patient can tolerate the cough, angiotensin converting enzyme inhibitors should be continued. Otherwise, switching to another ACE inhibitor is suggested.¹ Upon discontinuing the ACE inhibitor, the cough usually resolves within a few of days but can take months to fully resolve.⁵ There is a higher incidence of ACE inhibitors-induced coughing in Asian Americans.^2,4

Additional ACE inhibitors side effects that have not been previously discussed include:²

• Headache
• Pruritus
• Myalgia
• Rash
• Dizziness
• Syncope

Monitoring Parameters for ACE Inhibitors

Monitoring parameters for angiotensin converting enzyme inhibitors at the start of therapy should include:⁶

• Serum creatinine and blood urea nitrogen
• Serum electrolytes especially potassium and sodium
• CBC with differential especially in patients with collagen vascular disease
• Liver function tests
• Blood pressure
• Heart rate

Potassium and serum creatinine should be followed closely during the first month of therapy.¹ Patients with a collagen vascular disease should have CBC with differential monitored periodically throughout treatment.

ACE Inhibitors Contraindications

Patients who have a history of hereditary or idiopathic angioedema should be administered ACE inhibitors as it increases their risk of developing ACE inhibitor-induced angioedema.^2,6 Likewise, patients who had angioedema while taking ACE inhibitors or an angiotensin receptor blocker should not be rechallenged with a different ACE inhibitor.^2,6

Angiotensin converting enzyme inhibitors cause fetal harm; therefore, they are contraindicated during pregnancy.^2,6 ACE inhibitors should be discontinued once pregnancy is detected.² Caution is advised when prescribing ACE inhibitors to women of childbearing age who are not on an appropriate birth control method.

ACE inhibitors are contraindicated in patients who have received an angiotensin receptor/neprilysin inhibitor (ARNi) within the last 36 hours due to the increased risk of developing angioedema.⁷ ACE inhibitors and ARNi should not be used concurrently.

Drug Interactions

ACE inhibitors used concurrently with aliskiren in patients with diabetes should be avoided due to an increased risk of renal failure, stroke, hyperkalemia, and hypotension.²

Use caution when ACE inhibitors are used concurrently with:

• Potassium sparing medications and potassium supplements due to the increased risk of hyperkalemia
• Lithium, as the ACE inhibitor will increase serum levels of the lithium
• NSAIDs especially in volume depleted, renally impaired or elderly patients due to increased risk of acute renal failure
• Angiotensin receptor blockers, due to an increased risk of hyperkalemia and acute kidney injury

Primary ACE Inhibitors Indications

ACE Inhibitors for Hypertension: Diagnosis & Presentation

Hypertension is a major risk factor for cardiovascular disease (CVD) and accounts for more CVD deaths in the US than any other modifiable risk factor.⁴ A diagnosis of hypertension is made when the average of 2 or more seated blood pressure measurements during 2 or more office visits is greater than 140 mmHg systolic blood pressure (SBP) or 90 mmHg diastolic blood pressure (DBP).^4,8 Automated oscillometric blood pressure machines haven been shown to detect a lower blood pressure reading than manual measurement.⁸ This can lead to the misclassification of a patient’s blood pressure level. Once the average blood pressure is determined, it should be categorized into one of the following four levels to help aid in treatment decisions:⁴

• Normal: < 120 mmHg systolic blood pressure and < 80 mmHg diastolic blood pressure
• Elevated: 120-129 mmHg systolic blood pressure and < 80 mmHg diastolic blood pressure
• Stage 1: 130-139 mmHg systolic blood pressure or 80-89 mmHg diastolic blood pressure
• Stage 2: > 140 mmHg systolic blood pressure or > 90 mmHg diastolic blood pressure

Primary hypertension is a gradual increase in blood pressure due to weight gain, lifestyle factors, poor dietary habits, decreased physical activity, and/or a family history of hypertension.⁴ Patients with primary hypertension may experience headaches, vision changes, arrhythmias, chest pain, or nosebleeds; they may also be asymptomatic.

Secondary hypertension is when another medical condition causes high blood pressure. A physical exam and medical history are required to identify the potential causes. Patients with secondary hypertension may also experience the same symptoms as primary hypertension but may also present with signs or symptoms of the underlying disease causing the increase in blood pressure.⁴

Hypertension Diagnostic Workup

Diagnostic labs for primary hypertension should include fasting blood glucose, complete blood count, lipid profile, serum creatinine with eGFR, electrolytes including calcium, thyroid stimulating hormone, and urinalysis.⁴ Additional labs should be ordered to help rule out secondary causes.⁴ An electrocardiogram can be used to detect left ventricular hypertrophy and may be useful in the assessment of comorbid disease states.⁴

Hypertension Differential Diagnosis

Patients should be screened for primary and secondary causes of hypertension such as:⁴

• Obesity
• Dietary factors including excessive sodium or low potassium intake
• Renal parenchymal disease
• Renovascular disease
• Primary aldosteronism
• Obstructive sleep apnea
• Drug or alcohol induced

Hypertension Management

In patients with primary hypertension without a comorbid disease, ACE inhibitors used as monotherapy or in combination with a diuretic or calcium channel blocker are the first-line of treatment for non-black patients.^4,8 ACE inhibitors are less effective in black patients; therefore, they are second-line therapy in this population except for comorbid conditions that require the use of ACE inhibitors.^4,8 The decision to start monotherapy or combination therapy depends on how high a patient’s initial blood pressure is above the recommended target.

ACE inhibitors are considered first-line therapy in patients with hypertension and one of the following indications:^4,8

• Heart failure
• Stable ischemic heart disease
• Post stroke or transient ischemic attack
• Diabetes mellitus with nephropathy
• Chronic kidney disease regardless of race

Depending on the compelling indication, ACE inhibitors are used as either monotherapy or in combination with another medication per guideline directed treatment. ACE inhibitor doses should be titrated to the maximal beneficial dose as tolerated, or to achieve a goal blood pressure based on compelling indication.

ACE Inhibitors in Heart Failure: Diagnosis & Presentation

Heart failure is a clinical syndrome in which the heart is not capable of pumping enough blood to sustain bodily functions due to impaired ventricular function.^7,9 Patients experiencing heart failure typically present with signs or symptoms of volume overload or reduced cardiac output such as peripheral edema, pulmonary rales, recent weight gain, paroxysmal nocturnal dyspnea, exercise intolerance, abdominal swelling, and fatigue.⁹ Dyspnea on exertion is the most commonly observed symptom.⁷

A clinical diagnosis of heart failure is made based on history, physical examination, laboratory tests, and imaging.⁹ During the physical exam, the degree of a patient’s clinical congestion should be assessed. The degree of congestion can guide initial treatments and titrations as well as help determine prognosis.⁷

The Framingham diagnostic criteria for heart failure looks for the absence or presence of key components associated with heart failure during the initial evaluation.⁹ Studies have demonstrated these criteria to be highly sensitivity (97%) at detecting systolic heart failure; therefore, it is widely accepted as a tool for aiding in the diagnosis of heart failure.⁹ When the Framingham diagnostic criteria are not met, heart failure in general, and diastolic heart failure can be ruled out.⁹

After a diagnosis of heart failure is made, patients should be classified into one of the four categories based off their left ventricular ejection fraction (LVEF):⁷

• Heart failure with reduced ejection fraction (HFrEF): LVEF < 40%
• Heart failure with improved ejection fraction (HFimpEF): previous LVEF < 40% with a follow up measurement of LVEF > 40%
• Heart failure with mildly reduced ejection fraction (HFmrEF): LVEF 40-49%
• Heart failure with preserved ejection fraction (HFpEF): LVEF > 50%

It is important to classify patients as the prognosis, initial treatment, and response to treatment differs for each classification.⁷

Heart Failure Diagnostic Workup

Diagnostic information aids in the clinical diagnosis of heart failure. Initial lab tests should include B-type natriuretic peptide, CBC, liver and renal function, serum electrolytes including calcium and magnesium, iron studies, fasting lipid panel, glucose, thyroid stimulating hormone level, and urinalysis.^7,9 A B-type natriuretic peptide level is proven to be a more reliable test than N-terminal pro-BNP, especially in older populations, and have a high negative predictive value (therefore effectively ruling out heart failure if normal).⁹ However, obesity decreases the levels of BNP and NT-proBNP, thus reducing the diagnostic sensitivity in this population.⁷

A chest x-ray can be used to identify pulmonary congestion as well as to reveal alternative causes or sources of observed symptoms.⁷ A diagnosis of heart failure is more likely in the presence of pulmonary venous congestion and interstitial edema; however, it cannot be used as the only diagnostic factor.⁹ Electrocardiography helps to identify other cardiac causes that may require further workup.⁹

An echocardiogram confirms the diagnosis of systolic heart failure, and identifies the degree of dysfunction. Although an echocardiogram can assist with the diagnosis of diastolic heart failure it is not very sensitive. Echocardiography findings that support a diagnosis of diastolic heart failure include elevated left atrial pressure, impaired left ventricular relaxation, and decreased compliance.⁷ It is not uncommon to make a diagnosis of diastolic heart failure without a conclusive echocardiogram.⁹

Heart Failure Differential Diagnosis

In addition to coronary artery disease, the number one cause of heart failure, patients should be screened for:^7,9

• Hypertension
• Cardiomyopathy: idiopathic (most common type), postpartum, hypertrophic, toxic (alcohol, cocaine), restrictive
• Valvular heart disease
• Endocrine/metabolic disorders
• Infections causing myocarditis, pericarditis
• Arrhythmia
• Collagen vascular disease
• Cardiotoxicity from chemotherapy such as anthracyclines

Heart Failure Management

ACE inhibitors reduce morbidity and mortality in HFrEF thereby are first-line therapy in patient when an ARNi can’t be used.⁷ Patients that have HFrEF and hypertension should be started on ACE inhibitors and beta blockers.^4,8 Doses should be started low and titrated up to the target dose of the particular ACE inhibitor as tolerated.⁷ Patients who are asymptomatic may benefit from treatment with an ACE inhibitor.¹

Patients who have diabetes and symptomatic HFrEF benefit from ACE inhibitors in combination with a beta blocker to reduce risk of heart failure, hospitalization, and death.¹⁰ Caution should be taken in prescribing beta blockers to those with diabetes due to their decreased sensitivity to hypoglycemic symptoms.

ACE inhibitors decrease mortality and can prevent HFrEF.⁷ Therefore, there may be some benefit in starting an ACE inhibitor in patients with current or previous HFmrEF as a third line treatment option if the potential benefits outweigh the risks.⁷ Along the same lines, patients who are considered to have pre-heart failure with LVEF < 40% should be started on an ACE inhibitors to help prevent symptomatic heart failure from developing and reduce mortality.⁷

Chronic Kidney Disease Diagnosis & Presentation

Chronic kidney disease (CKD) is defined as having an abnormality in either the kidney structure or function for greater than 3 months.¹¹ Patients must have one or more of the following to meet the definition:¹¹

• GFR < 60 mL/min/1.73m2
• Albuminuria
• Urine sediment, histology or imaging suggestive of kidney damage
• Renal tubular disorder
• History of kidney transplant

Patients may present with gross hematuria complaints of foamy urine, nocturia, flank pain or decreased urine output; however, the majority of cases are identified through routine serum chemistry and urine studies.¹¹ Patients with advanced CKD can have changes in their mental status, fatigue, nausea, metallic taste, unintentional weight loss, peripheral edema, pruritus, vomiting, or dyspnea.¹¹

A detailed physical exam and history can help identify underlying causes of CKD as well as determine a timeline to distinguish chronic from acute kidney injury.¹¹ If it is determined that the abnormality in the kidney function or structure is less than 3 months, then it is acute kidney injury which is treated differently. A patient’s volume status should be assessed during the initial evaluation to help guide treatment.¹¹

CKD Diagnostic Workup

Diagnostic labs include renal function, lipid panel, serum bicarbonate, electrolytes including calcium and phosphate, parathyroid hormone, vitamin D, iron and urine levels. A kidney ultrasound can help detect urinary obstruction.¹¹

CKD Differential Diagnosis

It is important to determine if there are underlying causes of CKD as this can help with treatment decisions. Common causes of CKD are:

• Urinary obstruction
• Medication toxicity
• Exposure to nephrotoxins in the environment
• Chronic infection
• Diabetes
• Hypertension
• Malignancy
• Autoimmune disease

CKD Management

In addition to the cardio- and renoprotective benefits that ACE inhibitors have, they also slow kidney disease progression.⁵ Therefore, ACE inhibitors are first-line therapy in patients with CKD with albuminuria, with or without hypertension or diabetes.^5,11

ACE Inhibitors and Diabetes: Diagnosis & Presentation

Polyuria, polydipsia, polyphagia, blurry vision, poor wound healing, fatigue, numbness, and tingling are the main signs and symptoms associated with diabetes; however, not all patients present with symptoms.¹² Asymptomatic patients with two or more risk factors for developing diabetes should be screened annually.¹² Risk factors include, but are not limited to:¹²

• Overweight or obesity
• Sedentary lifestyle
• Family history of diabetes
• Presence of CVD
• Medication exposure, including to antipsychotics, chronic glucocorticoids
• Hypertension

A diagnosis of diabetes can be made when patients have classic symptoms of hyperglycemia or hyperglycemic crisis with random glucose of > 200 mg/dL or when one or more of the following criteria are met on two separate occasions:^12,13

• Fasting blood glucose > 126 mg/dL
• 2 hour plasma glucose > 200 mg/dL during an oral glucose tolerance test with a 75 g oral glucose tolerance test
• Hemoglobin A1c (HbA1c) > 6.5%

The HbA1c can be falsely low or elevated in certain conditions. For instance, chronic liver disease, and acute blood loss can falsely lower the HbA1c while hypertriglyceridemia, iron deficiency anemia, and splenectomy falsely elevate it.¹²

Diabetes Diagnostic Workup

Fasting plasma glucose or 2 hour plasma glucose tolerance test (for pregnant patients) and HbA1c tests are the gold standard for diagnosing diabetes.¹³ Fasting plasma glucose must be obtained from a venous blood draw, as glucometer or continuous glucose monitoring measurements should not be used for diagnosis.¹² Likewise, HbA1c should also be measured from a venous blood sample.¹² It is important that HbA1c tests are conducted in a National Glycohemoglobin Standardization Program (NGSP) certified laboratory and is consistent with the Diabetes Control and Complications Trial (DCCT) reference assay.^10,12

Diabetes Management

ACE inhibitors decrease the risk of cardiovascular events and offer renal protection in patients with diabetes. Because of this, they are first-line therapy in patients that have diabetes and one of the following compelling indications: heart failure, hypertension without albuminuria, hypertension with presence of microalbuminuria, albuminuria, proteinuria, or LV hypertrophy, CKD or coronary artery disease.^4,10,11

Depending on the compelling indication, ACE inhibitors are used as either monotherapy or in combination with another medication per guideline directed treatment. ACE inhibitor doses should be titrated to the maximal beneficial dose tolerated. ACE inhibitors can also decrease the onset of new diabetes in patients with an impaired fasting blood glucose or glucose tolerance test.¹⁰

ACE Inhibitors Post MI Management

ACE inhibitors reduce the incidence of both nonfatal and fatal major cardiovascular events in patients that have suffered an ST elevation MI (STEMI). ACE inhibitors should be initiated in all patients with STEMI of anterior location, heart failure or LVEF < 40% unless there are known contraindications. The greatest benefit was seen when ACE inhibitors were started within the first 24 hours of the MI.¹⁴

Patients can develop severe heart failure post STEMI; therefore, ACE inhibitors should be administered provided there are no contraindications. It is reasonable to give ACE inhibitors to all patients post STEMI unless contraindicated.

Narrow ACE Inhibitors Indications

ACE Inhibitors and Migraines

Lisinopril and enalapril have been shown to decrease the frequency and severity of migraine attacks. Thus, ACE inhibitors can be used for prophylactic management of migraines in patients that do not respond to or have a contraindication to conventional therapies.¹⁵

Scleroderma

ACE inhibitors are first-line therapy for patients in scleroderma renal crisis which is characterized by a sudden onset of severe hypertension. A calcium channel blocker can be added as a second line agent when blood pressure is not adequately controlled with ACE inhibitors alone.¹⁶

Glomerular Disease

Proteinuria, hypertension, and edema are common complications associated with glomerular disease. ACE inhibitors can reduce proteinuria up to 50% in a dose dependent manner. This makes them a favorable option in glomerular disease, especially when hypertension is also present.¹⁷

Nephrotic Syndrome with Proteinuria

ACE inhibitors reduce proteinuria by up to 50% and are considered first-line therapy for nephrotic syndrome when proteinuria is present. A reduction in proteinuria decreases the risk of thromboembolic and metabolic complications, and infection risk can contribute to the development of nephrotic syndrome.¹⁷

Summary

Angiotensin converting enzyme inhibitors are used for a variety of indications and have been shown to reduce morbidity and mortality through cardio and renoprotective benefits. ACE inhibitors should be used according to guidelines in patients with no known contraindications to their use.

References

1. Bicket D. Using ACE Inhibitors Appropriately. Am Fam Physician. 2002;66(3):461-469.

2. Angiotensin Converting Enzyme (ACE) Inhibitors. Clinical Pharmacology [database]. Elsevier. 2021. Accessed September 18 2022.

3. Fountain JH, Lappin SL. Physiology, Renin Angiotensin System. StatPearls. NCBI Bookshelf version. StatPearls Publishing; 2022. Accessed October 7, 2022.

4. Whelton PK, Carey RM, Aronow WS, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the prevention, detection, evaluation and management of high blood pressure in adults: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol. 2018;71e127-248. doi:10.1016/j.jacc.2017.11.006

5. Kidney Disease: Improving Global Outcomes (KDIGO) Blood Pressure Work Group. KDIGO 2021 Clinical Practice Guideline for the Management of Blood Pressure in Chronic Kidney Disease. Kidney Int.2021;99(3S):S1-S87. doi:10.1016/j.kint.2020.11.003

6. Goyal A, Cusick AS, Thielemier B. ACE Inhibitors. StatPearls. NCBI Bookshelf version. StatPearls Publishing; 2022. Accessed October 7, 2022.

7. Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA guidelines for management of heart failure:a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2022;145:e895-1032. doi:10.1161/CIR.0000000000001063

8. Ferdinand, KC, Nasser SA. Management of Essential Hypertension. Cardiol Clin. 2017;35:231-246. doi:10.1016/j.ccl.2016.12.005

9. King M, Kingery J, Casey B. Diagnosis and evaluation of heart failure. Am Fam Physician. 2012;85(12);1162-1168.

10. Cosentino F, Grant PJ, Aboyans V, et al. 2019 ESC Guidelines on diabetes, pre-diabetes and cardiovascular diseases developed in collaboration with the EASD. Eur Heart J. 2020;41:2330-2323. doi:10.1093/eurheartj/ehz486

11. Chen TK, Knicely DH, Grams ME. Chronic Kidney Disease Diagnosis and Management A Review. JAMA. 2019;322(13):1294-1304. doi:10.1001/jama.2019.14745

12. Pippitt K, Li M, Gurgle HE. Diabetes Mellitus: Screening and Diagnosis. Am Fam Physician. 2016:93(2):103-109.

13. American Diabetes Association. Classification and diagnosis of Diabetes: Standards of Medical care in Diabetes – 2019. Diabetes Care. 2019;42(S1):S13-S28.

14. O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA Guideline for Management of ST Elevation Myocardial Infarction. A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2013;127:e362-e425.doi:10.1161/CIR.0b013e3182742cf6

15. Nandha Rm Singh H. Renin angiotensin system: a novel target for migraine prophylaxis. Indian J Pharmacol. 2012;44(2):157-160. doi:10.4103/0253-7613.93840

16. Fernandez-Codina A, Walker KM, Pope JE. Treatment Algorithms for Systemic Sclerosis According to Experts. Arthritis Rheumatol. 2018;70(11):1820-1828. doi:10.1002/art.40560C

17. Kidney Disease: Improving Global Outcomes (KDIGO) Blood Pressure Work Group. KDIGO 2021 Clinical Practice Guideline for the Management of Glomerular Diseases. Kidney Internal. 2021;100(45):S2-S276. doi:10.1016/j.kint.2021.05.021

Author Bio

Emilie White, PharmD is a residency trained clinical pharmacist and medical writer. She has provided direct patient care to hospitalized patients for over a decade. Her clinical practice areas of interest include critical care, infectious diseases, and autoimmune disorders.

The post ACE Inhibitors: Class & Utilization Review appeared first on The Cardiology Advisor.

Overview of Acute Heart Failure

Heart failure is a chronic, progressive condition in which the heart muscle cannot pump enough blood to meet the body’s demands. Acute heart failure is the rapid onset of new or worsening signs and symptoms of heart failure. It can occur on the left, right, or both sides of the heart, with right-sided failure usually caused by left-sided failure. Acute decompensated heart failure shows the same signs or symptoms as heart failure and occurs in patients with heart conditions like coronary artery disease.^1-3

There are two types of left-sided heart failure:⁴

• Acute systolic heart failure. Also known as heart failure with reduced ejection fraction (HFrEF). Occurs when the left ventricle loses its ability to contract normally. The heart then cannot pump with enough force to transport blood throughout the body.
• Acute diastolic heart failure. Also known as heart failure with preserved ejection fraction (HFpEF). Occurs when the left ventricle loses its ability to relax normally due to heart muscle stiffness. The heart then cannot fill correctly with blood during the resting period between each beat.

Right-sided heart failure occurs when the right ventricle becomes damaged and loses pumping power, typically due to issues stemming from left-sided failure. Right-sided failure causes blood to get backed up in the veins, leading to congestion throughout the body.⁵

Acute congestive heart failure is a term that is often used interchangeably with acute heart failure, but it refers explicitly to acute heart failure that results in an accumulation of blood in other parts of the body, most commonly in the lungs and lower extremities. Additionally, acute decompensated heart failure presents the same signs and symptoms as acute heart failure. No matter the type, acute heart failure is a potentially life-threatening medical emergency that requires immediate medical attention.

De novo acute heart failure refers to patients presenting for the first time with the typical symptoms and signs of heart failure. Acute decompensated heart failure applies to patients experiencing acute heart failure who have pre-existing cardiomyopathy. While de novo acute heart failure occurs in patients without a history of heart disease, it should be noted that these patients typically have other ongoing health conditions that damage the heart.⁵

Causes of Acute Heart Failure & Presentation

Acute heart failure can present with a variety of symptoms, with one of the most common being shortness of breath (dyspnea). Other symptoms can include:⁵

• Fatigue and weakness
• Rapid or irregular heartbeat
• Swelling in the legs, ankles, feet, abdomen, and veins of the neck
• Persistent cough or wheezing
• Chest pain
• Difficulty concentrating or decreased alertness
• Rapid weight gain from fluid buildup
• Reduced ability to exercise
• Nausea and lack of appetite

There is a wide variety of etiologies of acute heart failure. Anything that damages the heart or makes it work too hard can lead to acute heart failure. This includes lifestyle factors as well as pre-existing medical conditions. Some conditions that can potentially lead to heart failure are:³

• Abnormal heart rhythm (arrhythmia or dysrhythmia)
• Abnormal heart valves
• Advanced kidney disease
• Alcoholism
• Blood clot in the lung (pulmonary embolism)
• Heart defects present at birth (congenital heart disease)
• Coronary artery disease
• Diabetes
• Heart muscle disease (dilated cardiomyopathy or hypertrophic cardiomyopathy)
• Heart muscle inflammation (myocarditis)
• High blood pressure (hypertension)
• Low red blood cell count (severe anemia)
• Obesity
• Overactive thyroid (hyperthyroidism)
• Past heart attack (myocardial infarction)
• Severe lung disease
• Stroke

Acute Heart Failure Diagnostic Workup

The diagnostic workup for acute heart failure begins with a rapid assessment of the patient’s health history, including a detailed account of any symptoms, history of heart disease in the family, whether the patient smokes, what medications they take, and if they have any other medical conditions.

The physical examination should be comprehensive. Patients with acute decompensated heart failure will present a general appearance that includes anxiety, diaphoresis, and poor nutritional status.⁶

Physicians often use the Framingham Diagnostic Criteria for Heart Failure, which requires the presence of either two major criteria or one major and two minor criteria to make the diagnosis.⁵ The criteria are as follows:⁵

Major Acute Heart Failure Criteria

• Acute pulmonary edema
• Cardiomegaly
• Hepatojugular reflex
• Neck vein distention
• Paroxysmal nocturnal dyspnea or orthopnea
• Pulmonary rales
• Third heart sound (S3 Gallop)
• Weight loss of 4.5 kg or more in 5 days in response to treatment
• Central venous pressure greater than 16 cm of water
• Radiographic cardiomegaly

Minor Acute Heart Failure Criteria

• Ankle edema
• Dyspnea on exertion
• Hepatomegaly
• Nocturnal cough
• Pleural effusion
• Tachycardia (heart rate greater than 120 beats per minute)
• A decrease in vital capacity by one-third of the maximal value recorded

Diagnostic testing that can also be used to help diagnose acute heart failure, as well as potential underlying etiologies, includes blood tests, chest x-ray, electrocardiogram, echocardiogram, stress tests, cardiac computerized tomography (CT) scan, magnetic resonance imaging (MRI), coronary angiogram, and myocardial biopsy.⁷

Acute Heart Failure Differential Diagnosis

There is a broad differential diagnosis of heart failure, including the following:

• Acute kidney injury
• Acute respiratory distress syndrome
• Bacterial pneumonia
• Cardiogenic pulmonary edema
• Chronic obstructive pulmonary disease
• Cirrhosis
• Community-acquired pneumonia
• Goodpasture syndrome
• Idiopathic pulmonary fibrosis
• Interstitial (non-idiopathic) pulmonary fibrosis
• Myocardial infarction
• Nephrotic syndrome
• Neurogenic pulmonary edema
• Pulmonary embolism
• Pneumothorax
• Respiratory failure
• Viral pneumonia
• Venous insufficiency

Acute Heart Failure Management (Nonpharmacotherapy and Pharmacotherapy)

Acute heart failure management largely depends on the severity of the symptoms. Two main classification systems are used to determine the severity based on symptoms. Often, both systems are used to decide which treatment options are best for the patient.

American College of Cardiology/American Heart Association Classification

• Stage A: At high risk for heart failure but no structural heart disease or symptoms of heart failure
• Stage B: Asymptomatic left ventricular dysfunction: structural heart disease but no symptoms or signs of heart failure
• Stage C: Overt heart failure: structural heart disease with symptoms of heart failure
• Stage D: Refractory heart failure

*Symptoms of heart failure are only in stages C and D.

New York Heart Association Classification¹

• Class I: Asymptomatic left ventricular dysfunction with no limitations on physical activity or symptoms.
• Class II: Mild symptoms with slight limitation of physical activity. Ordinary activities lead to symptoms.
• Class III: Moderate symptoms with marked limitation of physical activity. Less than ordinary activities lead to symptoms.
• Class IV: Severe symptoms while at rest.

Nonpharmacological treatment is always indicated, with the ultimate goal of preventing overt heart failure by controlling the risk factors. This mainly comprises behavioral and lifestyle modifications, including dietary and nutritional consultation; strict adherence to therapy and diet; daily weight and diuretic dosing adjustment for sudden weight changes; aerobic exercise training; controlling of high blood pressure, heart rhythm abnormalities, or anemia; and discontinuing the use of tobacco, alcohol, and illicit drugs.

Other more serious nonpharmacological treatments include the use of implantable cardioverter-defibrillators for ICD shock, cardiac resynchronization therapy (CRT), coronary revascularization, heart transplantation, ventricular assist devices (VADs), and surgical ventricular restoration (SVR).⁶ These treatment options should be carefully considered based on the individual case. In most instances, pharmacological intervention should be attempted first, if possible.

Pharmacological interventions include:⁸

• Angiotensin system blocker (ACE inhibitors, ARB, or ARNI)
• Aspirin and statin
• Beta blockers
• Continuous intravenous inotrope
• Digoxin
• Diuretics
• Ivabradine
• Mineralocorticoid Receptor Antagonists (MRAs)
• Nitrates Plus Hydralazine
• Sodium-glucose cotransporter 2 inhibitor

Acute Heart Failure Complications

Complications of acute heart failure depend on the patient’s overall health, the severity of heart disease, and other factors such as age and treatment determinations. Possible complications can include:⁸

• Arrhythmia/Dysrhythmia
• Decreased functional capacity
• Decreased quality of life
• Liver dysfunction (hepatic congestion)
• Myocardial infarction
• Pulmonary hypertension
• Renal dysfunction or failure (cardiorenal disease)
• Sudden cardiac death
• Unintentional weight loss (cardiac cachexia)
• Valvular dysfunction with dilated cardiomyopathy

Monitoring Acute Heart Failure Post Care

One of the most common causes of heart failure readmission is the failure to comply with diet or medications. Careful monitoring combined with patient education is critical in preventing the associated morbidity and mortality of this disease.

The ACC/AHA recommends patient education to facilitate self-care and compliance, as well as close supervision in home-based visits, telephone support, and remote monitoring to prevent adverse outcomes. Patients need frequent in-depth education and re-evaluation to ensure adherence to recommendations.

Acute Heart Failure ICD 10 Codes

Here are several relevant acute heart failure ICD 10 codes, including the acute on chronic diastolic heart failure ICD 10 code and the acute on chronic systolic heart failure ICD 10 code:

References

1. Kurmani S, Squire I. Acute Heart Failure: Definition, Classification and Epidemiology. Current Heart Failure Reports. 2017;14(5):385-392. doi:10.1007/s11897-017-0351-y

2. Acute Heart Failure: Types, Symptoms, Causes and Treatment. Cleveland Clinic. Accessed June 29, 2022.

3. Heart Failure. Centers for Disease Control and Prevention. Published September 8, 2020. Accessed June 29, 2022.

4. Heart Failure – What Is Heart Failure? National Heart, Lung, and Blood Institute. Published March 24, 2022. Accessed June 29, 2022.

5. Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2022;145(18). doi:10.1161/cir.0000000000001063

6. Understanding Heart Failure. Cleveland Clinic. Published 2015. Accessed June 29, 2022.

7. Malik A, Brito D, Vaqar S, Chhabra L. Heart Failure, Congestive (CHF). National Library of Medicine. Published 2018. Accessed June 29, 2022.

8. Hajouli S, Ludhwani D. Heart Failure And Ejection Fraction. NIH | National Library of Medicine. Published January 18, 2020. Accessed June 29, 2022.

Author Bio

Jonathan Poole is a freelance writer and copyeditor with a BSc in Exercise Science living in West Lafayette, IN. When not writing, he owns and operates a fitness training company, Unstoppable Athletes.

Updated: 03/29/2023

The post Acute Heart Failure appeared first on The Cardiology Advisor.

This article focuses on antianginal drug classes and oral antianginal drugs used to treat angina. Additional therapies to prevent cardiovascular events should be started according to guidelines.¹

Antianginal Drugs: Beta Blockers

Antianginal beta blockers decrease myocardial oxygen demand by decreasing contractility and heart rate and reducing total peripheral resistance.⁴ Beta blockers are classified as either cardio-selective or non-selective. Cardio-selective beta blockers have a greater affinity for beta₁ receptors with additional beta₂ receptor inhibition at higher doses while non-selective options have an affinity for beta₁, beta₂, and alpha₁ receptors.⁵

Beta blockers are effective in treating stable angina; however, not all beta blockers are FDA approved for this indication.² Beta blockers can worsen symptoms of vasospastic angina and severe peripheral arterial disease.⁴

Side effects include hypotension, exercise intolerance, bradycardia, fatigue, and insomnia.^3,4,5 Beta blockers can mask the symptoms of hypoglycemia in people with diabetes.^3,4,5 Bronchospasm can occur, therefore use cautiously in individuals with severe obstructive airway disease.^5,6 Taper beta blockers to avoid beta-blocker withdrawal, which increases the risk of an acute MI.⁴

Beta blockers are contraindicated in those with Raynaud’s phenomenon, pre-existing heart block, sinus bradycardia, cardiogenic shock, sick sinus syndrome without a pacemaker, and heart failure.^4,7,9,11 Beta blockers in combination with verapamil or diltiazem can cause symptomatic bradycardia, excessive fatigue, and heart block.^4,6,9

Cardio-selective Antianginal Beta blockers

Atenolol

Atenolol is not metabolized by the liver.⁹ Dosing starts at 50 mg orally once a day and can be titrated up to 200 mg daily.⁹  Atenolol is renally excreted requiring dose adjustments for CrCl < 35.⁹

In addition to the class side effects of beta blockers, atenolol can also cause cold extremities, dizziness, and depression.⁹ Atenolol crosses the placenta and can harm the fetus; therefore, it is pregnancy category D.⁹ Use caution in nursing mothers as atenolol is excreted in breast milk.⁹  

Metoprolol

Metoprolol is hepatically metabolized through CYP2D6.^6,10 Medications that inhibit or induce this enzyme system will alter plasma concentrations of either drug, which may require dose adjustments. Metoprolol is contraindicated in those that have, or are suspected to have, pheochromocytoma.^6,10

Metoprolol can mask clinical signs of hyperthyroidism. People who are at risk of developing thyrotoxicosis should be managed carefully as abrupt discontinuation can precipitate a thyroid storm.^6,10

Additional adverse events include dizziness, depression, cold extremities, diarrhea, and rash. 
Dosing recommendations are:

• Metoprolol tartrate⁸: 100 to 400 mg orally daily in divided doses 
• Metoprolol succinate¹⁰: 100 to 400 mg orally once daily

Regardless of the formulation, doses should be titrated up as tolerated. People may experience worsening cardiac failure during the titration.¹⁰

Non-selective Beta blockers

Propranolol

Propranolol is hepatically metabolized through CYP2D6,1A2 and 2C19.^7,11 Propranolol may cause impotence, vivid dreams, and worsen symptoms of depression.^7,11

Dosing recommendations differ based on the formulation:

• Immediate release⁵: 80 to 320 mg orally daily in divided doses 2 to 4 times per day
• Extended release⁷: 80 to 320 mg orally once a day

Antianginal Drugs: Calcium Channel Blockers

Calcium channel blockers decrease myocardial oxygen demand and increase oxygen supply by causing coronary artery vasodilation, reducing total peripheral resistance, and decreasing heart rate and ventricular contractility.^4,12

Calcium channel blockers are classified as either non-dihydropyridine or dihydropyridines. Non-dihydropyridines have a greater effect on the myocardium compared to dihydropyridines.^3,4  Calcium channel blockers treat stable and vasospastic angina; however, not all calcium channel blockers are FDA-approved for these indications.^2,12

Calcium channel blockers are contraindicated in sick sinus syndrome without a pacemaker, severe hypotension, acute MI, and pulmonary congestion.¹² Peripheral edema is common, especially when starting therapy.^4,12

Dihydropyridine Calcium Channel Blockers

Dihydropyridine calcium channel blockers mainly cause peripheral vasodilation.¹³ Side effects include lightheadedness, headache, and flushing.^4,12,13

Monitor individuals with severe obstructive coronary artery disease closely during initiation and dose titration due to the increased risk of worsening angina or acute MI.^13,14 Beta blockers can be used to help overcome dihydropyridine-induced tachycardia.^3,4

Amlodipine

Amlodipine has a long half-life, 30 to 50 hours, which increases in individuals with hepatic impairment.¹³ Steady state is reached in 7 to 8 days of consecutive dosing.¹³ Higher doses had more incidences of headache and edema compared to lower ones.¹³ Other side effects include fatigue, nausea, somnolence, and abdominal pain.¹³

Amlodipine dosing is 5 to 10 mg orally once a day, with a lower starting dose of 2.5 mg in individuals with hepatic impairment, and in the elderly.¹³ Amlodipine is pregnancy category C and is not recommended when nursing.¹³

Nifedipine

Nifedipine is hepatically metabolized through CYP3A4.¹⁴ Administration with strong CYP3A4 inducers is not recommended. Nifedipine should not be used in cardiogenic shock. Peripheral edema, the most common adverse event, is dose related to higher doses having more incidents.¹⁴ Fatigue, weakness, nausea, and constipation are other common adverse events.¹⁴

Dosing for the extended-release formulation is 30 to 60 mg orally once daily.¹⁴ Monitor patients for excessive hypotension during initiation and dose titration, especially if the individual is also on a beta blocker.¹⁴ Nifedipine is pregnancy category C and is not recommended when breastfeeding.¹⁴

Short-acting nifedipine should be avoided due to increased risk of cardiac events and death when used.^1,4,16

Non-dihydropyridine Calcium Channel Blockers

Non-dihydropyridines slow myocardial conduction and contractility due to inhibition at the SA and AV nodes.¹²  Because of these actions, non-dihydropyridines can worsen cardiac output and bradycardia, thus avoid in those with 2^nd and 3^rd-degree heart block and heart failure with a reduced ejection fraction.^3,4,12 Concurrent use with a beta-blocker is not recommended.^4,6,8

People with Wolff Parkinson White syndrome or wide complex tachycardia should not receive verapamil or diltiazem.^15,17 Although rare, incidents of gingival hyperplasia have been reported.²

Verapamil

Verapamil can be used to treat unstable angina.¹⁵ There have been reports of verapamil causing 1^st-degree heart block.¹⁵ Use caution in people with hypertrophic cardiomyopathy with an outflow tract obstruction especially those with high gradients, sinus bradycardia, and advanced heart failure.¹⁵ Verapamil can cause hypotension and thus should be avoided in people who are severely hypotensive (systolic blood pressure < 90 mmHg) or those in cardiogenic shock.¹⁵

Additional adverse events include severe constipation, dyspnea, peripheral edema, and fatigue.^2,15 Angina dosing for verapamil is 80 to 160 mg orally three times a day of the immediate release formulation.¹⁵ Verapamil is metabolized by the liver; therefore, those with liver impairment should start at a lower dose and titrated up as tolerated.¹⁵ Verapamil, pregnancy category C, can cross the placenta causing adverse effects on the fetus.¹⁵

Diltiazem

Diltiazem is a potent coronary artery vasodilator and is hepatically metabolized through CYP3A4.^3,17,18 Acute hepatic injuries have been reported which resolved with drug discontinuation.¹⁷ Diltiazem is contraindicated in severe hypotension and acute MI with pulmonary edema.^17,18

Although rare, erythema multiforme and/or exfoliative dermatitis have been reported.¹⁸ More common side effects include headaches, edema, nausea, dizziness, weakness, and generalized rash.^17,18

Diltiazem is available in multiple dosage forms and strengths with pharmacokinetics differing for each one. It is recommended to refer to specific product information as dosing varies.

Antianginal Drugs: Nitrates

Low-dose nitrates cause venodilation, thus decreasing preload while high doses lead to arterial vasodilation.³ The latter mechanism decreases afterload, with both mechanisms resulting in a reduction in myocardial oxygen demand.^1,4 Nitrates effectively treat all forms of angina.⁴

Headache, palpitations, flushing, and hypotension are side effects.⁴ Reflex tachycardia can occur due to reduction of afterload.³ Nitrates should be avoided in people with severe aortic valvular stenosis and used cautiously with those in hypertrophic obstructive cardiomyopathy.^1,4

People who take long-acting nitrates must have a nitrate-free period of 10 to14 hours per day to help prevent tolerance.^4,19 Anginal symptoms may occur during that time.²⁰ Abrupt discontinuation can intensify angina.⁴

Short-acting Antianginal Nitrates

Short-acting nitroglycerin is available as sublingual tablets, sprays, ointments, and powders, and is used for prevention and treatment of acute anginal symptoms.^1,2,4,8 Onset of action is 2 to 5 minutes with effects lasting 15 to 30 minutes.⁴ Nitrate tolerance doesn’t develop with short-acting products.⁴ Dosing varies depending on the product.

Long-acting Antianginal Nitrates

Long-acting nitrates in combination with 5-PDE inhibitors such as sildenafil, can cause excessive hypotension.^2,4 Nitroglycerin is available as extended-release capsules and patches for treating angina.⁴

Isosorbide

Isosorbide should not be used in individuals who have an allergy to another nitrate and people with right ventricular infarction or hypertrophic cardiomyopathy since isosorbide decreases the preload.²⁰

In addition to the above side effects, isosorbide can cause nausea, vomiting, dizziness, lightheadedness, and syncope.²⁰ There are two salt formulations of isosorbide available that differ in pharmacokinetics and dosing.

Isosorbide dinitrate has an onset of 15 to 30 minutes with effects lasting 4 to 6 hours.²⁰ Dosing for the dinitrate formulation is 10 to 40 mg orally three times a day.²⁰

Isosorbide mononitrate, an active metabolite of isosorbide dinitrate, has an onset of 30 minutes with effects lasting 6 to 10 hours.^4,20 Dosing for isosorbide mononitrate depends on formulation:

• Immediate release: 20 mg orally twice daily
• Extended release: 30 to 120 mg orally once a day

Antianginal Drugs: Late Sodium Current Blockers

Ranolazine, a late sodium current-blocker, reduces oxygen demand by indirectly decreasing myocardial calcium influx thus reducing ventricular wall tension.^{4, 21} Ranolazine has minimal effects on blood pressure and heart rate.^4,21 Side effects include constipation, nausea, headache, and dizziness.^4,19 Although rare, ranolazine-induced myopathy can occur.²¹

Ranolazine is hepatically metabolized through CYP3A4 and 2D6.^4,19 Hepatic impairment and renal failure (CrCl < 30) increases ranolazine concentrations warranting discontinuation or a dose adjustment.⁴ Ranolazine can prolong the QT interval.^4,19 Ranolazine is started at 500 mg orally twice a day. Dose can be titrated up to 1000 mg twice daily if tolerated and there are no antianginal drugs interactions limiting max dose.^19,21

Antianginal Drugs in Summary

In summary, antianginal drugs vary in mechanism of action, side effects, and contraindications. Angina treatment with antianginal drugs should be individualized based on the patient’s medical history and drug-specific information.⁸

References

1. Gibbons RJ, Chatterjee K, Daley J, et al. ACC/AHA/ACP-ASIM Guidelines for Management of Patients with Chronic Stable Angina: Executive Summary and Recommendations. Circulation. 1999;99:2829-2848.

2. Kloner RA, Chaitman B. Angina and its Management. J Cardiovascular Pharmacology and Therapeutics. 2017;22(3):199-209.

3. Balla C, Pavasini R, Ferrari R. Treatment of Angina: Where are we? Cardiology. 2018;140:52-67.

4. Fihn, SD, Gardin JM, Abrams J, et al. 2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS Guideline for the Diagnosis and Management of Patients With Stable Ischemic Heart Disease: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, and the American College of Physicians, American Association for Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. J Am Coll Cardiol. 2012;60(24):e44-e164.

5. Khashayar F, Arif J. Beta Blockers. In:StatPearls. NCBI Bookshelf version. StatPearls Publishing; 2022. Accessed September 9, 2022.

6. Lopressor (metoprolol tartrate). Package Insert. In: Novartis Pharmaceutical Corp.;2008.

7. Propranolol. Package Insert. In: Akrimax Pharmaceuticals;2010.

8. Rousan TA, Thadani U. Stable Angina Medical Therapy Management Guidelines: A Critical Review of Guidelines from the European Society of Cardiology and National Institute of Health and Care Excellence. Eur Cardiol Rev. 2019;14(1):18-22.

9. Tenormin (atenolol). Package Insert. In: AstraZeneca; 2011.

10. Toprol XL (metoprolol succinate). Package Insert. In: AstraZeneca;2009.

11. Propranolol hydrochloride extended release capsules. Package Insert. In: Rouses Point Pharmaceuticals;2010.

12. McKeever RG, Hamilton RJ. Calcium channel blockers. In:StatPearls. NCBI Bookshelf version. StatPearls Publishing; 2022. Accessed September 9, 2022.

13. Amlodipine. Package Insert. In: Pfizer; 2011.

14. Nifedipine. Package Insert. In: Cadila Healthcare limited;2019.

15. Fahie S, Cassagnol M. Verapamil. In:StatPearls. NCBI Bookshelf version. StatPearls Publishing; 2022. Accessed September 9, 2022.

16. Kannam JP, Aroesty JM, Gersh BJ. Chronic Coronary Syndrome: Overview of Care. UptoDate, June 3, 2021. Accessed: September 8, 2022.

17. Talreja O, Cassagnol M. Diltiazem. In:StatPearls. NCBI Bookshelf version. StatPearls Publishing; 2022. Accessed September 9, 2022.

18. Diltiazem. Package Insert. In: Valeant Pharmaceuticals;2014.

19. Ranolazine. Package Insert. In: Gilead Sciences, Inc;2010.

20. Balasubramanian S, Chowdhury YS. Isosorbide. In:StatPearls. NCBI Bookshelf version. StatPearls Publishing; 2022. Accessed September 9, 2022.

21. Reed M, Kerndt CC, Gopal S, Nicolas D. Ranolazine. In:StatPearls. NCBI Bookshelf version. StatPearls Publishing; 2022. Accessed September 9, 2022.

Author Bio

Emilie White, PharmD is a residency trained, clinical pharmacist and medical writer. She has practiced pharmacy for over a decade in various hospital settings. Her clinical practice areas of interest include critical care, infectious diseases, and autoimmune disorders.

The post Antianginal Drugs appeared first on The Cardiology Advisor.

A common type of cardiac arrhythmia, atrial fibrillation (AFib) is considered a tachyarrhythmia.¹ In the United States, there are more than 454,000 hospitalizations with atrial fibrillation listed as the primary diagnosis each year, and atrial fibrillation contributes to about 158,000 deaths each year.² Moreover, the number of people with atrial fibrillation and needing AFIB treatment is expected to double or triple by 2050.³

With atrial fibrillation, the atria do not contract in a strong, regular pattern.¹ During this disorganized atrial activity, the heart may not pump enough oxygen-rich blood to the body. These arrhythmias can be classified as paroxysmal, persistent, permanent, or long-standing.³

People with atrial fibrillation are five times more likely to have a stroke than people without this arrhythmia. Risk of heart failure is also elevated with atrial fibrillation due to the gradual weakening of the heart muscle.¹

Atrial fibrillation does not always present with symptoms, but when symptoms occur, they may include:³

• Fast heartbeat
• Irregular heartbeat
• Heart palpitations
• Lightheadedness
• Chest pain or pressure
• Nausea
• Dizziness
• Diaphoresis 
• Fatigue
• Lower extremity swelling
• Dyspnea on exertion
• Shortness of breath

Atrial Fibrillation Risk Factors

Atrial fibrillation risk factors may include:³

• Older age (prevalence of approximately 1% in general population worldwide compared to 22% in individuals aged 80 and older)
• Hypertension
• Underlying congenital valvular, structural, or ischemic heart disease
• Underlying lung disease
• Obstructive sleep apnea
• Obesity hypoventilation syndrome
• Smoking
• Illicit drug use
• History of rheumatic fever
• History of pericarditis
• Hyperlipidemia
• Hyperthyroidism

Atrial Fibrillation Quick Facts – Infographic Embed

<a href="https://www.thecardiologyadvisor.com/ddi/atrial-fibrillation-management/"><img style="width:100%;" src="https://www.thecardiologyadvisor.com/wp-content/uploads/sites/17/2023/01/AFIB-Management-510x1280.jpg"></a><br>Infographic by: Cardiology Advisor <a href="https://www.thecardiologyadvisor.com/ddi/atrial-fibrillation-management/">Cardiology Advisor - Atrial Fibrillation</a>

Atrial Fibrillation Differential Diagnosis & Diagnostic Workup

Patients with atrial fibrillation may present with mild or no symptoms or severe manifestations including heart failure or stroke.

Evaluating a patient for atrial fibrillation starts with taking a thorough history to uncover any potential risk factors and conducting a physical exam focusing on symptoms such as palpitations, chest pain, and shortness of breath.³ Moreover, extremities may be swollen and there may also be decreased pulses in both upper and lower extremities and integumentary signs of peripheral vascular disease including hair loss and skin breakdown.³

Healthcare providers should ask about symptom onset, duration of symptoms, and any aggravating factors leading up to symptoms.³ Also inquire about recent illnesses and the use of new medications, supplements, illicit drugs, or alcohol.

Patients may present with an irregularly irregular pulse. Heart rate usually ranges from 110 to 140/min.³ Still, this should be confirmed with electrocardiography.

Note that a normal test result does not completely rule out atrial fibrillation because electrocardiography may not capture a paroxysmal arrhythmia. For these reasons, a Holter or cardiac event monitor may be required to make an AFIB diagnosis.^{3, 4}

Look for potential underlying causes of atrial fibrillation during the physical exam.³ For example, listening to the neck may uncover signs of carotid artery or thyroid disease, pulmonary examination may show signs of heart failure such as rales or wheeze, and a cardiovascular exam consisting of careful auscultation can spot underlying valvular pathology.

In addition, an abdominal exam to look for an enlarged liver and/or distention may indicate heart failure. It is important to evaluate the central and peripheral nervous system for signs of transient ischemic attack or cerebrovascular accident.

Diagnostic tests should include blood pressure measurement, electrocardiogram (ECG), and laboratory work.³ Note that on the ECG, atrial fibrillation presents with a narrow complex “irregularly irregular” pattern and no distinguishable p-waves. Fibrillary waves may or may not be present, and ventricular rate typically ranges between 80 to 180 beats/min.

Laboratory testing may include:³

• Complete blood count (CBC) for infection or anemia
• Basic metabolic panel for electrolyte abnormalities
• Thyroid function tests for hyperthyroidism
• Cardiac biomarkers and B-type natriuretic peptide (BNP) to rule out underlying cardiac disorder
• Liver and kidney function tests
• Drug screening, if indicated
• Sleep study, if sleep apnea is suspected

Imaging tests for atrial fibrillation should include a chest X-ray to screen for lung disease, and an echocardiogram to identify any other heart-related problems.

Additional testing may be necessary depending on the patient’s history, including a stress echocardiography and cardiac catheterization for ischemia or coronary artery disease.³

Potential differential diagnoses include atrial flutter, atrial tachycardia, multifocal atrial tachycardia, Wolff Parkinson White syndrome, and atrioventricular nodal reentry tachycardia.³

AFIB Management

Atrial fibrillation management guidelines call for rhythm control, rate control, and prevention of thromboembolism.³ Additionally, it is important to manage risk factors for stroke, prevent other heart rhythm problems, and heart failure.

If the cause of the atrial fibrillation is identified during the diagnostic process, AFIB treatment can target the cause. For example, if atrial fibrillation is a result of underlying thyroid disease, AFIB treatment can involve treating the thyroid disease to correct the atrial fibrillation.

Stroke Prevention in Atrial Fibrillation & AFIB Treatment

Stroke prevention typically entails the use of blood-thinning drugs, namely warfarin, direct-acting oral anticoagulants (dabigatran, apixaban, rivaroxaban, or edoxaban), and aspirin (recommended only in rare cases).³

About 60% of strokes that occur after an atrial fibrillation diagnosis can be prevented with anticoagulants.³

Use the point-based CHA2DS2-VASc score to assess stroke risk in all atrial fibrillation patients:³

• Congestive heart failure
• Hypertension
• Age (75 or older; assigned double points)
• Diabetes
• Stroke (prior episode; assigned double points)
• Vascular disease (prior heart attack, peripheral artery disease or aortic plaque)
• Age 65-74
• Sex (female)

Each risk factor gets a certain number of points from 1 to 2.

People with atrial fibrillation and elevated CHA2DS2-VASc score of 2 or higher should receive oral anticoagulation. Non-vitamin K oral anticoagulants, including apixaban, dabigatran, edoxaban, and rivaroxaban, are recommended over warfarin in most cases.

Always assess renal and liver function before initiating non-vitamin K oral anticoagulants.³ Other medications to help control the heart rate during atrial fibrillation include beta blockers, certain calcium channel blockers, and digoxin.

Additionally, beta blockers or antiarrhythmics can restore normal heart rhythm in atrial fibrillation. In cases of paroxysmal atrial fibrillation, for example, heart rate can be reset with medications or cardioversion.⁵

Lifestyle modifications also play a role in AFIB treatment and preventing stroke or other downstream consequences.

Patients with atrial fibrillation should be advised to:^1-3

• Get regular physical activity
• Eat a heart-healthy diet
• Manage hypertension
• Avoid excessive alcohol and caffeine consumption
• Quit smoking or never start
• Control cholesterol
• Maintain a healthy weight

Nonpharmacotherapy for atrial fibrillation can be divided into two categories: surgical or nonsurgical. Procedures to stop or control the electrical impulses causing the arrhythmia include electrical cardioversion or catheter ablation, pacemaker, or other surgery.³ Pacemaker use is typically reserved for severe cases that led to heart failure.

Electrical cardioversion can “reset” the heart to a normal rhythm, but for some atrial fibrillation patients the arrhythmia may return.³ In these cases, antiarrhythmic medications are needed indefinitely to keep the heart’s rhythm and rate in the optimal range and help prevent irreversible structural and electrical remodeling that can occur with longstanding, persistent AF. It is important to note that a transesophageal echocardiogram should always be done prior to cardioversion in these patients to minimize the risk of stroke.³

Ablation is used when cardiac arrhythmias are not responding to long-term medications or electrical cardioversion.⁵ Types of ablation include pulmonary vein isolation ablation and AV node ablation with pacemakers. During pulmonary vein isolation ablation, radiofrequency (RF) or lasers are used in the pulmonary veins to block the abnormal electrical impulses.

During ablation of the AV node, catheters are guided to the heart where radiofrequency energy severs or injures the AV node. Device therapy is also an option. In these cases, an implantable atrial defibrillator can be used to treat symptoms and keep heart rhythm in check as part of AFIB treatment.⁶

Monitoring AFIB Treatment

Blood-thinning drugs can increase risk of bleeding. Patients on warfarin must take a monthly blood test to monitor their blood levels of international normalized ratio (INR).⁷ Patients should be told to call right away if they experience any unusual bleeding or bruising. The newer oral anticoagulants do not require monthly blood testing.⁸ Care must be taken for perioperative management in patients with atrial fibrillation who use a direct oral anticoagulant and are undergoing surgery to reduce risk of bleeding and stroke.

Monitoring can be continuous with implantable pacemakers, implantable cardioverter defibrillators or subcutaneous implantable cardiac monitors or only when symptoms occur.⁶

AFIB ICD 10 Codes

Here are several relevant ICD 10 codes for atrial fibrillation:

References

1. FAQ about afib. American Heart Association. Published 2021. Accessed August 24, 2022.

2. Atrial fibrillation. Centers for Disease Control and Prevention. Updated July 12, 2022. Accessed August 24, 2022.

3. Nesheiwat N, Goyal A, Jagtap M. Atrial fibrillation. In: Stat Pearls. NCBI Bookshelf version. StatPearls Publishing: 2022. Accessed August 24, 2022.

4. Diagnosis: Atrial fibrillation. National Health Service. Updated May 17, 2021. Accessed Aug. 24, 2022.

5. Non-surgical procedures for atrial fibrillation (AFib or AF). American Heart Association. Last reviewed July 31, 2016. Accessed August 24, 2022.

6. Devices for arrhythmia. American Heart Association. Last reviewed September 30, 2016. Accessed August 24, 2022.

7. A patient’s guide to taking warfarin. American Heart Association. Last reviewed September 30, 2016. Accessed August 24, 2022.

8. Atrial fibrillation medications. American Heart Association. Accessed August 24, 2022.

About the Author

Denise Mann, MS, is a veteran freelance health writer in New York. Her work has appeared on HealthDay, among other outlets. She was awarded the 2004 and 2011 journalistic Achievement Awards from the American Society for Aesthetic Plastic Surgery. She was also named the 2011 National Newsmaker of the Year by the Community Anti-Drug Coalitions of America.

She has also been awarded the Arthritis Foundation’s Northeast Region Prize for Online Journalism, the Excellence in Women’s Health Research Journalism Award, the Gold Award for Best Service Journalism from the Magazine Association of the Southeast, a Bronze Award from The American Society of Healthcare Publication Editors, and an honorable mention in the International Osteoporosis Foundation Journalism Awards.

She was part of the writing team awarded a 2008 Sigma Delta Chi award for her part in a WebMD series on autism. Mann has a graduate degree from the Medill School of Journalism at Northwestern University in Evanston, Ill.

Updated: 03/29/2023

The post Atrial Fibrillation & AFIB Management appeared first on The Cardiology Advisor.

Atrial Tachycardia Definition & Epidemiology

Atrial tachycardia is a heart rhythm in which the heart beats faster than 100 beats per minute due to an electrical signal in the atria. It is one type of paroxysmal supraventricular tachycardia (PSVT), a term referring to a group of arrhythmias that originate above the atrioventricular junction (AVJ) and that generally begin and end abruptly.¹

Collectively, the PSVTs are thought to affect 36 per 100,000 persons per year in the United States. Women are at twice the risk of PSVT compared to men, while older people face a fivefold risk compared with younger people.^2,3

Of all PSVTs, atrial tachycardia is the least common, accounting for approximately 1 in 10 cases. Among patients referred for supraventricular tachycardia (SVT) ablation, focal atrial tachycardia (FAT) is present in 3% to 17%.⁴

Etiology and Risk Factors

In atrial tachycardia, the AVJ is not part of the circuit. This distinguishes it from related arrhythmias such as atrioventricular nodal reentrant tachycardia (AVNRT) and atrioventricular reentrant tachycardias (AVRT).

There are two main types of atrial tachycardia: unifocal and multifocal.

• Unifocal. In the unifocal type, also called focal or ectopic atrial tachycardia, the abnormal electrical impulse begins at a single spot somewhere in either atrium. A subtype of unifocal is called sinus node reentry tachycardia; it involves micro re-entry that arises at the sinus node.
• Multifocal. In multifocal atrial tachycardia (MAT), several areas give rise to these electrical signals.

When FAT arises from reentrant electrical impulses, it is associated with structural heart disease. It may also occur incessantly due to enhanced automaticity in a structurally normal heart, a condition that can result in cardiomyopathy and heart failure.⁵ Atrial tachycardia commonly occurs after ablation for atrial fibrillation.

By contrast, MAT is closely associated with lung diseases, such as asthma or chronic obstructive pulmonary disease (COPD). It can also result from hypomagnesemia.⁶

Digoxin and theophylline are among the drugs that can cause atrial tachycardia. Others include β-agonists, phosphodiesterase inhibitors, dobutamine, and milrinone. Substances such as caffeine, cocaine, amphetamines, and alcohol use or withdrawal may also provoke arrhythmia.⁷

Presentation

Symptoms of paroxysmal supraventricular tachycardia commonly include palpitations, chest pain, fatigue, and/or lightheadedness. Syncope is less common, while sudden cardiac death may rarely occur.

Patients with incessant atrial tachycardia resulting in cardiomyopathy may report heart failure symptoms such as progressive exertional dyspnea. Symptoms of intermittent focal or multifocal atrial tachycardia may relate to underlying heart or pulmonary disease.

An electrocardiogram (ECG) reveals a regular, narrow-complex tachycardia in which P waves differ from their appearance in sinus rhythm. P waves may sometimes disappear into the preceding T waves.⁴

Atrial Tachycardia Physical Examination Findings & Workup

Because bouts of tachycardia can be short-lived and episodic, the patient may not be experiencing symptoms during the clinical encounter. The history should elicit a description of episodes, including any triggers; if the episodes occur with activity or amid known heart disease, a ventricular origin may be present. It is also helpful to establish age of onset, abrupt vs gradual onset (the latter suggests sinus tachycardia), and symptom duration.⁴

The provider should also ask about heart disease, cardiac surgery, and medications, including those that may cause electrolyte disturbance. Inquiries about substance use or withdrawal are important.

Physical examination may reveal only tachycardia. If the atria contract against a closed tricuspid valve, blood may backflow into the jugular veins, resulting in visible bulging known as the frog sign.⁸ (However, the frog sign can also be seen in AVNRT; it is not specific to atrial tachycardia.) Vital signs, including orthostatic blood pressure measurements, may point to other causes of tachyarrhythmia.

For unifocal tachycardia, ECG shows a fast, regular rhythm with isoelectric segments between P-waves. It may be difficult to distinguish from other regular SVTs. The P waves outnumber the QRS complexes, helping to distinguish atrial tachycardia from sinus tachycardia.

With MAT, the ECG shows an irregular rhythm with at least three different P-wave morphologies, typically with isoelectric periods between them.

If the patient is not tachycardic at the time of evaluation, outpatient monitoring may be indicated.⁴

Some diagnostics can also be therapeutic. Vagal maneuvers such as the Valsalva maneuver or unilateral carotid sinus massage can slow down conduction through the atrioventricular node.⁹ However, massage should be avoided in older patients with carotid bruits.

Pharmacological interventions such as adenosine, which should be administered in a monitored environment, can also block atrioventricular conduction. If the arrhythmia stops in response to adenosine, it indicates AVNRT or AVRT. With unifocal atrial tachycardia, the ventricular rate will typically slow down in response to adenosine. Transient atrioventricular block with persistent atrial tachycardia suggests a unifocal origin.¹⁰

Cardioversion is rarely necessary and is indicated if the patient is hemodynamically unstable and has not responded to other measures. It is not useful to treat MAT.

Laboratory studies should include complete blood count, basic metabolic panel, magnesium, and thyroid-stimulating hormone.¹⁰ Patients with known or suspected heart disease may also require measurement of B-type natriuretic peptide and cardiac enzymes.

A chest X-ray may reveal cardiomegaly, while an echocardiogram may reveal structural heart disease.³ In some cases, an invasive electrophysiology study is indicated, especially if ablation of the abnormal atrial impulse(s) is planned. Mapping during such a study can help determine the origin of a unifocal atrial tachycardia.

Differential Diagnosis

The differential diagnosis of narrow-complex tachycardias, including the PSVTs, is important because treatment differs depending on the arrhythmia. This requires scrutiny of the ECG with close attention to P-wave and QRS shapes and to the PR and RR intervals. Practitioners may wish to consult an algorithm to help distinguish atrial tachycardia from other SVTs, including AVNRT, AVRT, permanent junctional reciprocating tachycardia (PJRT), atrial fibrillation, and atrial flutter.³

Briefly, unifocal atrial tachycardia is typically regular, as are reentry tachycardias and sinus tachycardia. By contrast, multifocal atrial tachycardia and atrial fibrillation are irregular. Atrial flutter and atrial tachycardia may also present with variable conduction and irregular rhythm, however. 

Unifocal atrial tachycardia’s atrial rate is typically 100 to 250 beats per minute.¹¹ MAT’s isoelectric periods between its three or more P-wave types can help to distinguish it from atrial fibrillation.

Atrial tachycardia and the other PSVTs may be misdiagnosed as panic disorder or anxiety disorder, which may be hazardous if an incessant arrhythmia is overlooked.³

Atrial Tachycardia Prognosis

Prognosis depends on the underlying cause. Unifocal atrial tachycardia is usually benign in adults and may not require treatment if it is not sustained. On the other hand, incessant atrial tachycardia can contribute directly to tachycardic cardiomyopathy and reversible heart failure.¹¹The prognosis of MAT will relate in large part to underlying lung disease.

Treatment for paroxysmal supraventricular tachycardia includes a variety of antiarrhythmic drugs and/or catheter ablation of the abnormal focus or foci. Unifocal atrial tachycardia may respond to medication; ablation with 3-dimensional mapping technology is frequently successful.

Collectively, the SVTs are thought to be a common reason patients visit a primary care provider or emergency department. However, these arrhythmias seldom result in inpatient admission.

Atrial Tachycardia ICD 10 Codes

Here are relevant ICD 10 codes for atrial tachycardia:

References

1. Helton MR. Diagnosis and Management of Common Types of Supraventricular Tachycardia. Am Fam Physician. 2015;92(9):793-800.

2. Orejarena LA, Vidaillet H Jr, DeStefano F, et al. Paroxysmal supraventricular tachycardia in the general population. J Am Coll Cardiol. 1998 Jan;31(1):150-7. doi:10.1016/s0735-1097(97)00422-1

3. Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society [published correction appears in Circulation. 2016 Sep 13;134(11):e234-5]. Circulation. 2016;133(14):e506-e574. doi:10.1161/CIR.0000000000000311

4. Mahtani AU, Nair DG. Supraventricular Tachycardia. Med Clin North Am. 2019;103(5):863-879. doi:10.1016/j.mcna.2019.05.007

5. Liwanag M, Willoughby C. Atrial Tachycardia. In: StatPearls. Treasure Island (FL): StatPearls Publishing; 2022 Jan-.

6. Custer AM, Yelamanchili VS, Lappin SL. Multifocal Atrial Tachycardia. In: StatPearls. Treasure Island (FL): StatPearls Publishing; 2022 Jan-.

7. Tisdale JE, Chung MK, Campbell KB, et al. Drug-Induced Arrhythmias: A Scientific Statement From the American Heart Association. Circulation. 2020;142(15):e214-e233. doi:10.1161/CIR.0000000000000905

8. Velibey Y, Durak F, Türkkan C, Alper AT. “Frog Sign” in paroxysmal supraventricular tachycardia. Anatol J Cardiol. 2018 Apr;19(4):E7. doi: 10.14744/AnatolJCardiol.2018.78045

9. Niehues LJ, Klovenski V. Vagal Maneuver. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-.

10. Kusumoto FM, Schoenfeld MH, Barrett C, et al. 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Circulation. 2018;140(8)e382-e482.

11. Atrial Tachycardia. Cleveland Clinic. Published 2021. Accessed June 20 2022.

Author Bio

Jenny Blair, MD, is an award-winning journalist and writer based in Vermont.

Updated: 03/29/2023

The post Atrial Tachycardia: Diagnosis appeared first on The Cardiology Advisor.

β-ARs are expressed on cardiomyocytes. β1-AR is the most abundant receptor subtype expressed in the heart with four times more expression than β2, while β3-AR is the least expressed.² In cardiomyocytes, β1-ARs are coupled to G-proteins.¹ They have stimulatory effects on the heart, increasing cardiac contractility, rate of myocardial relaxation, and chronotropy.

β2-ARs are associated with activating and inhibitory G-proteins, and although they primarily stimulate activating G-proteins, they can also have inhibitory effects on the heart. β3-ARs are coupled to inhibitory G-proteins and have negative effects on heart inotropy.¹ They can also activate nitric oxide synthase (NOS), guanylate cyclase (GC), and the production of cGMP.

Beta Blockers Mechanism of Action

Three generations of β-AR antagonists currently exist.¹ They differ based on their selectivity which allows them to elicit different responses. The first generation of beta blockers are nonselective antagonists of β1 and β2 receptors. The second generation of beta blocker shows dose-dependent cardioselectivity for β1 receptors over β2 receptors. The third generation of beta blockers inhibits β1 receptors on cardiomyocytes, and function as cardiovascular vasodilators by blocking α1-adrenoreceptor activity and activation of β3-ARs.

Beta blocker activity can decrease heart rate, heart strength, cardiac output, activity of renin-angiotensin system, and blood pressure.¹ Due to its vasodilating properties, third generation β-blockers decrease peripheral vascular resistance. Through activation of NOS and GC, third generation beta blockers exhibit angiogenic, antioxidant, antifibrotic, and anti-apoptotic properties, which reduces cardiac remodeling, and endothelial and cardiac dysfunction.

Pharmacokinetics and Pharmacodynamics of Beta Blockers

Sotalol and propranolol are first-generation beta blockers, and propranolol is the first of its class used in clinical practice.¹ Second generation beta blockers include atenolol and metoprolol, and labetalol. Carvedilol, and nebivolol are third generation β-blockers.¹ β-blocker can be lipophilic (propranolol, metoprolol, third generation) or hydrophilic (atenolol).¹ They show a range of values in serum availability and half-life. They are often metabolized by the liver or can be cleared without biotransformation (atenolol).¹

Beta blocker inhibitory activity has been demonstrated by: (1) reduction in resting and exercise heart rate and cardiac output, (2) reduction of systolic and diastolic blood pressure, (3) decreased atrioventricular nodal conduction and increased atrioventricular nodal refractoriness, (4) inhibition of isoproterenol induced tachycardia, (5) reduction in reflex orthostatic tachycardia.^3–9

Precautions and Warnings

• β-adrenergic inhibition may lead to more severe cardiac failure due to lowered myocardial contractility
• In patients with aortic or mitral valve disease, or compromised left ventricular function, continued β-adrenergic depression may lead to cardiac failure
• Abrupt therapy interruption in patients with coronary artery disease, worsening of angina pectoris, and in some cases myocardial infarction and death can happen
• Beta blocker treatment can worsen symptoms of arterial insufficiency in patients with peripheral or mesenteric vascular disease due to reduced cardiac output
• β-blockers should be avoided in patients with bronchospastic disease
• β-blockers should not be routinely discontinued prior to major surgery. However, there is an increased risk of general anesthesia and surgical procedure due to the impaired heart response to adrenergic stimuli
• β-blockers may mask hypoglycemia and should be used with caution in diabetic patients
• β-blockers may mask some sign of hyperthyroidism. Abrupt withdrawal may lead to thyroid storm
• Patients with a history of severe anaphylactic reaction may be more reactive to repeated challenge and unresponsive to the usual dose of epinephrine while taking β-blockers
• β-blockers should be used with caution in patients with impaired liver function
• Pheochromocytoma
• Prinzmetal’s variant angina
• β−blocker withdrawal syndrome: condition of adrenergic hypersensitivity that can arise after abrupt discontinuation of the therapy. Symptoms include elevated blood pressure and high heart rate. In patients with stable angina, abrupt discontinuation of medicine can lead to unstable angina and myocardial infarction (MI). If discontinuation is needed, beta blocker tapering is required to prevent adverse cardiac effects of adrenergic hypersensitivity^3-10

Beta Blockers Indications

• Hypertension
• Ventricular arrhythmia
• Delay in recurrence of atrial fibrillation/atrial flutter
• Angina pectoris due to coronary atherosclerosis
• Acute myocardial infarction
• Heart failure
• Left ventricular dysfunction following myocardial infarction^3-9

Side Effects of Beta Blockers

• Cardiovascular (chest pain, edema, hypotension, bradycardia, heart failure, and syncope)
• Central nervous system (depression, dizziness, fatigue, headache, insomnia, abnormal dreams, anxiety, impotence, and paraesthesia)
• Dermatological (rash, pruritus)
• Gastrointestinal problems (constipation, diarrhea, dyspepsia, flatulence, nausea, vomiting, and abdominal pain)
• Metabolic (hyperglycemia, weight gain, increased blood urea nitrogen, and nonprotein nitrogen, hypercholesterolemia, and peripheral edema)
• Genitourinary (micturition, dysuria, and nocturia)
• Musculoskeletal (arthralgia, myalgia, back pain, and joint pain)
• Respiratory (cough, dyspnea, rhinitis, pharyngitis, and wheezing)
• Special senses (abnormal vision, conjunctivitis, and dry eye)
• Liver and biliary system (increased bilirubin and alkaline phosphatase)^3-9

Beta Blockers Contraindications

• Persistent severe bradycardia
• Second- and third-degree heart block
• Overt cardiac failure
• Cardiogenic shock
• Sick sinus syndrome (except when permanent pacemaker present)
• Severe hepatic impairment
• Bronchospastic conditions
• Severe hypersensitivity^3-9

Drug Interactions with Beta Blockers

• Other β-blocking drugs
• Catecholamine-depleting drugs (reserpine and guanethidine)
• Calcium antagonist (verapamil and diltiazem)
• Digitalis glycosides
• CYP2D6 inhibitors
• Rifampin^3-9

Primary Beta Blockers Indications

Beta Blockers for Angina

Angina: Presentation and Diagnosis

Patients with angina present with retrosternal chest pain, sensation of pressure, tightness or discomfort in chest, and pain in the shoulders, arms, neck, back, upper abdomen, or jaw.¹¹ Symptoms of angina may include dyspnea, nausea, and lightheadedness.

Angina can be stable or unstable. Unstable angina is one of the conditions of acute coronary syndrome, that also includes ST-elevation myocardial infarction (STEMI) and non-ST-elevation myocardial infarction (NSTEMI).¹⁹ Stable angina happens in response to physical and emotional stress, whereas unstable angina occurs without physical or minimal exertion.¹⁹ Symptoms of stable angina generally dissipate with the use of nitroglycerin.¹¹ 

Angina: Diagnostic Workup

Diagnostic workup for angina includes physical exam and assessment of medical history. A physical exam can differentiate angina from other causes of chest pain, like aortic stenosis, hypertrophic cardiomyopathy, or pulmonary hypertension. A crescendo-decrescendo systolic murmur is indicative of aortic stenosis and hypertrophic cardiomyopathy, and they can be distinguished with Valsalva maneuver, squatting, and hand grip. Loud and widely dispersed P2 component of the second heart sound or a right ventricular heave can indicate pulmonary hypertension.

Electrocardiogram (ECG) should be performed to screen for evidence of prior myocardial infarction (MI) or left ventricular hypertrophy. Functional stress testing to provoke ischemia in combination with ECG is the primary diagnostic tool for stable angina. Testing used to diagnose stable angina includes Coronary computed tomographic angiography (CCTA), which is able to detect nonobstructive plaque that may be missed by stress testing. It has recently become one of the first-line tests used to diagnose angina¹¹

Angina: Differential Diagnosis

• Cardiovascular conditions (unstable angina, NSTEMI, STEMI, myocarditis, and pericarditis)
• Gastrointestinal conditions (esophageal spasm, and gastroesophageal reflux)
• Pulmonary conditions (asthma, chronic obstructive pulmonary disease (COPD), and pulmonary embolism)
• Musculoskeletal conditions (costochondritis and injury)¹²

Beta Blockers for Angina: Indication Management by Drug-Class Use

Beta blockers are used as first-line antianginal drugs for therapy and to manage symptoms unless contraindication or intolerance is present.¹¹ The selection of an appropriate therapeutic drug to treat angina is guided by a patient’s comorbidities.¹³ Therefore, the combination of a beta blocker and calcium channel blocker is the primary combination for the treatment of angina in patients with prior MI and left ventricular dysfunction.¹³

However, in patients with stable coronary disease without prior MI or decreased left ventricular function, who have undergone percutaneous coronary intervention, long term use of beta blockers does not associate with reduction of future cardiovascular events.^14,15

Prevention of Recurrent Myocardial Infarction (RMI)

Recurrent myocardial infarction (RMI) is one of the most concerning of the adverse cardiovascular events in survivors of acute myocardial infarction (AMI).¹⁶ Approximately, 10% of the all MI patients are at risk of developing a RMI within the year of AMI.¹⁷

Prevention of RMI: Presentation and Diagnosis

Chest pain that occurs at rest or with minimal exertion for more than 10 minutes is the most common symptom of MI.¹⁸ Pain frequently starts in the retrosternal area and radiates into the left arm, neck, and jaw. Chest pain can be accompanied by palpitation, nausea, syncope, dyspnea, and excessive sweating.^18,20

MI can be divided into ST-elevated (STEMI) and non-ST-elevated (NSTEMI) MI based on ST segment elevation. STEMI is diagnosed based on ECG findings of ST elevation.¹⁹ NSTEMI is diagnosed based on elevated cardiac biomarkers in the absence of ST elevation.²¹ Cardiac troponins are the most sensitive and specific biomarkers of NSTEMI. They become elevated within a few hours upon the onset of symptoms and can be elevated for several days or even longer depending on the size of the infarction.²¹

Prevention of RMI: Diagnostic Workup

Diagnostic workup includes physical examination that can alternatively diagnose chest pain, some of which can be life threatening.²¹ A 12-lead ECG should be done and interpreted within 10 minutes of arrival to the emergency room. If initial ECG is not diagnostic, serial ECG should be performed.

Biomarkers of myocardial necrosis (serial cardiac troponin I or T) should be measured.²¹ A troponin value above the 99^th percentile of the upper reference level is the appropriate cutoff point for the diagnosis of myocardial necrosis.²⁰ Additional diagnostic workup may include imaging using x-ray, computed tomography (CT), and transthoracic echocardiogram.

Prevention of RMI: Differential Diagnosis

Imbalance in myocardial oxygen consumption and demand, is a hallmark of MI caused by coronary artery obstruction can happened as a result of other conditions including:

• Excessive oxygen demand in the presence of stable flow-limited lesion
• Acute coronary insufficiency due to vasospastic angina (prinzmetal), coronary embolism, and coronary arteritis
• Non-coronary causes (hypotension, severe anemia, hypertension, tachycardia, hypertrophic cardiomyopathy, and severe aortic stenosis)
• Nonischemic myocardial injury (myocarditis, cardiac contusion, and cardiotoxic drugs)
• Stress cardiomyopathy
• Pulmonary embolism
• Severe heart failure
• Sepsis
• Nonischemic cardiovascular causes of chest pain (aortic dissection, expanding aortic aneurysm, pericarditis, and pulmonary embolism)
• Noncardiovascular causes of chest, back, and upper abdominal pain (pneumonia, pneumothorax, gastroesophageal reflux, esophageal spasm, peptic ulcer, pancreatitis, biliary disease, costochondritis, cervical radiculopathy, psychiatric disorders, sickle cell crisis, and herpes zoster) ²¹

Prevention of RMI: Indication Management by Drug-Class Use

According to the American Heart Association (AHA)/ American College of Cardiology (ACC) guidelines²¹, oral beta blocker therapy should be initiated in the first 24 hours following MI if the patients don’t have signs of heart failure, evidence of low-output state, increased risk for cardiogenic shock, and other contraindication to β−blocker therapy (class of recommendation (CoR) I, level of evidence (LoE) A).

The 2014 AHA/ACC guidelines also state that continuous use of beta blockers is reasonable in patients with normal left ventricular function and without angina after initial MI (CoR IIa, LoE C).²¹ The 2013 AHA/ACC and 2017 ESC guidelines recommend long term use of beta blockers in patients after STEMI with preserved left ventricular ejection function (LVEF) and no angina (Class I for ACC/AHA; class IIA for ESC).^22,23

However, most of the studies of the long term benefits of beta blockers were conducted before the widespread use of percutaneous coronary intervention and use of antiplatelets and statins; therefore, the long-term benefits of beta blockers for the prevention of recurrent MI and other cardiovascular events are not fully established.²³ Holt et al. found no association between long-term beta blocker therapy and reduction of cardiovascular death, recurrent MI, or a composite outcome of cardiovascular events.²⁴

Beta Blockers for Hypertension

Hypertension is the leading cause of the death worldwide, with 10.4 million deaths per year attributed to elevated blood pressure. ²⁵

Hypertension: Presentation and Diagnosis

The following guidelines are used to diagnose hypertension:

• Office blood pressure measurement:
  • Grade I 140-159 mmHg systolic and 90-99 mmHg diastolic
  • Grade II ≥ 160 mmHg systolic ≥ 100 mmHg diastolic
• Ambulatory blood pressure measurement:
  • 24-hour average ≥ 130 mmHg systolic and ≥ 80 mmHg diastolic
  • Awake average ≥ 135 mmHg systolic and ≥ 85 mmHg diastolic
  • Asleep average ≥ 120 mmHg systolic and ≥ 70 mmHg diastolic
• Home blood pressure measurement ≥ 135 mmHg (systolic) and ≥ 85 mmHg diastolic²⁵

Blood pressure measurement in the office is the most common method of diagnosing hypertension. The diagnosis should be made based on 2 to 3 office visits spaced 1 to 4 weeks apart. Hypertension can be diagnosed based on a single visit if the measured blood pressure is ≥ 180 mmHg and other signs of cardiovascular disease are present.

Patients with hypertension are often asymptomatic or they can present with chest pain, dyspnea, palpitations, claudication, peripheral edema, headaches, blurred vision, nocturia, hematuria, and vertigo. Signs of secondary hypertension may be present like muscle weakness, cramps, arrhythmias, flash pulmonary edema, sweating, snoring, daytime sleepiness, or symptoms of thyroid disease.

Hypertension: Diagnostic Workup

Diagnostic workup includes blood pressure measurement in both arms, preferably simultaneously in a comfortable environment. Measurements should be taken 3 times at 1 minute intervals. Physical exams can assist with confirmation of diagnosis and identification of hypertension-mediated organ damage or secondary hypertension.

Medical history including a history of cardiovascular disease, family history of hypertension, assessment of overall cardiovascular risk scored based on BP levels, and additional risk factors according to the ESC/ESH guidelines.²⁶ Laboratory tests include sodium, potassium, serum creatinine, and estimated filtration rate, and if available lipid profile, fasting glucose, urine test, and 12-lead ECG.

Hypertension: Differential Diagnosis

• Secondary hypertension
• Hyperaldosteronism
• Coarctation of the aorta
• Renal artery stenosis
• Chronic kidney disease
• Aortic valve disease²⁷

Beta Blockers for Hypertension: Indication Management by Drug-Class Use

Beta blockers are one of the five major drug classes recommended for the treatment of hypertension.²⁵ When compared to placebo, beta blockers significantly reduce the risk of stroke, heart failure, and major cardiovascular events in patients with hypertension.²⁸ Beta blockers are equally as effective as other blood pressure-lowering drug classes in preventing cardiovascular events in hypertensive patients, with the exception of stroke.²⁶

Beta blockers are associated with an increased risk of diabetes in predisposed patients.²⁶ β-blockers are the treatment of choice in hypertensive patients with symptomatic angina, post-MI, HFrEF, need for the heart rate control, or as an alternative to angiotensin-converting enzyme or ACE inhibitors (ACEi) and angiotensin II receptor blockers in younger hypertensive women.²⁶

In the case of uncomplicated hypertension, hypertension with chronic kidney disease, beta blockers can be added if hypertension proved to be resistant to treatment combination consisting of ACEi or angiotensin II receptor blockers with calcium channel blockers and diuretic.²⁶

The vasodilating β-blocker, labetalol, is considered the first-line of treatment in hypertensive emergencies, including malignant hypertension, hypertensive encephalopathy, acute coronary event, eclampsia, and severe pre-eclampsia.²⁶ Beta blockers with the exception of metoprolol should be used as blood pressure controlling medicine in hypertensive psychiatric patients with drug-induced tachycardia.²⁵  

Beta Blockers for Heart Failure

Heart failure is a complex clinical syndrome with symptoms resulting from deficits in ventricular blood pumping. The ACC/AHA classify development and progression of heart failure into four categories²⁹:

Stage A – At risk for heart failure (asymptomatic and without structural heart disease, but with risk-increasing disease present, like hypertension, cardiovascular disease, diabetes, obesity, exposure to cardiotoxic agent, genetic marker of cardiomyopathy, and familiar myopathy)

Stage B – Pre-heart failure (asymptomatic with structural heart disease, evidence of filling pressure, increased natriuretic peptide, and persistent elevated levels of cardiac troponin in the absence of competing diagnosis)

Stage C – Symptomatic heart failure

Stage D – Advanced heart failure that interferes with daily activities and requires hospitalization

Another important classification of heart failure is based on the LVEF. LVEF classification is important because of its prognostic values in response to treatment.²⁹ Most clinical trials select patients based on their LVEF values. According to the ACC/AHA, heart failure is classified as:²⁹

• Heart failure with reduced LVEF if LVEF value is less or equal 40% (HFrEF)
• Heart failure with improved LVEF if previous LVEF less or equal 40% and the follow-up value more than 40% (HFimpEF)
• Heart failure with preserved LVEF if LVEF value is equal or more than 50 % (HFpEF)
• Heart failure with mid-range LVEF if LVEF values are between 40 and 50%

Heart Failure: Presentation and Diagnosis

Symptoms of heart failure include:³⁰

• Dyspnea – exertional dyspnea, orthopnea (dyspnea that develops in recumbent position, and it is relieved with head elevation), paroxysmal nocturnal dyspnea (dyspnea that develops during the night after several hours of sleep and it requires longer positional relief), and dyspnea at rest
• Ankle swelling
• Chest pain
• Palpitations
• Weakness
• Nocturia and oliguria
• Cerebral symptoms -confusion, memory problems, anxiety, insomnia, and headaches

Diagnosis of heart failure requires 2 major criteria, or 1 major and 2 minor criteria.³¹ Major criteria include:

• Paroxysmal nocturnal dyspnea
• Neck vein distention
• Rales
• Cardiomegaly
• Acute pulmonary edema
• S3 gallop
• Increased central venous pressure
• Hepatojugular reflux
• Weight loss of more than 4.5 kg in 5 days in response to treatment

Minor criteria include:

• Bilateral ankle edema
• Nocturnal cough
• Exertional dyspnea
• Hepatomegaly
• Pleural effusion
• Decrease in vital capacity by 1/3 from maximum recorded
• Tachycardia

Heart Failure: Diagnostic Workup

Diagnostic workup for heart failure includes a physical exam and medical history. A critical component of a physical exam is to look for signs of clinical congestion that are the result of elevated cardiac filling pressure. Clinical congestion can be assessed by jugular venous distention, orthopnea, a square-wave response to the Valsalva maneuver, and leg edema.³²

Laboratory testing includes CBC, electrolytes, complete metabolic profile, TSH levels, and urine analysis. Per the recommendation of the AHA/ACC (COR = 1 and LOE = A), specific laboratory tests that measure B-type natriuretic peptide (BNP) and N-terminal natriuretic peptide (NT-proBNP) are recommended to support or exclude the diagnosis of heart failure in symptomatic patients, to risk stratify patients with previous diagnosis of heart failure, or to determine the prognosis in patients hospitalized with heart failure. An ECG is a part of the routine evaluation of patients with suspected heart failure.³³

A chest X-ray is also used in patients with suspected heart failure to evaluate heart size and pulmonary congestion, and to detect other possible cardiac or pulmonary causes contributing to patient symptoms. A transthoracic echocardiogram is an integral part of the diagnostic workup. LVEF values from the transthoracic echocardiogram are essential for the classification of heart failure and in determining the appropriate therapy.

Additional imaging techniques can be used such as CMR, SPECT or radionuclide ventriculography, PET, cardiac CT, or ICA.²⁹ Genetic testing may be used if genetic causes of cardiomyopathy are suspected.

Heart Failure: Differential Diagnosis

• Acute renal failure
• Acute respiratory distress syndrome (ARDS)
• Cirrhosis
• Pulmonary fibrosis
• Nephrotic syndrome
• Pulmonary embolism³⁴

Beta Blockers for Heart Failure: Indication Management by Drug-class Use

For patients in stage B (pre-heart failure) with LVEF less than or equal 40 %, beta blockers should be used to prevent symptomatic heart failure. For these patients in stage B with LVEF less than or equal 40 %, and a recent or remote history of MI or acute coronary syndrome, beta blockers are categorized as a Class I recommendation per the AHA/ACC guidelines, and should be used to reduce mortality.^35,36 This treatment can improve LVEF, lessen the symptoms of heart failure, and improve clinical status.

Even if symptoms do not improve, long-term treatment should be maintained to reduce the risk of major cardiovascular events. Three β-blockers are recommended bisoprolol, sustained-release metoprolol, and carvedilol.

Beta Blockers for Arrhythmia

Arrhythmia is a condition of irregular heartbeat that includes changes in the rate and the heartbeat rhythm.³⁷ Broadly, arrhythmias include tachycardias (increased heartbeat) and bradycardia (slower heartbeat).³⁷ Based on its site of origin, tachycardias are divided into two main categories, supraventricular tachycardias (SVT), and ventricular tachycardias (VT), characterized by the narrow and wide QRS complex on ECG, respectively.

Occasionally, SVTs can present with wide QRS, as in case of SVT with bundle-branch block and SVT with AV conduction through an accessory pathway.³⁷

SVTs include a wide range of arrhythmias originating in the atrium of the atrioventricular node that can be divided into two groups based on the rhythm pattern.^38,39:

1. Regular SVTs:

• Atrial flutter
• Atrioventricular recurrent tachycardia
• Atrioventricular recurrent tachycardia
• Atrial tachycardia
• Sinus tachycardia

2. Irregular SVTs:

• Atrial fibrillation
• Atrial tachycardia with variable block
• Atrial flutter with variable block
• Multifocal atrial tachycardia
• Frequent premature atrial bloc

SVT: Presentation and Diagnosis

SVTs can be symptomatic or asymptomatic (identified by surface ECG). ECG documentation is required for the diagnosis of SVT.^38,40 Patients with symptomatic SVTs present with palpitations, dyspnea, fatigue, chest pain or tightness, poor effort tolerance, dizziness, syncope, and troubled sleeping. In the case of hemodynamically unstable atrial fibrillation, the following conditions may be observed: syncope, symptomatic hypotension, acute heart failure, pulmonary edema, myocardial ischemia, and cardiogenic shock.⁴⁰

Atrial fibrillation is a supraventricular tachyarrhythmia with uncoordinated atrial electrical activation and consequently ineffective atrial contraction.⁴⁰ It is the most common type of cardiac arrhythmia.⁴¹ Atrial fibrillation is diagnosed based on irregular R-R intervals in the absence of p-waves and irregular atrial activation on a 12-lead ECG recording or a single-lead ECG tracing of > 30 seconds.⁴⁰

SVT: Diagnostic Workup

Diagnostic workup for all SVT patients should include a physical exam, complete medical history and concurrent conditions, 12-lead ECG to establish diagnosis and asses ventricular rate, and the identification of ischemia, structural defects, and conductivity problems. Complete blood work (full blood count, electrolytes, thyroid, and kidney function) and transthoracic echocardiogram should be part of diagnostic workup.

Selected atrial fibrillation patients should be evaluated for the presence of pulmonary embolisms and examined by transesophageal echocardiogram to evaluate for atrial thrombus.⁴⁰

SVT: Differential Diagnosis

1. Atrioventricular nodal reentry tachycardia
2. Multifocal atrial tachycardia
3. Paroxysmal supraventricular tachycardia
4. Wolff-Parkinson-White Syndrome
5. Regular tachycardia:

If Yes:

• No Visible P waves AVNRT
• Visible P waves:
  • Atrial rate greater than ventricular rate = Atrial flutter or Atrial tachycardia
  • Atrial rate not greater than ventricular rate:
    • Long RP (RP longer than PR) = Atrial tachycardia, PJRT, Atypical AVNT
    • Short RP interval – Less than 70 ms = AVNRT
    • Short RP interval – More than 70 ms = AVRT, AVNRT, AT

If No:

• Atrial fibrillation, AT/flutter with variable AT conductivity, MAT³⁷

Beta Blockers for SVT: Indication Management by Drug-Class Use

In patients with atrial fibrillation with minimal symptoms, rate control is the initial treatment strategy and beta blockers are one class of drugs that can be used to achieve an adequate heart rate. β-blockers are preferred for the management of atrial fibrillation in patients with a history of heart failure with reduced ejection fraction (HFrEF) and acceptable with in patients with heart failure with preserved ejection fraction (HFpEF).⁴¹ β-blockers are used as synergistic reagents in the rhythm control strategy for atrial fibrillation or AFIB management.⁴¹

The beta blockers currently used in clinical practice include metoprolol, carvedilol, and esmolol. Adverse effects include hypotension, bradycardia, masking of hypoglycemia in diabetic patients, and worsening symptoms in patients with asthma or chronic obstructive pulmonary disease (COPD).⁴¹ In the patients with reactive airways disease, atrial fibrillation rate control therapy should be initiated with β-1 receptor selective β-blocker to minimize the risk of bronchospasm.⁴¹

Contraindications include second or third degree heart block.⁴¹ In patients with hemodynamically stable regular SVTs, β-blockers are considered a reasonable choice if vagal maneuvers and adenosine administration fails to terminate SVTs. In patients with Wolff Parkinson White syndrome or new pre-excitation pattern on ECG, AV-nodal blockers, including β-blockers should be avoided because of their potential to cause life-threatening ventricular arrhythmia.^38,43

Narrow Beta Blockers Indications

Beside the treatment for cardiovascular conditions, beta blockers are used in treatment of hyperthyroidism, essential tremor, portal hypertension, glaucoma and migraine.⁴⁴ Although not approved by FDA, beta blockers are also used by some individuals for management of anxiety due to its strong anxiolytic properties.⁴⁴

References

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2. Lucia C de, Eguchi A, Koch WJ. New Insights in Cardiac β-Adrenergic Signaling During Heart Failure and Aging. Front Pharmacol. 2018;9:904. doi:10.3389/fphar.2018.00904

3. Atenolol [package insert]. AstraZeneca Pharmaceuticals LP; 2011.

4. Bisoprolol Fumarate [package insert]. Duramed Pharmaceuticals, Inc; 2007.

5. Carvedilol [package insert]. GlaxoSmithKline; 2008.

6. Labetalol Hydrochloride [package insert]. Prometheus Laboratories Inc; 2010.

7. Metoprolol Tartrate [package insert]. Novartis Pharmaceuticals Corporation; 2008.

8. Nebivolol [package insert]. Forest Pharmaceuticals, Inc; 2011.

9. Acebutolol Hydrochloride [package insert]. Promius Pharma LLC; 2010.

10. Frishman WH. Beta-adrenergic blocker withdrawal. Am J Cardiol. 1987;59(13):F26-F32. doi:10.1016/0002-9149(87)90038-5

11. Joshi PH, Lemos JA de. Diagnosis and Management of Stable Angina. JAMA. 2021;325(17):1765-1778. doi:10.1001/jama.2021.1527

12. Gillen C, Goyal A. Stable Angina. StatPearls. NCBI Bookshelf version. StatPearls Publishing; 2022. Accessed September 19, 2022.

13. Sorbets E, Steg PG, Young R, et al. β-blockers, calcium antagonists, and mortality in stable coronary artery disease: an international cohort study. Eur Heart J. 2018;40(18):1399-1407. doi:10.1093/eurheartj/ehy811

14. Motivala AA, Parikh V, Roe M, et al. Predictors, Trends, and Outcomes (Among Older Patients ≥65 Years of Age) Associated With Beta-Blocker Use in Patients With Stable Angina Undergoing Elective Percutaneous Coronary Intervention Insights From the NCDR. JACC Cardiovasc Interv. 2016;9(16):1639-1648. doi:10.1016/j.jcin.2016.05.048

15. Nappi AG, Boden WE. Should Beta-Blockers Continue to Be Used in Post-Percutaneous Coronary Intervention Patients Without Myocardial Infarction?∗. Jacc Cardiovasc Interv. 2016;9(16):1649-1651. doi:10.1016/j.jcin.2016.07.001

16. Nair R, Johnson M, Kravitz K, et al. Characteristics and Outcomes of Early Recurrent Myocardial Infarction After Acute Myocardial Infarction. J Am Heart Assoc. 2020;10(16):e019270. doi:10.1161/jaha.120.019270

17. Jernberg T, Hasvold P, Henriksson M, Hjelm H, Thuresson M, Janzon M. Cardiovascular risk in post-myocardial infarction patients: nationwide real world data demonstrate the importance of a long-term perspective. Eur Heart J. 2015;36(19):1163-1170. doi:10.1093/eurheartj/ehu505

18. Ferry AV, Anand A, Strachan FE, et al. Presenting Symptoms in Men and Women Diagnosed With Myocardial Infarction Using Sex‐Specific Criteria. J Am Heart Assoc. 2019;8(17):e012307. doi:10.1161/jaha.119.012307

19. O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. 2013;127(4):e362-e425. doi:10.1161/CIR.0b013e3182742cf6

20. Hamm CW, Bassand JP, Agewall S, et al. ESC Guidelines for the Management of Acute Coronary Syndromes in Patients Presenting Without Persistent ST-Segment Elevation: The Task Force for the management of acute coronary syndromes (ACS) in patients presenting without persistent ST-segment elevation of the European Society of Cardiology (ESC). Eur Heart J. 2011;32(23):2999-3054. doi:10.1093/eurheartj/ehr236

21. Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guideline. J Am Coll Cardiol. 2014;64(24):e139-e228. doi:10.1016/j.jacc.2014.09.017

22. O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction: Executive Summary. Circulation. 2013;127(4):529-555. doi:10.1161/cir.0b013e3182742c84

23. Ibanez B, James S, Agewall S, et al. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation:The Task Force for the management of acute myocardial infarction in patients presenting with ST–segment elevation of the European Society of Cardiology (ESC). Eur Heart J. 2018;39(2):119-177. doi:10.1093/eurheartj/ehx393

24. Kumar, M., Malouf A, C, Beavers, C. Are Long-Term Beta Blockers Following MI inthe Absence of Angina and HF Indicated in the PCI Era? American College of Cardiology website. Published October 25, 2021. Accessed September 19, 2022.

25. Unger T, Borghi C, Charchar F, et al. 2020 International Society of Hypertension Global Hypertension Practice Guidelines. Hypertension. 2020;75(6):1334-1357. doi:10.1161/hypertensionaha.120.15026

26. Williams B, Mancia G, Spiering W, et al. 2018 ESC/ESH Guidelines for the management of arterial hypertension:The Task Force for the management of arterial hypertension of the European Society of Cardiology (ESC) and the European Society of Hypertension (ESH). Eur Heart J. 2018;39(33):3021-3104. doi:10.1093/eurheartj/ehy339

27. Iqbal AM, Jamal SF. Essential Hypertension. StatPearls. NCBI Bookshelf version. StatPearls Publishing; 2022.  Accessed September 19, 2022.

28. Thomopoulos C, Parati G, Zanchetti A. Effects of blood pressure-lowering on outcome incidence in hypertension: 5. Head-to-head comparisons of various classes of antihypertensive drugs – overview and meta-analyses. J Hypertens. 2015;33(7):1321-1341. doi: 10.1097/HJH.0000000000000614

29. Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: Executive Summary: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2022;145:e895–e1032. doi: 10.1161/CIR.0000000000001063

30. Bozkurt B, Coats AJ, Tsutsui H, et al. Universal Definition and Classification of Heart Failure: A Report of the Heart Failure Society of America, Heart Failure Association of the European Society of Cardiology, Japanese Heart Failure Society and Writing Committee of the Universal Definition of Heart Failure.  J Card Fail. 2021;S1071-9164(21)00050-6. doi:10.1016/j.cardfail.2021.01.022

31. Mahmood SS, Wang TJ. The epidemiology of congestive heart failure: the Framingham Heart Study perspective. Glob Heart. 2013;8(1):77-82. doi:10.1016/j.gheart.2012.12.006

32. Thibodeau JT, Drazner MH. The Role of the Clinical Examination in Patients With Heart Failure. JACC Heart Fail. 2018;6(7):543-551. doi:10.1016/j.jchf.2018.04.005

33. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013;62(16):e147-e239. doi:10.1016/j.jacc.2013.05.019

34. Malik A, Brito D, Vaqar S, et al. Congestive Heart Failure.  StatPearls. NCBI Bookshelf version. StatPearls Publishing; 2022. Accessed September 19, 2022.

35. Dargie HJ. Effect of carvedilol on outcome after myocardial infarction in patients with left-ventricular dysfunction: the CAPRICORN randomised trial. Lancet. 2001;357(9266):1385-1390.

36. Exner DV, Dries DL, Waclawiw MA, Shelton B, Domanski MJ. Beta-adrenergic blocking agent use and mortality in patients with asymptomatic and symptomatic left ventricular systolic dysfunction: a post hoc analysis of the studies of left ventricular dysfunction. J Am Coll Cardiol. 1999;33(4):916-923. doi:10.1016/s0735-1097(98)00675-5

37. Blomström-Lundqvist C, Scheinman MM, Aliot EM, et al. ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias–executive summary. a report of the American college of cardiology/American heart association task force on practice guidelines and the European society of cardiology committee for practice guidelines (writing committee to develop guidelines for the management of patients with supraventricular arrhythmias) developed in collaboration with NASPE-Heart Rhythm Society. J Am Coll Cardiol. 2003;42(8):1493-1531. doi:10.1016/j.jacc.2003.08.013

38. Bibas L, Levi M, Essebag V. Diagnosis and management of supraventricular tachycardias. CMAJ. 2016;188(17-18):E466-E473. doi:10.1503/cmaj.160079. doi:10.1503/cmaj.160079

39. Sims JM, Miracle V. Sinus tachycardia. Nursing. 1996;26(6):49. doi:10.1097/00152193-199606000-00018

40. Hindricks G, Potpara T, Dagres N, et al. 2020 ESC Guidelines for the diagnosis and management of atrial fibrillation developed in collaboration with the European Association of Cardio-Thoracic Surgery (EACTS): The Task Force for the diagnosis and management of atrial fibrillation of the European Society of Cardiology (ESC) Developed with the special contribution of the European Heart Rhythm Association (EHRA) of the ESC. Eur Heart J. 2021;42(5):373-498. doi:10.1093/eurheartj/ehaa612

41. Lacoste JL, Szymanski TW, Avalon JC, et al. Atrial Fibrillation Management: A Comprehensive Review with a Focus on Pharmacotherapy, Rate, and Rhythm Control Strategies. Am J Cardiovasc Drugs. 2022;22(5):475-496. doi:10.1007/s40256-022-00529-6

42. Gestel YRBM van, Hoeks SE, Sin DD, et al. Impact of Cardioselective β-Blockers on Mortality in Patients with Chronic Obstructive Pulmonary Disease and Atherosclerosis. Am J Respir Crit Care Med. 2008;178(7):695-700. doi:10.1164/rccm.200803-384OC

43. Redfearn DP, Krahn AD, Skanes AC, Yee R, Klein GJ. Use of medications in Wolff-Parkinson-White syndrome. Expert Opin Pharmaco. 2005;6(6):955-963. doi:10.1517/14656566.6.6.955

44. Farzam K, Jan A. Beta Blockers. StatPearls. NCBI Bookshelf version. StatPearls Publishing; 2022. Accessed September 19, 2022.

Author Biography

Ivana Celic, PhD, is a biomedical scientist and freelance medical and scientific writer. Her research interests include genome plasticity, cancer, aging, neurodegenerative disease, and infertility. She actively participates in laboratory research, scientific writing, and presentations.

The post Beta Blockers appeared first on The Cardiology Advisor.

History & Epidemiology

A bifurcation lesion is a common health issue that occurs when a coronary artery narrows, adjacent to or involving a significant side branch.¹ These are caused by plaque deposits comprised of fat. Bifurcations are a type of coronary artery disease, a serious medical condition that ranks as the leading cause of death in the US.²

Coronary bifurcation lesions can be either simple or complex, accounting for approximately 20% of all percutaneous coronary interventions.³​​ They represent a challenge to medical professionals since this condition is known for its cardiac side effects and lower interventional success rates. Although a number of treatment options have been used, provisional side branch stenting is the most commonly used treatment and the intervention associated with the lowest risk of failure.

Patients with bifurcation lesions will need to be monitored carefully as they also have an increased risk of developing atherosclerosis.⁴

Bifurcation Lesion Presentation & Diagnosis

If a patient presents with the following symptoms, they should undergo testing for coronary artery disease, which may include bifurcation lesions⁵:

• Discomfort or pain in the chest area
• Pain in the shoulder or arms
• Shortness of breath
• Nausea
• Cold sweats
• Lightheadedness

If patients are diagnosed with coronary artery disease, they should undergo additional testing to look for the presence of bifurcation lesions.

A bifurcation lesion can only be identified via diagnostic imaging, primarily computed tomography coronary angiography (CTCA) and invasive coronary angiography (ICA). While ICA is effective in diagnosing coronary artery disease, it has limitations when used for identifying the size and extent of bifurcation lesions, as only the lumen and not the plaque accumulations within can be visualized.

Research indicates that since 64-slice CTCA provides three-dimensional imaging, it is one of the most accurate diagnostic tools, particularly for complex bifurcations, and so should be the primary tool used for identifying bifurcation lesions.⁶

Diagnostic Workup

If bifurcation lesions are present, they can then be classified to determine the best possible treatment option for the patient; the most commonly used is the Medina classification of bifurcation lesions.¹

The Medina bifurcation lesion classification is popular for its simplicity compared to other classification methods, as a binary number (0 or 1) is assigned to the proximal, distal, and side branches based on the absence or presence of a stenosis.

In terms of frequency, research has found that Medina subtypes 1.1.1 and 1.1.0 are the most prevalent. Patients with either Medina 1.1.1 or Medina 0.0.1 should be more closely monitored as these classification subtypes generally have worse outcomes and a higher risk of failure after one year.⁷

Bifurcation Lesion Differential Diagnosis

Coronary artery disease, including bifurcation lesions, can appear similar to a wide range of other health issues. Initial complaints of chest discomfort can include the following differential diagnoses:

• Pericarditis
• Gastroesophageal reflux disease
• Myocarditis
• Pneumonia
• Pericardial effusion
• Prinzmetal angina
• Pleuritis
• Pleural effusion

To determine the exact cause of a patient’s discomfort, a thorough medical history should be taken, along with a physical exam and diagnostic testing.⁸

Management (Nonpharmacotherapy and Pharmacotherapy)

In the past, a range of interventions has been used for bifurcation lesions, including balloon angioplasty and bare-metal stents. But today, provisional side branch stenting is considered to be the default treatment option for the majority of cases.

Drug-eluting stenting is most often used, which contains drugs to reduce tissue growth, keeping the artery from re-narrowing. Either one or two stents can be placed. A second stent is used when the side branch is greater than 2.5 mm with greater than 50% stenosis.³

During the stenting procedure, the main vessel should be treated first. Side branches should then be treated if they meet the following classifications:

• Major flow limitation
• A large myocardial territory
• Difficult side branch access

Compared to bare-metal stenting, drug-eluting stenting results in a lower mortality rate and a lower risk of recurrence. These stents are also shown to reduce repeat revascularization and restenosis rates.⁹

Monitoring Side Effects, Adverse Events, and Drug-Drug Interactions

All patients should be carefully monitored during and after treatment. Because stenting involves inserting foreign material into the body, patients can be at risk for developing stent thrombosis when a blood clot forms within the stent. This can occur months or even years after the stent has been inserted; however, newer stent technology has reduced this risk compared to first-generation stents.

To reduce the risk of developing stent thrombosis, patients can be given anti-clotting medicine (dual antiplatelet therapy) after a review of the patient’s other medications to avoid any adverse drug reactions. Completion of the therapeutic course is crucial for preventing side effects, so patients should be reminded to finish the complete course of medication, as well as given guidelines on the importance of dietary and exercise changes, if needed. Monitor patients for side effects and instruct them to seek medical assistance if they experience any of the following:

• Chest pain
• Shortness of breath
• Nausea or vomiting
• Headaches
• Rash
• Bleeding or frequent bruising¹⁰

In rare cases, other complications relating to stents can include¹¹:

• Failure of stent deployment (occurs primarily with first-generation stents)
• Infection
• Coronary aneurysm

All patients and their primary care providers should be given a copy of the ongoing recovery plan.

References

1. Louvard Y, Medina A. Definitions and classifications of bifurcation lesions and treatment. EuroIntervention. 2015;11(suppl V:V23-26). doi:10.4244/EIJV11SVA5

2. Centers for Disease Control and Prevention. Leading Causes of Death. Updated September 6, 2022. Accessed September 16, 2022.

3. Sawaya FJ, Lefèvre T, Chevalier B, et al. Contemporary approach to coronary bifurcation lesion treatment. JACC Cardiovasc Interv. 2016;9(18):1861-78.

4. Raphael CE, O’Kane PD.  Contemporary approaches to bifurcation stenting. JRMS Cardiovas Dis. 2021. doi:10.1177/2048004021992190

5. Centers for Disease Control and Prevention. Coronary Artery Disease (CAD).Updated July 19, 2021. Accessed September 16, 2022. 

6. Van Mieghem CAG, Thury A, Meijboom WB, et al. Detection and characterization of coronary bifurcation lesions with 64-slice computed tomography coronary angiography. Eur Heart J. 2007;28(16):1968-76.

7. Mohamed MO, Lamellas P, Roguin A, et al. Clinical outcomes of percutaneous coronary intervention for bifurcation lesions according to Medina Classification. J Am Heart Assoc. 2022;11(17):e025459.

8. Shahjehan RD, Bhutta BS. Coronary artery disease. StatPearls Publishing. Updated February 9, 2022. Accessed September 16, 2022.

9. Généreux P, Mehran R. Are drug-eluting stents safe in the long term? CMAJ. 2009;180(20):154-5.

10. Yelamanchili VS, Hajouli S. Coronary artery stents. StatPearls Publishing. Updated June 11, 2022. Accessed September 16, 2022.

11. Maisel W, Laskey W. Cardiology patient page. Drug-eluting stents. Circulation. 2007;115(17):e426-e427.

Author Bio

Katie Dundas is American freelance medical writer and travel blogger based in Sydney, Australia.

The post Bifurcation Lesion appeared first on The Cardiology Advisor.

Presentation & Cause

A pacemaker is any device that sends controlled electrical impulses to certain areas of the heart in order to stimulate cardiac contraction when the heart’s intrinsic electrical system is not functioning normally. The overall purpose of pacemakers is to restore normal electrical activity, improve heart function, and regulate cardiac pacing as part of cardiac resynchronization therapy (CRT).

Based on current guidelines, approximately 40% of patients with systolic heart failure are cardiac resynchronization therapy candidates. For patients with heart failure, myocardial dysfunction, and prolonged ventricular depolarization on a surface electrocardiogram (ECG), CRT has been proven effective.

Delivery methods for CRT include a pacemaker or a combined pacemaker-defibrillator. The most ideal CRT device type for specific populations with regard to patients’ longevity, quality of life, and cost of care is not clearly defined despite extensive research conducted over the past 2 decades.¹

CRT: Diagnostic Workup & Differential Diagnosis

Pacemakers consist of a pulse generator, pacing leads or wires, and an electrode at the end of each lead to carry the electrical signals to the relevant area of the heart. The pulse generator is implanted under the skin, most commonly in the left anterior chest wall or the left axilla. The pacing leads are inserted into the relevant chambers of the heart.

Modern pacemakers rely on a computer that monitors the electrical activity and tailors the function of the pacemaker to the electrical activity that already exists in the heart. Pulse generators can also be utilized for implantable or external pacemakers as necessary.²

Most commonly used pacemakers are permanent, single, and dual chamber pacemakers. Common cardiac pacing indications for a permanent pacemaker are symptomatic sinus node dysfunction (sinus bradycardia or sinus pauses), third or type 2 second atrioventricular (AV) -block, and permanent atrial fibrillation with symptomatic bradycardia.

Symptomatic indicators that may be treated with a pacemaker include symptomatic chronotropic incompetence and symptomatic pronounced AV block. A common indication for the use of a pacemaker is severe heart failure.³

When a patient already has a pacemaker implanted, an ECG, which detects the heart’s rhythm and electrical activity, can be interpreted and then used to identify the type of pacemaker the patient currently has.

The pacemaker intervention on an ECG can be seen as a sharp vertical line on all the leads on the ECG as electricity is transferred to the heart. More specifically, a line before the P wave indicates that the lead has been inserted into the atria. Alternatively, a line before the QRS complex (Q wave, R wave, and S wave) indicates that the lead is in the ventricles.⁴

CRT Device Overview & Selection Options

There are several different ways in which pacemakers can be categorized and chosen for a particular patient. They are often referred to by the number of the heart’s chambers they can pace.

• A single chamber pacemaker can either pace the right atrium or the right ventricle. The lead is placed in the right atrium if the AV conduction in the heart is normal and the issue is with the sinoatrial node. This stimulates depolarization in the right atrium, and then the electrical activity passes to the left atrium, through the AV node, and to the ventricles, promoting normal contraction of the heart. If the AV conduction in the patient is abnormal, the physician may place a single chamber pacemaker in the right ventricle, allowing it to bypass the atrium and stimulate the ventricular contraction directly.¹  

• A dual chamber pacemaker can pace both the right atrium and the right ventricle. By doing so, it can synchronize the contractions of the atria and the ventricles.¹

• A biventricular pacemaker can pace the right atrium, right ventricle, and left ventricle. The use of a biventricular pacemaker is indicated by ventricular dyssynchrony, which can occur from either right ventricular pacing and/or from underlying cardiomyopathy. This pacemaker synchronizes the contractions of all the chambers, optimizing overall heart function. A common indication for the use of a biventricular pacemaker to conduct cardiac resynchronization therapy is severe heart failure.³

Pacemakers are also categorized based on their duration. There are permanent pacemakers that contain a battery that typically lasts for 5 to 10 years, after which the generator needs to be replaced. While cardiac pacing is most commonly accomplished using a permanent pacemaker, temporary pacing can be lifesaving in critical care patients with severe symptoms and acute instability.⁵ Temporary pacemakers remain implanted for several days or a week and can establish normal sinus rhythm in cases of bradyarrhythmias, tachyarrhythmias, and heart block.⁵

• Transvenous pacemakers are those from which the wires are implanted into the internal jugular vein, yet the power source and circuitry remain external.⁶

• Transcutaneous pacemakers conduct an electrical current applied to the patient’s skin. A transcutaneous pacemaker is only used during bradycardic arrests in order to buy the necessary time to place a transvenous pacemaker.⁶

• Epicardial pacemakers are occasionally placed at the time of cardiac surgery.⁶ Contrary to conventional pacemakers, temporary epicardial pacing wires are almost always implanted at the conclusion of cardiac surgery to treat bradydysrhythmias, particularly AV block, or to control heart rate.²

Pacemakers can also be categorized by whether they have the ability to defibrillate the heart in the event of ventricular fibrillation (VF) or sustained ventricular tachycardia (VT). This ability would classify those pacemakers as implantable cardioverter defibrillators (ICD).⁷

ICDs are used to terminate VT and VF in high-risk patients. ICDs have both typical pacing/sensing electrodes and 1 to 2 defibrillation electrodes composed of coils and wire. The metal housing of the generator itself can serve as a third electrode. These defibrillators continually monitor the heart and, in the case of a patient having a shockable arrhythmia, an ICD shocks the heart in order to return the heart rate to proper rhythm.

The first indication is secondary prevention of cardiac arrest or sustained VT in the absence of a completely reversible cause. The second indication is the primary prevention of sudden cardiac death.⁷

Patient & Special Populations Consideration

Regardless of cardiac pacing indication, reversible ideologies of the conduction disease must be ruled out first before placing the device. Reversible ideologies can include medications, infection, electrolyte disturbances, and ongoing ischemia. For patients who require a rhythm control strategy, cardioversion is a vital option for atrial flutter and atrial fibrillation management through synchronized direct current, electrical shock, or application of antiarrhythmic drugs.⁸

Cardioversion is a medical procedure that replaces an irregular heart rhythm with brief, low-energy shocks. In the emergency room, patients can be cardioverted quickly to treat their immediate symptoms and enable discharge. This eliminates the need for anticoagulation in low-risk patients as well as the requirement for heart-rate control prescriptions.⁹

Electrical cardioversion is the best treatment option for severely hemodynamically compromised patients with new-onset atrial fibrillation or atrial flutter because it stops atrial fibrillation in over 90% of cases.⁸

Monitoring Cardiac Pacers

Because permanent and temporary cardiac pacers expire over a certain period of time and can have dangerous complications, they require constant monitoring. Implantation-related complications that could arise from the use of a pacemaker include pocket hematoma, pocket infection, pneumothorax, hemothorax, lead dislodgement, and, rarely, a cardiac perforation/tamponade.

Many complications could also be delayed, giving even more reason to continue monitoring the patient. These delayed complications include a lead fracture, insulation break, infection (pocket or lead), thrombosis/stenosis of veins, pacing-induced cardiomyopathy, pacemaker syndrome, and pacemaker-mediated tachycardia.¹⁰

References

1. Canterbury A, Saba S. Cardiac resynchronization therapy using a pacemaker or a defibrillator: Patient selection and evidence to support it. Prog Cardiovasc Dis. 2021;66:46-52. doi:10.1016/j.pcad.2021.04.003

2. Cronin B, Dalia A, Goh R, Essandoh M, O’Brien EO. Temporary epicardial pacing after cardiac surgery. J Cardiothorac Vasc Anesth. 2022. doi:10.1053/j.jvca.2022.08.017

3. Glikson M, Nielsen JC, Kronborg MB, et al. 2021 ESC Guidelines on cardiac pacing and cardiac resynchronization therapy. Europace. 2022;24(1):71-164. doi:10.1093/europace/euab232

4. Prutkin JM. ECG tutorial: Pacemakers. UpToDate. Updated April 13, 2021. Accessed September 15, 2022.

5. Gammage MD. Temporary cardiac pacing. Heart. 2000;83(6):715-720. doi:10.1136/heart.83.6.715

6. Cunningham MA, Ferrara E. Temporary Cardiac Pacing. In: L’Ecuyer KM, Young E, eds. Cardiac Vascular Nurse Certification Review. Springer Publishing Company, LLC; 2022:179-192.

7. Ellenbogen KA, Kaszala K. Cardiac Pacing and ICDs. 7th ed. Hoboken, NJ: John Wiley & Sons Ltd; 2020.

8. Brandes A, Crijns HJGM, Rienstra M, et al. Cardioversion of atrial fibrillation and atrial flutter revisited: current evidence and practical guidance for a common procedure. Europace. 2020;22(8):1149-1161. doi:10.1093/europace/euaa057

9. Stiell IG, Sivilotti MLA, Taljaard M, et al. Electrical versus pharmacological cardioversion for emergency department patients with acute atrial fibrillation (RAFF2): a partial factorial randomised trial. Lancet. 2020;395(10221):339-349. doi:10.1016/S0140-6736(19)32994-0

10. Asirvatham SJ, Friedman PA, Hayes DL. Cardiac Pacing, Defibrillation and Resynchronization: A Clinical Approach. 4th ed. Hoboken, NJ: John Wiley & Sons Ltd; 2021.

Author Bio

Sydney Murphy is the Associate Editor of HealthDay Physicians Briefing and a freelance science writer based in New York City. You can follow her on Twitter @SydneyLiz_Murph.

The post Cardiac Resynchronization Therapy & Cardiac Pacing appeared first on The Cardiology Advisor.

As a prevalent medical complaint, chest pain differential diagnosis often is needed. There are numerous causes of chest pain, some of them life-threatening, and it accounts for 5% of all emergency hospital visits.¹ It is most commonly caused by acute coronary syndrome, but chest pain also can be caused by factors including: gastrointestinal reflux disease (the most common non-cardiac cause of chest pain),² pulmonary embolisms, pericarditis, and musculoskeletal factors.

Chest pain is reported in 7% to 24% of primary care visits,³ with the risk increasing after the age of 30. When a patient presents to a health care facility with chest pain, this chest pain should be triaged with a high priority level. An ECG should be administered to patients with suspected cardiac etiology of their chest pain, and the ECG results used to determine the necessary care plan.⁴

Chest Pain Risk Factors

There is a wide range of risk factors that can increase a patient’s risk of experiencing chest pain.

• Risk factors for acute coronary syndrome can include a family history of cardiac disease, prior myocardial infarction, hypertension and/or hyperlipidemia, and diabetes.¹
• Pulmonary embolism risk factors include previous incidences of pulmonary embolism or deep vein thrombosis, use of hormonal medication, recent incidents of surgery, cancer, or an inability to walk.¹
• Other risk factors can include drug and tobacco use, recent endoscopies, bleeding disorders, or kidney disease.¹

Prognosis

Chest pain can be life-threatening in some cases, but the prognosis will vary based on the causes of chest pain. For acute coronary syndrome patients, the prognosis remains poor, despite many modern advancements in diagnosis and treatments. In patients whose chest pain symptoms were caused by myocardial infarction, research estimates that, within a year, 23% of women and 18% of men aged 40 and over will have died.⁵

For patients with non-cardiac chest pain, prognosis is good, with less severe effect on mortality. However, ongoing non-cardiac chest pain can decrease a person’s quality of life.²

Chest Pain Diagnosis & Presentation

If a patient presents with chest pain, it can often be difficult for them to describe it or identify its precise point of origin. This creates a challenge for medical professionals in chest pain diagnosis. If they can identify the source of the pain, health professionals should ask questions about the chest pain, including:

• When the chest pain began
• How long the chest pain has lasted
• What the patient was doing when the chest pain began
• If they can identify exactly where they feel the chest pain

For visceral pain, which is chest pain associated with internal organs, the pain tends to be described as deep, dull, and aching, and can also include vomiting and nausea. In contrast, somatic pain tends to be a stabbing, sharp pain that can be traced to one clear location in the body.⁶ Note that not every case presents with typical symptoms. Women and people with diabetes tend to have atypical symptoms or no symptoms of myocardial infarction.

The evaluation of the patient with chest pain should begin with a full physical examination. Clinicians should ask plenty of questions to get them to describe how the chest pain feels, as mentioned above. A chest pain physical exam should include the following:

• A check of the patient’s general appearance and distress levels
• Vital signs
• Skin and neck exams
• Chest, skin, heart, lung, and abdominal exams
• A check of the limbs for swelling and calf pain

Patients should be asked about potential risk factors and have a thorough review of their medical history, including family history of cardiac disease and the patient’s history of tobacco and drug use.

When the patient presents with chest pain symptoms, it’s important to rule out life-threatening conditions like acute coronary syndrome. The patients with the highest risk of acute coronary syndrome may present with the following:

• Male gender
• Over the age of 60
• Chest pain that feels like pressure and moves into the shoulder, arm, and/or neck

Once it’s determined the chest pain is not cardiac in origin, pleuritic or chest wall pain may also be considered. Pleuritic chest pain differential diagnosis often is identified by the following symptoms⁶:

• Muscle tension localized to one part of the body
• No coughing
• Chest pain that’s described as ‘stinging’
• Reproducibility on palpation

Chest Pain Workup & Chest Pain Physical Exam Findings

When diagnosing chest pain, there are many effective tools. When determining the causes of chest pain, one effective tool is HEART, a chest pain differential diagnosis mnemonic. HEART⁷ was developed in the Netherlands in 2008 as a risk assessment tool for cardiac heart pain. HEART stands for:

• H: History
• E: Electrocardiogram (ECG)
• A: Age
• R: Risk factors
• T: Troponin (Levels of troponin above 0.4 can indicate that the patient has experienced myocardial infarction.)

Each factor above corresponds to a numeric ranking, which is then added up and used to group patients into low, moderate, or high risk of life-threatening cardiac emergencies. Low-risk patients may be safe to discharge, while patients with higher risk levels may need further examination or urgent medical treatment.

Other diagnostic tools include:

• Chest X-rays
• Complete blood work
• Computed tomography
• Pulmonary angiography
• Ultrasound

Chest Pain Differential Diagnosis

Due to the vague nature of chest pain, it can be representative of a wide range of medical conditions.⁸ Chest pain differential diagnosis can be broken down into categories:

• Cardiac: acute coronary syndrome, pericarditis, congestive heart failure, post-cardiac injury syndrome
• Hematologic: sickle cell anemia, pleural effusion
• Gastrointestinal: pancreatitis, inflammatory bowel disease, bacterial pleurisy
• Infections: abscesses to the liver, lung, or spleen, bacterial and viral infections

Other categories of chest pain differential diagnosis are iatrogenic, pulmonary, rheumatologic, and renal.

Once a thorough examination has been performed, medical professionals should be able to accurately diagnose the causes of chest pain and recommend the appropriate treatment. If, after examination, the exact cause of chest pain still can not be identified, the patient should be referred to a specialist for further testing.

Chest Pain ICD 10 Codes

Here are chest pain ICD 10 codes relevant to any differential diagnosis for chest pain, specified or otherwise:

References

1. Johnson, K, Ghassemzadeh, S. Chest Pain. In: StatPearls. NCBI Bookshelf version. StatPearls Publishing, 2022. Accessed September 6, 2022.

2. Fass, R, Achem, S. Noncardiac Chest Pain: Epidemiology, Natural Course and Pathogenesis. J Neurogastroenterol Motil. 2011 Apr; 17(2): 110–123. doi: 10.5056/jnm.2011.17.2.110

3. Katerndahl, D. Chest Pain and Its Importance in Patients With Panic Disorder: An Updated Literature Review. Prim Care Companion J Clin Psychiatry. 2008; 10(5): 376–383. doi: 10.4088/pcc.v10n0505

4. Herren, K, Mackway-Jones, K. Emergency management of cardiac chest pain: a review. Emergency Medicine Journal.  2001;18:6-10.

5. Kolansky, D. Acute coronary syndromes: morbidity, mortality, and pharmacoeconomic burden. Am J Manag Care. 2009 Mar; 15(2 Suppl): S36-41.

6. Clarke, J. Introductory Chapter: The Patient Presenting with Chest Pain. Differential Diagnosis of Chest Pain. 2020. doi: 10.5772/intechopen.91925

7. Brady, W, de Souza, K. The HEART score: A guide to its application in the emergency department. Turk J Emerg Med. 2018 Jun; 18(2): 47–51. doi: 10.1016/j.tjem.2018.04.004

8. Reamy, B, Williams, P, Ryan, M. Pleuritic Chest Pain: Sorting Through the Differential Diagnosis. Am Fam Physician. 2017;96(5):306-312.

Author Bio

Katie Dundas is an American health writer currently based in Sydney, Australia. After moving overseas, she worked for seven years with the Prostate Cancer Foundation of Australia, managing health awareness and advocacy programs, and has been a freelance health writer for the last three years, with a focus on patient care.

Updated: 04/12/2023

The post Chest Pain Differential Diagnosis appeared first on The Cardiology Advisor.

Arterial catheterization may occur through the radial, ulnar, axillary, brachial, dorsalis pedis, posterior tibial, or femoral arteries.¹ In the case of femoral artery catheterization, the catheter is inserted into the femoral artery, one of the main arteries of the lower limb,² through a small incision in the groin. This catheter can then be used to measure blood pressure or to inject contrast medium into the artery for angiography.

Arterial catheterization is a medical procedure that typically occurs in the intensive care or surgical setting.¹ This procedure requires the insertion of a catheter into an artery to monitor blood pressure, allowing access to frequent blood sampling and evaluation of intravascular volume status.¹ Other indications include cardiac catheterization, transfusions, and extracorporeal membrane oxygenation.¹

Femoral artery catheterization is commonly used for cardiac catheterization, a procedure that may be used for diagnostic or therapeutic purposes.³ For example, patients may have first-line non-invasive testing for common cardiac complaints such as chest pain or cardiac arrhythmias, and if this initial testing does not yield adequate data, cardiac catheterization via the femoral artery may be used for further evaluation.³

Left heart catheterization is considered the gold standard of coronary artery disease diagnosis; however, the procedure is also used therapeutically in patients with congenital heart defects, arrhythmias, or those requiring cardiac valve replacement.³

Diagnostic Workup/Differential Diagnosis to Identify Appropriateness

The assessment for contraindications to the placement of an arterial catheter is an essential part of the diagnostic workup to identify the appropriateness of the procedure. Important contraindications to catheterization include arterial insufficiency, vascular disease, and infection at the catheterization site.¹

To assess for arterial insufficiency, the femoral artery anatomic site should be inspected carefully, and peripheral pulses should be documented.³

Though there are no absolute contraindications to cardiac catheterization, relative contraindications include severe uncontrolled hypertension, unstable arrhythmias, acute cerebrovascular accidents, and severe coagulopathies.³ If radiographic contrast dye is used during the catheterization procedure, history of allergy to radiographic contrast dye, as well as renal function must be assessed.³

In preparation for the femoral artery catheterization procedure, hemoglobin, platelets, creatinine, and coagulation profile should also be analyzed.³

Femoral Artery Catheterization: Device Overview & Selection Options

Equipment for artery catheterization procedures is typically packaged in commercially bundled kits containing catheter-related equipment and infection control materials.¹ These kits typically comprise appropriately-sized catheter and search needle, lidocaine, chlorhexidine solution, gauze tissue, sterile gloves, masks and gowns, and a guidewire.¹

Equipment required specifically for cardiac catheterization include coronary wires, balloons, stents, and ultrasound.³ Cardiac catheterization is usually performed in a cardiac catheterization laboratory equipped with a fluoroscopy machine and hemodynamic monitors.³

After the femoral artery catheterization procedure, a vascular closure device may be used to achieve hemostasis at the catheterization site.² Although mechanical compression at the site can be used to achieve hemostasis, this method can be especially challenging in patients who are obese and medically anticoagulated.² These vascular closure devices may be passive (eg, devices that help healthcare workers with mechanical compression) or active (eg, suture devices, collagen plugs, and clips that expedite hemostasis).²

Patient & Special Populations Considerations

Due to the risk of bleeding associated with femoral artery catheterization, patients with anticoagulation disorders and patients undergoing medical anticoagulation represent an important special population.¹ These patients should be considered especially carefully when assessing the appropriateness of the femoral catheterization procedure.¹ Although severe coagulopathies represent a relative contraindication to cardiac catheterization, the procedure may still be performed in this patient population after the appropriate risk-benefit analysis.³

For patients who are medically anticoagulated, oral anticoagulants are typically stopped at least 24 hours before the catheterization procedure.³

Due to the relatively small size of arteries, multiple catheter insertion attempts may required; as a result, pediatric patients represent another special population for arterial catheterization procedures.^1,4 Previously identified pediatric risk factors for complications related to catheterization procedures include infants and children aged 5 months to 2 years, the presence of systemic infection, and the number of days in hospital.⁴ Due to the increased likelihood of complications of catheterization procedures in the pediatric population, the risks-benefit analysis of performing the procedure must be carefully considered.¹

Patients with burns or surgical interventions at the catheterization site also should be given special consideration.¹

Monitoring After Femoral Artery Catheterization

In adult patients, complications related to artery catheterization have been reported in 10 to 13% of cases; therefore, monitoring for complications is especially important.¹

Hematomas and active bleeding represent some of the most common complications.⁵ To prevent bleeding, mechanical compression at the site or a closure device may be used.² Mechanical compression remains the “gold standard” for achieving hemostasis and involves at least 10 minutes of firm pressure proximal to the puncture site.² After hemostasis is achieved via mechanical compression or closure device, patients also require bed rest and monitoring for any retroperitoneal bleeding for at least 8 hours.²

Additional complications of primary importance include infection and inflammation at the site, mechanical complications related to the medical equipment used for the procedure, embolic or thrombotic events, and amputation due to ischemic injury.¹ To prevent infection, appropriate aseptic techniques should be used.¹

Amputation due to ischemic injury can occur due to obstruction of the femoral artery during or after the catheterization procedure, because no other major collateral arterial vessels exist in the lower limb.¹

Complications specifically due to cardiac catheterization include myocardial infarction, pericardial effusion, cardiac tamponade, and aortic or coronary artery dissection.³

Finally, if contrast dye is used, additional contrast-related complications may include allergic reaction or renal dysfunction.³

Implementation of ultrasound guidance reduces the risk of cardiovascular complications, and ultrasound-guided catheterization is currently the standard of care.^1,6 As previously stated, the use of vascular closure devices may also improve patient outcomes.⁵

References

1. Pierre L, Pasrija D, Keenaghan M. Arterial Lines. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022. Updated May 8, 2022. Accessed August 30, 2022.

2. Rao SS, Agasthi P. Femoral Vascular Closure Devices After Catheterization Procedure. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022. Updated Jun 21, 2022. Accessed August 30, 2022.

3. Ahmed I, Hajouli S. Left Heart Cardiac Catheterization. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022. Updated 2022 Jul 1. Accessed August 30, 2022.

4. Hebal F, Sparks HT, Rychlik KL, Bone M, Tran S, Barsness KA. Pediatric arterial catheters: Complications and associated risk factors. J Pediatr Surg. 2018;53(4):794-797. DOI: 10.1016/j.jpedsurg.2017.08.057

5. Castillo-Sang M, Tsang AW, Almaroof B, et al. Femoral artery complications after cardiac catheterization: a study of patient profile. Ann Vasc Surg. 2010;24(3):328-335. DOI: 10.1016/j.avsg.2009.06.025

6. Rashid MK, Sahami N, Singh K, Winter J, Sheth T, Jolly SS. Ultrasound Guidance in Femoral Artery Catheterization: A Systematic Review and a Meta-Analysis of Randomized Controlled Trials. J Invasive Cardiol. 2019;31(7):E192-E198.

Author Bio

Anna Courant is a nurse practitioner and writer.

The post Femoral Artery Catheterization appeared first on The Cardiology Advisor.

Fractional flow reserve (FFR) is a diagnostic cardiac catheterization technique used to measure blood flow and pressure in an isolated segment of the coronary artery. FFR is the current standard of care for the evaluation of lesions in intermediate-grade stenosis. It is more precise than non-invasive techniques in determining the functional significance and ischemic potential of the observed lesion.^1,2

FFR Definition & Description

FFR is defined as ratio of pressure measured in coronary segment distal to stenosis (Pd) and pressure measured proximal to stenosis, usually aortic pressure (Pa) or pressure measured in healthy proximal coronary segment. Fractional flow reserve formula is FFR = Pd/Pa.³ FFR is measured using guidewires equipped with micromanometer pressure sensors.² The coronary guidewires are inserted via transradial or transfemoral catheterization.⁴

FFR was originally defined as the ratio of proximal and distal blood flow across the coronary stenosis. The blood flow is related to pressure through coronary arterial resistance (R = pressure/flow). Under the condition of minimal distal resistance, the relationship between pressure and flow becomes linearized, and the pressure, which is easier to measure, can be used as a proxy for the blood flow across the coronary stenosis.^2,5

For measurement accuracy, it is necessary to achieve stable pressure under hyperemia, a physiological state of maximal coronary blood flow and minimal vascular resistance.⁶ This is achieved by administration of adenosine by intravenous continuous infusion (140 mcg/kg/min) or intracoronary bolus (50 to 100 mcg into the right coronary artery, 100 to 200 mcg into left coronary artery). In a healthy coronary artery with normal blood flow, the FFR value equals 1, indicating no obstruction to blood flow present. The presence of coronary stenosis lowers Pd/Pa ratio. An FFR of 0.8 or lower identifies coronary stenosis that induces ischemia with 90% accuracy.^6,7

FFR Indication

FFR is indicated in patients with stable coronary artery disease (CAD) to determine ischemic potential of intermediate coronary stenosis observed on invasive coronary angiograms (ICA).^7,8 ICAs alone cannot reliably identify hemodynamically significant stenosis.⁹ FFR can overcome this limitation. When noninvasive tests are inconclusive in patients that present with persistent chest pain and moderate coronary stenosis, FFR reliably indicates functionally significant coronary stenosis and guides revascularization decision avoiding unnecessary interventions.⁷

Several large-scale clinical trials have evaluated FFR for use in assessment of coronary stenosis severity and guidance for revascularization.^4,10 The DEFER trial demonstrated safety and efficacy on deferral of percutaneous coronary intervention (PCI) in patients with FFR of 0.75 or higher.¹¹ The FAME trial showed a reduction in major adverse cardiac events (MACE – death, myocardial infarction and revascularization) and in revascularization in patients with multivessel disease undergoing FFR-guided PCI compared to PCI alone.¹²

The FAMEII trial demonstrated that FFR-guided PCI in stable CAD patients with FFR of 0.8 or lower, combined with optimal medical therapy, decreased the incidence of MACE relative to optimal medical therapy alone.¹³ The efficacy of FFR-guided PCI was confirmed at 3 and 5 years follow-up in the FAMEII trial.^14,15 Based on the results of clinical trials, FFR was given class I, level A recommendation by the European Society of Cardiology and European Association for Cardio-Thoracic Surgery for identification of hemodynamically relevant stenosis and to guide PCI in patients with multivessel disease.¹

The American College of Cardiology/American Heart Association/Society for Cardiovascular Angiography and Intervention (SCAI) designated FFR as reasonable for the evaluation of intermediate stenosis and helpful in guiding revascularization decisions in patients with stable ischemic heart disease (class IIa, level A).¹⁶ A recent SCAI consensus statement recommends expanded use of FFR when non-invasive imaging is unavailable or inconclusive.¹⁷

Other Indications

FFR has been evaluated in the following special clinical scenarios:⁶

• Acute coronary syndrome to assess non-culprit artery lesions
• Left main coronary artery stenosis
• Multivessel disease
• Assessment prior to coronary artery bypass grafting (CABG)
• Diffuse atherosclerosis
• Sequential stenosis
• Bifurcation and ostial branch stenosis

Relevant Metrics

Table 1. Main hyperemic and non-hyperemic indices for assessment of coronary lesions:²

FFR Complications & Contraindications

There are no absolute contraindications for FFR tests.³ Second and third degree atrioventricular blocks, sick sinus syndrome without pacemaker, prolong QT- interval, severe hypotension, heart failure and obstructive pulmonary disease are relative contraindications for intravenous administration of adenosine. Generally, invasive diagnostic procedures should not be attempted if invasive therapeutic options don’t exist.

FFR test measurements have limitations in patients with small-vessel disease, diffuse coronary artery disease and left ventricular hypertrophy.¹⁸ These conditions may lead to underestimation of severity of coronary stenosis due to the restriction in blood flow after pharmacological vasodilation and corresponding decrease in distal coronary blood pressure.

Several comorbidities can influence performance and safety of FFR tests.³ The accuracy of FFR tests may be affected in older patients due to the age-associated changes in microvasculature, leading to higher observed FFR values independent of degree of stenosis. Similarly, patients with diabetes mellitus can have falsely elevated FFR values due to microvasculature pathology and impaired response to vasodilators administered during the test. This could lead to reduced treatment of elderly and diabetic patients when FFR values are used as guidelines.

Although the true effect of the diseased microvasculature on FFR values is still debated, it has been shown that PCI interventions guided by FFR are equally beneficial in patients older than 65 years of age with multivessel disease as in younger patients with the same disease and in patients with and without diabetes, compared to angiography-guided PCI.

References

1. Neumann FJ, Sousa-Uva M, Ahlsson A, et al. 2018 ESC/EACTS Guidelines on myocardial revascularization. Eur Heart J. 2018;40(2):87-165.

2. Okutucu S, Cilingiroglu M, Feldman MD. Physiologic Assessment of Coronary Stenosis: Current Status and Future Directions. Curr Cardiol Rep. 2021;23(7):88.

3. Peper J, Becker LM, Kuijk JP van, Leiner T, Swaans MJ. Fractional Flow Reserve: Patient Selection and Perspectives. Vasc Heal Risk Management. 2021;17:817-831.

4. Achenbach S, Germany D of C Friedrich Alexander University (FAU) Erlangen Nuremberg, Rudolph T, et al. Performing and Interpreting Fractional Flow Reserve Measurements in Clinical Practice: An Expert Consensus Document. Interventional Cardiol Rev. 2017;12(02):97.

5. Pijls NH, Son JA van, Kirkeeide RL, Bruyne BD, Gould KL. Experimental basis of determining maximum coronary, myocardial, and collateral blood flow by pressure measurements for assessing functional stenosis severity before and after percutaneous transluminal coronary angioplasty. Circulation. 1993;87(4):1354-1367.

6. Chowdhury M, Osborn EA. Physiological Assessment of Coronary Lesions in 2020. Curr Treat Options Cardiovasc Medicine. 2020;22(1):2.

7. Pijls NHJ, Bruyne B de, Peels K, et al. Measurement of Fractional Flow Reserve to Assess the Functional Severity of Coronary-Artery Stenoses. New Engl J Medicine.1996;334(26):1703-1708.

8. Bruyne BD, Fearon WF, Pijls NHJ, et al. Fractional Flow Reserve–Guided PCI for Stable Coronary Artery Disease. New Engl J Medicine. 2014;371(13):1208-1217.

9. Tonino PAL, Fearon WF, Bruyne BD, et al. Angiographic Versus Functional Severity of Coronary Artery Stenoses in the FAME Study Fractional Flow Reserve Versus Angiography in Multivessel Evaluation. J Am Coll Cardiol. 2010;55(25):2816-2821.

10. Bertolone DT, Gallinoro E, Esposito G, et al. Contemporary Management of Stable Coronary Artery Disease. High Blood Press Cardiovasc Prev. 2022;29(3):207-219.

11. Zimmermann FM, Ferrara A, Johnson NP, et al. Deferral vs. performance of percutaneous coronary intervention of functionally non-significant coronary stenosis: 15-year follow-up of the DEFER trial. Eur Heart J. 2015;36(45):3182-3188.

12. Pijls NHJ, Fearon WF, Tonino PAL, et al. Fractional Flow Reserve Versus Angiography for Guiding Percutaneous Coronary Intervention in Patients With Multivessel Coronary Artery Disease 2-Year Follow-Up of the FAME (Fractional Flow Reserve Versus Angiography for Multivessel Evaluation) Study. J Am Coll Cardiol. 2010;56(3):177-184.

13. Bruyne BD, Pijls NHJ, Kalesan B, et al. Fractional Flow Reserve–Guided PCI versus Medical Therapy in Stable Coronary Disease. New Engl J Medicine. 2012;367(11):991-1001.

14. Fearon WF, Nishi T, Bruyne BD, et al. Clinical Outcomes and Cost-Effectiveness of Fractional Flow Reserve–Guided Percutaneous Coronary Intervention in Patients With Stable Coronary Artery Disease. Circulation. 2018;137(5):480-487.

15. Nunen LX van, Zimmermann FM, Tonino PAL, et al. Fractional flow reserve versus angiography for guidance of PCI in patients with multivessel coronary artery disease (FAME): 5-year follow-up of a randomised controlled trial. Lancet. 2015;386(10006):1853-1860.

16. Members WC, Levine GN, Bates ER, et al. 2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention. Circulation. 2011;124(23):e574-e651.

17. Patel MR, Calhoon JH, Dehmer GJ, et al. ACC/AATS/AHA/ASE/ASNC/SCAI/SCCT/STS 2017 Appropriate Use Criteria for Coronary Revascularization in Patients With Stable Ischemic Heart Disease A Report of the American College of Cardiology Appropriate Use Criteria Task Force, American Association for Thoracic Surgery, American Heart Association, American Society of Echocardiography, American Society of Nuclear Cardiology, Society for Cardiovascular Angiography and Interventions, Society of Cardiovascular Computed Tomography, and Society of Thoracic Surgeons. J Am Coll Cardiol. 2017;69(17):2212-2241.

18. Pijls NHJ, Bruyne B de, Peels K, et al. Measurement of Fractional Flow Reserve to Assess the Functional Severity of Coronary-Artery Stenoses. New Engl J Medicine.1996;334(26):1703-1708.

Author Bio

Ivana Celic, PhD, is a biomedical scientist and freelance medical and scientific writer. Her research interests include genome plasticity, cancer, aging, neurodegenerative disease, and infertility. She actively participates in laboratory research and scientific writing and presentations.

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Glycoprotein IIb/IIIa inhibitors are a class of drugs that prevent the binding of fibrinogen to platelets. This class of drugs includes abciximab, eptifibatide, and tirofiban.¹ Glycoprotein IIb/IIIa inhibitors are approved by the FDA to treat acute coronary syndromes (ACS) including unstable angina and non-ST elevation myocardial infarction that needs percutaneous coronary intervention (PCI).^1-3

Symptoms of ACS include chest pain, nausea, sweating, dizziness or lightheadedness, shortness of breath, and discomfort or pain in the jaw, neck, back, stomach, or arms.⁴ Myocardial infarction symptoms can appear quickly, whereas symptoms of unstable angina often do not follow a pattern and may actually get worse during rest.

Risk factors for ACS include diabetes, smoking, high cholesterol, hypertension, obesity or overweight, family history of heart disease, stroke, or chest pain.⁴

The American College of Cardiology/American Heart Association currently recommends use of glycoprotein IIb/IIIa inhibitors in the treatment of ACS in patients:

• Unable to tolerate P2Y12 inhibitors, such as clopidogrel, ticlopidine, ticagrelor, prasugrel, and cangrelor⁵
• With allergy to P2Y12 inhibitors¹
• Undergoing PCI who have gotten P2Y12 inhibitors but have a high risk of thrombus and an aspirin allergy.¹

Diagnostic Workup/Differential Diagnosis

Patients presenting with chest pain should undergo a 12-lead electrocardiogram.⁶ Treatment is based on whether there is ST-segment elevation myocardial infarction (STEMI) present or not. If there is STEMI, the patient should undergo PCI or fibrinolytic therapy. If there is no STEMI, ACS risk should be classified as low, intermediate, or high. Cardiac troponin levels aid in determining risk.

Other causes of chest pain to rule out include:⁶

• Acute aortic dissection
• Pericarditis
• Heart failure
• Gallbladder disease
• Gastroesophageal reflux
• Nonulcer dyspepsia
• Peptic ulcer
• Pancreatitis
• Costochondritis
• Strained chest muscle
• Panic attack
• Somatoform disorder
• Pulmonary causes, such as pneumonia, pneumothorax, or pulmonary embolism

Before a decision is made to initiate a glycoprotein IIb/IIIa inhibitor, check INR, PT, and aPTT levels, ask about any drug allergies or intolerances, and review possible contraindications of treatment with glycoprotein IIb/IIIa inhibitors.¹

Glycoprotein IIb/IIIa Inhibitors: Pharmacotherapy Management

Glycoprotein IIb/IIIa (GP IIb/IIIa) inhibitors block subunits α and β on glycoprotein receptors of the platelet’s membrane. The GPIIb/IIIa receptor is the primary platelet receptor in platelet aggregation. This inhibition interferes with fibrinogen and von Willebrand factor binding. Drugs in this class are given intravenously along with aspirin and include abciximab, tirofiban, and eptifibatide.¹

Abciximab is approved to prevent ischemic complications in patients who are undergoing percutaneous coronary intervention (PCI), or with unstable angina that does not respond to antianginal drugs when PCI is scheduled within 24 hours.⁷

The recommended dosage of abciximab in adults is a 0.25 mg/kg intravenous bolus given 10 to 60 minutes before PCI. This is followed by a continuous intravenous infusion of 0.125 µg/kg/min (to a maximum of 10 µg/min) for 12 hours.

Patients with unstable angina that is not responsive to medical therapy and who are scheduled to undergo PCI within 24 hours may receive a bolus dose of abciximab 0.25 mg/kg followed by an 18- to 24-hour intravenous infusion of 10 µg/min, stopping one hour after the PCI.

Eptifibatide is approved in patients with ACS, and those undergoing PCI and stenting to lower the risk of death or new myocardial infarction.² The dosage is as follows:

• ACS: 180 mcg/kg IV bolus immediately after diagnosis followed by continuous infusion at 2 mcg/kg/min
• PCI: 180 mcg/kg IV bolus immediately before PCI followed by continuous infusion at 2 mcg/kg/min Add a second 180 mcg/kg bolus at 10 minutes

Tirofiban is approved in patients with non-ST-elevation acute coronary syndrome (NSTE-ACS) to lower the rate of death, myocardial infarction, refractory ischemia, and need to repeat cardiac procedure.³ The dosage is 25 mcg/kg given intravenously within 5 minutes and then 0.15 mcg/kg/min for up to 18 hours.

Complications of Glycoprotein IIb/IIIa Inhibitors

Glycoprotein IIb/IIIa inhibitors side effects include bleeding, hypotension, bradycardia, and thrombocytopenia.¹ Other complications to monitor include the risk of anaphylaxis.⁷

Absolute contraindications to treatment with glycoprotein IIb/IIIa inhibitors include major bleeding diathesis, active internal bleeding, and history of hemorrhagic stroke within 30 days.¹ Relative contraindications include history of thrombocytopenia, stroke, severe hypertension, or major surgery in the past six weeks. Possible contraindications include renal impairment and intracranial disease.

Monitoring

Patients should be monitored for thrombocytopenia which may occur as soon as 24 hours after treatment with glycoprotein IIb/IIIa inhibitors.¹ The platelet count should be checked within four hours of the start of the infusion and again at 24 hours. Signs and symptoms of bleeding, such as blood in the urine or vomit, should also be monitored.⁷

The infusion of glycoprotein IIb/IIIa inhibitors should be stopped if the platelet count drops below 100,000/mm.¹ Patients at high risk for thrombus should remain in intensive care if the glycoprotein IIb/IIIa inhibitors need to be continued. Typically, it takes up to two weeks for the platelet count to return to normal.

Because eptifibatide is cleared by the kidneys, patients with decreased renal function (ie, estimated creatinine clearance less than 50 ml/min) should receive the following adjusted dosage of eptifibatide: 180 mcg/kg IV bolus just before PCI followed by continuous infusion of 1 mcg/kg/min and a second bolus of 180 mcg/kg.²

References

1. Tummala R, Rai MP. Glycoprotein IIb/IIIa Inhibitors. In: StatPearls. NCBI Bookshelf version. StatPearls Publishing; 2022.

2. U.S. Food and Drug Administration. Integrilin (eptifibatide) injection, for intravenous use. February 2021. Accessed September 8, 2022.

3. U.S. Food and Drug Administration. Aggrastat (tirofiban hydrochloride) injection, for intravenous use. May 2019. Accessed September 8, 2022.

4. Acute Coronary Syndrome.  American Heart Association. 2022. Accessed September 8, 2022.

5. U.S. National Library of Medicine. Antiplatelet drugs – P2Y12 inhibitors. July 2020. Accessed September 8, 2022.

6. Barstow C, Rice M, McDivitt JD. Acute Coronary Syndrome: Diagnostic Evaluation. Am Fam Physician. 2017;95(3):170-177.

7. U.S. Food and Drug Administration. ReoPro® abciximab for intravenous administration. August 2019. Accessed September 8, 2022.

Author Bio

Jen Seabright, PharmD, is a freelance medical writer located in Pittsburgh, PA.

The post Glycoprotein IIb/IIIa Inhibitors appeared first on The Cardiology Advisor.

Epidemiology

Cardiovascular diseases in general cause an estimated 17.9 million deaths annually, accounting for 32% of all-cause mortality globally.¹  Heart failure (HF) affects approximately 26 million people around the world, and its prevalence increases each year, impacted by an aging population and improvements in survival.²

The American Heart Association (AHA) reported that 6.2 million people had heart failure in the United States between 2013 and 2016. In 2021, the AHA Statistical Update estimated the prevalence of heart failure to be 6 million, approximately 1.8% of the total US population.³ Researchers predict a 46% increase in heart failure prevalence by 2030, reaching more than 8 million people in the US.¹

Congestive heart failure (CHF) is more prevalent in older age groups. A 2012 study showed a 4.3% prevalence of CHF in people between 65 and 70 years old.⁴

Etiology of Heart Failure and Risk Factors

Heart failure is the inability to provide sufficient cardiac output for adequate oxygenation and perfusion of the body’s tissues while maintaining normal filling pressures.⁵  It can present as acute heart failure or with gradual progression of symptoms.

The most common causes of heart failure are:^4,6

• Diabetes
• Hypertension
• Hyperlipidemia
• Sedentarism
• Smoking
• Obesity
• Coronary artery disease
• Myocardial infarction

Genetics can play an important role as a risk factor for heart failure because many of the previously listed conditions are heritable, such as diabetes and hypertension. Arrhythmias and connective tissue disorders, such as Marfan syndrome, are heritable conditions with high risk of heart failure. Patients who have a medical history of these conditions should seek out a health care provider to regularly monitor for potential indications of heart failure.

Healthy lifestyle practices can lower heart failure risk. Common practices that can help maintain a healthy lifestyle and lower this risk include avoiding smoking tobacco, excessive alcohol consumption, high-fat foods, and high-sodium foods; practicing regular physical activity; and managing stress.

Heart Failure Prognosis in Case Studies

Research shows better patient outcomes when heart failure is diagnosed at younger ages. Poorer outcomes are associated with older age at time of diagnosis and in patients with kidney disease, diabetes, or who fall into class III or IV for heart failure in the New York Heart Association Functional Classification (see section below “Presentations of Heart Failure”).⁷

A meta-analysis that included 60 different studies with survival data for 1.5 million heart failure patients showed:⁸

• 1 month survival in 95.7% (95% CI, 94.3%-96.9%) of the studied patients
• 1 year survival in 86.5% (95% CI, 85.4%-87.6%) of the studied patients
• 2 years survival in 72.6% (95% CI, 67.0%-76.6%) of the studied patients
• 5 years survival in 56.7% (95% CI, 54.0%-59.4%) of the studied patients
• 10 years survival in 34.9% (95% CI, 24.0%-46.8%) of the studied patients

This analysis also showed that an increased age at diagnosis was significantly associated with a reduced survival time. In a US-only data analysis, it was shown that the death rate caused by heart failure in the United States varies by state.⁹

Presentations

Heart failure is a chronic condition that has no cure, but it can be controlled with lifestyle changes, medication, and surgery. Heart failure symptoms can appear acutely or develop over time. Common signs and symptoms of heart failure are shortness of breath, fatigue, weakness, swelling of the lower extremities, and a rapid or irregular heartbeat.^10,11,12

Two classification tables are used to determine levels of heart failure in the United States. These tables are used in tandem to determine the functionality and objective level of a person’s heart failure. ¹³

Table 1. Functional Classification

Table 2. Objective Classification

Heart Failure Diagnosis

To properly diagnose chronic heart failure, a health care provider first needs to know about the patient’s lifestyle (e.g., tobacco and alcohol consumption, diet, physical activity) and medical history, including family medical history, to understand if there are any underlying conditions (e.g., diabetes or high blood pressure) that may lead to heart failure.

It is also important to know if the patient has received cancer treatments because cancer is considered a risk factor for heart failure.

Classifications of heart failure depend on the left ventricle ejection fraction (LVEF)¹:

• Heart failure with preserved ejection fraction (HFpEF). This classification is also referred to as diastolic heart failure. The LVEF is greater than or equal to 50%, and it accounts for at least 50% of HF cases.
• Heart failure with mildly reduced ejection fraction (HFmrEF). HFrEF is also known as systolic heart failure. The LVEF is less than or equal to 40%. Patients with HFrEF can show severe symptoms and need immediate treatment.¹⁴
• Heart failure with reduced ejection fraction (HFrEF). This classification is for those cases in between HFrEF and HFpEF, with a LVEF in between 41% and 49%.¹⁴
  

Patients with Suspected Heart Failure Physical Exam Findings

• Heart murmurs. Cardiac arrhythmias can indicate abnormal movement of the blood in the heart, and pulmonary rales.¹⁵
• Blood pressure. A reading of 130/80 mm Hg or higher suggests hypertension, which can increase the risk for heart failure. A low blood pressure reading can also be indicative of late-stage heart failure in correlation with signs and symptoms suggestive of heart failure.
• Blood flow. Examination of proper blood circulation from the arteries can reveal elevated jugular venous pressure in those with heart failure.
• Edema. Edema in legs, feet, and ankles can indicate chronic heart failure.
  

Diagnostic Heart Failure Workup

In some cases of early heart failure, a physical examination won’t show any immediate signs, such as pulmonary rales or peripheral edema. In these cases, specific tests can be performed:⁶

Radiology

• Electrocardiogram (ECG) measures the heart’s electrical activity, which may include a stress test. The ECG may show signs of low voltage indicative of amyloid heart disease, or evidence of a prior myocardial infarction.
• Echocardiogram to search for abnormalities in the heart’s morphology, such as measuring the atrial and ventricular sizes, which could explain changes in ejection fraction, valvular dysfunction, or a structural remodeling. It also measures the filling pressure that, if elevated, could be a sign of HFpEF or HFmrEF.
• Chest radiography to observe the heart size, look for pulmonary congestion, or identify the placing of an implanted cardiac device.¹⁶ In this radiography, the health care provider would look for a cardiac to thoracic width ratio above 50 percent, cephalization of the pulmonary vessels, Kerley B-lines, and pleural effusions.

Lab Tests for Heart Failure

Lab tests are used to search for metabolic abnormalities, including:

• Complete blood count (CBC). The CBC may show a low level of red blood cells, a sign of heart failure.
• Thyroid stimulating hormone (TSH). With the counting of TSH, thyroid disease can be assessed. This and other endocrine metabolic diseases are signs of heart failure.
• Ferritin. Ferritin levels <100 mg /L are a sign of iron deficiency that causes anemia. Anemia is a common symptom of heart failure associated with reduced exercise capacity in patients with heart failure.
• Troponin. Elevated troponin concentration occurs in 15% to 70% of patients with heart failure.
• B-type natriuretic peptide (BNP) and N-terminal-pro-BNP (NT-pro-BNP). Increases in BNP and NT-pro-BNP are a sign of elevated ventricular pressure and volume, helping define heart failure in patients with shortness of breath.
• Creatinine

Myocardial Biopsy

In exceptional cases, a myocardial biopsy could be considered when heart failure is suspected to be caused by a muscular disease.

Heart Failure Differential Diagnosis

There are many other diseases or conditions with similar symptoms to heart failure.¹⁷

Table 3. Similar Symptoms Presented in Other Conditions

Management of Heart Failure

A health care provider can recommend different types of therapy depending on the stage of heart failure and severity of symptoms. Therapies may be recommended for long-term use to help manage heart failure and prevent or slow its progression. In some cases, heart surgery or implantation of a heart device may improve the patient’s condition.

Non pharmacotherapy

In cases where heart failure is established but the symptoms are minor, lifestyle modifications can help the patient effectively manage their symptoms.¹⁸

Table 4. Lifestyle Modifications to Manage HF

Pharmacotherapy

Depending on the type of heart failure, a health care provider can prescribe one or a combination of drugs to manage heart failure symptoms.^19,20,4

Table 5. Common Heart Failure Medications

Heart Failure Surgery

In cases of severe heart failure when lifestyle modifications and medication cannot improve symptoms, surgery might be needed to repair heart function.

Table 6. Surgical Options for HF²⁵

Severe Heart Failure and Palliative Care for Patients

In severe cases of heart failure where treatments are insufficient to improve symptoms, a health care provider can recommend palliative care to ease the symptoms and improve the quality of life of the patient.²⁵

Side Effects of Heart Failure Medications

Although they can be effective at treating heart failure symptoms, many drugs can cause side effects including indigestion, nausea, loss of appetite, constipation, and diarrhea. In these cases, switching medication or using other treatments may be recommended. Specific side effects of the most common heart failure medications are listed in Table 7. ²⁰

Table 7. HF Medication Side Effects

Heart Failure Treatment: Drug-Drug Interactions

Heart failure is normally treated with multiple medications so drug interactions are common and should be carefully monitored. Drugs that treat heart failure comorbidities can interact with medication prescribed to treat other pre-existing conditions. Following are some common examples of drug-drug interactions to be aware of:³¹

• Triple pharmacotherapy with ACE inhibitor, angiotensin II receptor blocker, and the hypertension drug, spironolactone, should be avoided since it can lead to severe hyperkalemia.
• Special attention should be taken when treating heart failure patients who are also receiving chemotherapy. Many chemotherapy treatments can cause severe reactions with heart failure medication.
• Analgesics of the NSAID family can exacerbate heart failure symptoms by producing peripheral vasoconstriction and sodium retention that can damage the kidneys. Additionally, NSAID can decrease the efficacy and increase toxicity of diuretics and ACE inhibitors.
• Calcium channel blockers used to treat arrhythmias or hypertension may worsen heart failure by increasing the risk of cardiovascular events. An exception to these problems has been shown when using vasoselective calcium channel blockers which avoids activation of the sympathetic nervous system.
• Antiarrhythmic medication used to correct heart rhythm can sometimes have a proarrhythmic effect that may worsen heart failure.
  

Complications of Heart Failure

Patients living with heart failure may also experience complications from the condition itself. The most common heart failure complications that arise and ways to manage them are listed in Table 8.¹⁸

Table 8. Heart Failure Complications and Management

Heart Failure Guidelines, 2022

Current US guidelines for the treatment of heart failure can be found in the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines.

Heart Failure ICD 10 Codes

Here are all relevant heart failure ICD 10 codes:

References

1. World Heart Organization. Cardiovascular diseases. Accessed July 4, 2022.
2. Savarese G, Lund LH. Global public health burden of heart failure. Card Fail Rev. 2017;3(1):7-11. doi: 10.15420/cfr.2016:25:2
3. Virani SS, Alonso A, Benjamin EJ, et al. Heart disease and stroke statistics—2020 update: A report from the American Heart Association. Circulation. 2020;141(9):e139-e596. doi:10.1161/CIR.0000000000000757
4. American Heart Association. What is heart failure? Updated May 31, 2017. Accessed July 4, 2022.
5. Van Nuys KE, Xie Z, Tysinger B, Hlatky MA, Goldman, DP. Innovation in heart failure treatment: Life expectancy, disability, and health disparities. JACC Heart Fail. 2018;6(5):401-409. doi:10.1016/j.jchf.2017.12.006
6. Ezekowitz JA, O’Meara E, McDonald MA, et al. 2017 Comprehensive Update of the Canadian Cardiovascular Society Guidelines for the Management of Heart Failure. Canadian Journal of Cardiology. 2017;33(11):1342-1433. doi:10.1016/j.cjca.2017.08.022
7. Newton JD, Blackledge HM, Squire IB. Ethnicity and variation in prognosis for patients newly hospitalised for heart failure: A matched historical cohort study. Heart. 2005;91(12):1545-1550. doi:10.1136/hrt.2004.057935
8. Jones NR, Roalfe AK, Adoki I, Hobbs FD, Taylor CJ. Survival of patients with chronic heart failure in the community: A systematic review and meta‐analysis. Eur J Heart Fail. 2019;21(11):1306-1325. doi:10.1002/ejhf.1594
9. Centers for Disease Control and Prevention. Heart failure. Reviewed September 8, 2020. Accessed June 22, 2022.
10. American Heart Association. Heart failure signs and symptoms. Updated May 31, 2017. Accessed July 4, 2022.
11. Roger VL. Epidemiology of heart failure. A contemporary perspective. Circ Res. 2021;128(10):1421-1434. doi:10.1161/CIRCRESAHA.121.318172
12. American Heart Association. Types of heart failure. Updated May 31, 2017. Accessed July 4, 2022.
13. American Heart Association. Classes of heart failure. Reviewed May 31, 2017. Accessed June 22, 2022.
14. Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. JACC. 2022;79(17):e263-e421. doi:10.1016/j.jacc.2021.12.012    
15. History and physical exam for heart failure. Kaiser Permanente. Updated December 19, 2017. Accessed June 22, 2022.
16. Dumitru I. What is the role of chest radiographs in the diagnosis of heart failure? Medscape. Updated March 2, 2021. Accessed June 22, 2022.
17. Heart Failure: Differential Diagnosis. Ioana Dumitru. Updated July 02, 2022. Medscape. Accessed June 22, 2022.
18. Heart Failure. Overview. Mayo Clinic Staff. Updated December 10, 2021. Accessed June 22, 2022.
19. Dumitru I. Heart failure medication. Updated May 13, 2022. Medscape. Accessed June 22, 2022.
20. American Heart Association. Medications used to treat heart failure. Updated May 31, 2017. Accessed July 4, 2022.
21. Heart Failure. Diagnosis. Mayo Clinic Staff. Updated December 10, 2021. Accessed June 22, 2022.
22. Velazquez EJ, Lee KL, Jones RH, et al. Coronary-artery bypass surgery in patients with ischemic cardiomyopathy. N Engl J Med. 2016;374(16):1511-1520. doi:10.1056/NEJMoa1602001
23. Casu G, Merella P. Diuretic therapy in heart failure – Current approaches. Eur Cardiol Review. 2015;10(1):42-47. doi:10.15420/ecr.2015.10.01.42
24. Miller SE, Alvarez RJ. Aldosterone antagonists in heart failure. J Cardiovasc Nurs. 2013;28(6):e47-e54. doi:10.1097/JCN.0b013e3182675e2a
25. Al-Mohammad A. Hydralazine and nitrates in the treatment of heart failure with reduced ejection fraction. ESC Heart Fail. 2019;6(4):878-883. doi:10.1002/ehf2.12459
26. Greenberg B, Neaton JD, Anker SD et al. Association of rivaroxaban with thromboembolic events in patients with heart failure, coronary disease, and sinus rhythm. A post hoc analysis of the COMMANDER HF Trial. JAMA Cardiology. 2019;4(6):515-523. doi:10.1001/jamacardio.2019.1049
27. Moss AJ, Hall WJ, Cannom DS, et al. Cardiac-resynchronization therapy for the prevention of heart-failure events. N Engl J Med. 2009; 361(14):1329-1338. doi:10.1056/NEJMoa0906431
28. Popov AF, Hosseini MT, Zych B, et al. Clinical experience with HeartWare left ventricular assist device in patients with end-stage heart failure. Ann Thorac Surg. 2012;93(3):810-815. doi:10.1016/j.athoracsur.2011.11.076
29. Enriquez-Sarano M, Schaff HV, Orszulak TA, Bailey KR, Tajik AJ, Frye RL. Congestive heart failure after surgical correction of mitral regurgitation. A long-term study. Circulation. 1995;92(9):2496–2503. doi: 10.1161/01.CIR.92.9.2496
30. Alraies MC, Eckman P. Adult heart transplant: Indications and outcomes. J Thorac Dis. 2014;6(8):1120-1128. doi:10.3978/j.issn.2072-1439.2014.06.44
31. Zorn SZ, Thohan V. Drug-drug interactions of common cardiac medications and chemotherapeutic agents. American College of Cardiology. Published December 21, 2018. Accessed July 4, 2022.

Author Bio

Francina Agosti is a freelance science and medical writer based in Canada. She holds a PhD in neuroscience, and she worked in academia for 10 years. Now she writes scientific and medical articles for digital magazines, and she also works as a scientific consultant for biotech and biopharma companies.

The post Heart Failure in the United States appeared first on The Cardiology Advisor.

History

Heart failure is a clinical syndrome that occurs when the heart muscle cannot pump blood effectively.¹ Heart failure is further classified based on symptoms and how well the left ventricle functions.² When the function of the left ventricle is impaired, left ventricular ejection fraction is reduced.² When left ventricular ejection fraction is less than 40%, this is known as heart failure with reduced ejection fraction (HFrEF).² When left ventricular ejection fraction is preserved (i.e., greater than 50%), this is known as heart failure with preserved ejection fraction (HFpEF).²

Some patients are also classified as having mildly reduced ejection fraction (HFmrEF) if their ejection fraction is between 41% and 49%.³ Additional classifications include heart failure with improved ejection fraction (HFimpEF), which is reserved for those who have improved ejection fraction greater than 40% after having previously had reduced ejection fraction that was less than 40%.³ The focus of this article is the subclassification of HFpEF. Heart failure with preserved ejection fraction can be caused by a variety of factors, mostly age-related, including hypertension, diabetes, and obesity.

HFpEF Epidemiology

Between 2013 and 2016, there were approximately 6.2 million people who had heart failure in the US.² More than 50% of patients who have heart failure are classified as having heart failure with preserved ejection fraction.¹ In fact, the incidence of heart failure with preserved ejection fraction (HFpEF) has grown in recent years when compared to the incidence of heart failure with reduced ejection fraction (HFrEF).⁴ Since 2017, heart failure hospitalization also has increased.³

Heart failure is more common in people who are older.¹ Patients who have HFpEF are typically older than patients who have heart failure with reduced ejection fraction (HFrEF).⁵ Heart failure is also more common in African American patients, with a 25% greater prevalence in African Americans compared with Caucasians.² Non-Hispanic African American patients also have the highest death rate per capita due to heart failure.³ Although women are less likely to have HFrEF, the risk for HFpEF is similar between men and women.⁵ Additionally, about half of the patients who have heart failure with preserved ejection fraction (HFpEF) also have five or more major comorbid conditions.⁵

HFpEF Etiology & HFpEF Risk Factors

Heart failure can occur due to diverse etiologies.¹ Common etiologies for heart failure include coronary artery disease, high blood pressure, chronic obstructive pulmonary disease, valvular heart disease, and cardiomyopathies.¹ Other possible causes include congenital heart disease, obesity, diabetes mellitus, and infections.¹ Risk factors for heart failure with preserved ejection fraction (HFpEF) specifically include hypertension in addition to diabetes, kidney disease, atrial fibrillation (AF), and obesity.^1,4,6

HFpEF Prognosis

Patients with HFpEF (heart failure with preserved ejection fraction) have a mortality rate of about 2.9%.¹ Mortality is more likely in patients who have more comorbidities.⁵ Death can occur due to cardiovascular causes or noncardiovascular causes. Noncardiovascular causes are more likely to cause death in patients with heart failure with preserved ejection fraction (HFpEF) when compared with patients with heart failure with reduced ejection fraction (HFrEF).⁵

HFpEF Diagnosis & Presentation

Some patients with stable heart failure with preserved ejection fraction (HFpEF) may have no clinical signs and symptoms.⁵ Patients with HFpEF who do have symptoms present with symptoms that are similar to those of patients with heart failure with reduced ejection fraction (HFrEF).¹ Common symptoms of both HFrEF and HFpEF include dyspnea, orthopnea, edema, abdominal discomfort, fatigue, anorexia, and weakness.¹ If present, these symptoms typically become more severe with exertion.¹ Patients who progress to advanced heart failure may present with symptoms such as resting sinus tachycardia, diaphoresis, narrow pulse pressure, and peripheral vasoconstriction.¹

Diagnosis is based on multiple sources of data including history, clinical signs and symptoms, laboratory findings, and imaging.¹ It is important to note that while findings may be abnormal in patients with HFpEF (heart failure with preserved ejection fraction) who have progressed to decompensated disease, determining the diagnosis is more difficult in patients who are stable or in patients who have only exertional symptoms.⁵

The clinical composite score H₂FPEF may also be used to aid risk stratification and to guide diagnostic workup.³ This score combines patient risk factors, such as obesity, AF, age greater than 60, into a weighted score.³ Patients with a score of less than 2 have low likelihood of having HFpEF, whereas patients with a score greater than 6 have a high likelihood of this disorder.³ A further workup is indicated for patients in the midrange of the score.³

Based on symptoms, laboratory findings, and imaging, the diagnosis of heart failure may be further classified. According to the 2022 ACCF/AHA Guidelines, heart failure may be divided into four stages based on presence of structural changes and presence of symptoms:

• Stage A: At risk for heart failure; patients at high risk for heart failure but no structural heart disease or symptoms of heart failure
• Stage B: Pre-heart failure; patients who have asymptomatic left ventricular dysfunction but no symptoms
• Stage C: Symptomatic heart failure; patients who have heart failure symptoms
• Stage D: Advanced heart failure; patients with refractory heart failure despite optimized treatment³

Additionally, heart failure is classified into New York Heart Association (NYHA) classes based on how heart failure symptoms affect the patient’s daily physical activities and functioning:

• Class I: Patients who have asymptomatic left ventricular dysfunction with no limitations on physical activity or symptoms
• Class II: Patients who have mild symptoms with slight limitation of physical activity
• Class III: Patients who have moderate symptoms with marked limitation of physical activity
• Class IV: Patients who have severe symptoms at rest.¹

Finally, several established criteria for the diagnosis of heart failure based on clinical symptoms are available.⁵ One example is the Framingham criteria, which base the diagnosis on the presence of major symptoms (such as, nocturnal dyspnea and orthopnea, among others) as well as minor symptoms (such as, edema of the extremities and exertional dyspnea, among others).⁵

HFpEF Physical Examination Findings

To assist with diagnosis, a detailed patient history should be collected, and a complete physical exam should be performed.⁴ However, some individuals with heart failure with preserved ejection fraction (HFpEF) who are stable may not present with clinical signs and symptoms.⁵

Patients who do present with symptoms may present with nonspecific physical exam findings such as peripheral edema due to fluid retention.⁷ Orthopnea or bendopnea (shortness of breath when bending forward) may also be present.³

Physical exam should include measurement of patient height and weight, an assessment of the cardiovascular system (including auscultation of heart sounds for irregular rhythm and orthostatic BP measurement), and an assessment of volume status (including peripheral edema, jugular venous distention, and gallop heart sounds).^4,7 Patients may report symptoms including breathlessness, exercise intolerance, or fatigue.^6,7

Collecting past medical history is important because risk factors such as diabetes, AF, hypertension, and kidney disease increase the probability of a heart failure with preserved ejection fraction or HFpEF diagnosis and are included as part of the clinical composite score H₂FPEF.^3,4

Finally, family history focused on history of familial cardiomyopathy or other cardiac history can be an important component for those who may have a heart failure with a genetic component.³

HFpEF Diagnostic Workup

Labs

Important components of the diagnostic workup can include complete blood count (CBC), serum electrolytes, blood urea nitrogen (BUN), serum creatinine, B-type natriuretic peptide (BNP) or N-terminal pro-brain natriuretic peptide (NT-proBNP), glucose, fasting lipid profile, lipid function test, thyroid-stimulating hormone (TSH), and iron studies.^1,3,6 Elevated natriuretic peptide levels of BNP greater than 35 pg/mL or NT-proBNP greater than 125 pg/mL may indicate heart failure with preserved ejection fraction (HFpEF) in patients who are asymptomatic.⁶

These values are especially useful for ruling out heart failure during the diagnostic workup process; however, increased values can occur due to other cardiac causes, such as acute coronary syndrome, and noncardiac causes, such as anemia, pneumonia, renal failure.³ Additionally, higher levels are associated with an increased risk of poor outcomes such as hospitalization and death.³ It is important to note that patients who are obese may have reduced levels of these BNP and NT-proBNP biomarkers.³ Additional genetic testing may also be appropriate in patients who are suspected of having cardiomyopathy due to genetic factors based on gathered family history.³

Imaging

An electrocardiogram (ECG) should be performed and rhythm, rate, and QRS morphology and duration noted.^1,3 Because atrial fibrillation is a risk factor for HFpEF, identifying AF on ECG may be a useful component of the diagnostic workup and is included as part of the clinical composite score H₂FPEF as described above.^3,6 Other abnormal ECG findings such as abnormal repolarization are not specific to the diagnosis of HFpEF.⁶

Other important imaging approaches include chest X-ray and especially the transthoracic echocardiogram (TTE).¹ The chest x-ray may be helpful in assessing for pulmonary etiologies or pulmonary congestion, as well as providing information about the size of the heart.^3,4 The TTE is considered a very useful component of the diagnostic workup because it provides both diagnostic and prognostic information.³ For example, the results of the TTE are used to determine whether the patient has heart failure with reduced ejection fraction (HFrEF) or HFpEF, and this determines the appropriate management approaches.^1,3

Left ventricular ejection fraction, as well as left ventricular diameter, and volume are typically measured.⁶ Echocardiogram findings, such as a nondilated left ventricle with left ventricular ejection fraction greater than 50%, as well as left ventricular hyperplasia and left atrium enlargement are consistent with heart failure with preserved ejection fraction (HFpEF).⁶

Serial TTE may be used to assess patient progress, including any changes to the structures of the heart and changes to the ejection fraction. Repeat imaging is recommended only if the patient experiences new clinical signs and symptoms or to guide management decisions.³ Other imaging modalities that may be performed if more information is needed after the TTE include cardiac MRI, CT, PET.³

Additional Tests & Procedures

Exercise stress testing may be useful for unmasking heart failure symptoms in patients with heart failure with preserved ejection fraction (HFpEF) who are otherwise asymptomatic and can help identify the common comorbidity of coronary artery disease.⁶ Additionally, exercise testing can help assess the functional impact of heart failure, which can aid with heart failure classification.³ Tests that may be used include the cardiopulmonary exercise test (CPET) and the 6 minute walk test.³ Invasive exercise stress testing is also available.⁴

Cardiac catheterization or coronary angiography may also be performed if more information is needed after noninvasive testing.¹ Cardiac catheterization or coronary angiography may also be appropriate for the assessment of heart failure; catheterization for hemodynamic monitoring can be used within the context of acute events such as acute respiratory distress or cardiogenic shock.³

HFpEF Differential Diagnosis

The differential diagnosis for heart failure is broad and spans many body systems. They may include:

• Pulmonary disease: Such as respiratory failure and pulmonary embolism
• Renal disease: Such as acute kidney injury and nephrotic syndrome
• Liver disease: Such as cirrhosis
• Cardiac disease: Such as myocardial infarction
• Infection¹

Identifying the specific etiology is important because treatment can vary based on underlying disease.³

HFpEF Management (Nonpharmacotherapy and Pharmacotherapy)

Patients with heart failure are typically managed by an interdisciplinary team that includes cardiologists, nurses, dieticians, and social workers.³

Nonpharmacotherapy

All patients with heart failure should be advised regarding the nonpharmacotherapy approach of lifestyle changes, including behavioral, dietary modifications, and regular exercise.^1,4 This approach lowers the risk of developing heart failure in those at risk, and also includes smoking cessation and maintaining normal weight, blood pressure (BP), and blood glucose levels.³

While sodium restriction has typically been included in dietary recommendations, there are concerns about the impact of sodium restriction on dietary quality.³ The Dietary Approaches to Stop Hypertension (DASH) diet can help patients restrict sodium while still maintaining appropriate nutrient intake.³

Pharmacotherapy

Whereas many pharmacologic approaches are described for treatment for heart failure in patients with HFrEF, there are no known disease-modifying therapies that improve the outcomes of patients with heart failure with preserved ejection fraction (HFpEF).¹

Because hypertension is one of the main risk factors for HFpEF, controlling blood pressure is the focus of treatment; however, there are no known optimal antihypertensive regimens specifically for patients with HFpEF.^1,3 Therefore, to control BP, medications such as beta blockers, angiotensin-converting enzyme inhibitors (ACEis), angiotensin receptor blockers (ARBs), angiotensin receptor–neprilysin inhibitors (ARNi), or mineralocorticoid receptor agonists (MRAs) may be used.¹

Typically, beta blockers may be preferred in patients with a history of myocardial infarction, symptomatic coronary artery disease, or atrial fibrillation with a rapid ventricular response.³ Treatment of symptoms such as fluid overload may include the use of diuretics.¹

The specific medications which have been studied in patients with HFpEF are the mineralocorticoid antagonist spironolactone and the ARNi sacubitril/valsartan.⁴ Spironolactone, a potassium-sparing diuretic, was shown to improve diastolic function in patients with HFpEF, while sacubitril/valsartan was shown to lower NT-proBNP levels.³

Because patients with HFpEF may have other comorbidities, such as coronary artery disease or AF, pharmacologic management of these conditions via medications such as statins and anticoagulants are also part of the management plan.⁴ Digoxin may be appropriate for rate control of comorbid AF in patients with HFpEF.³

Patients with comorbid diabetes, medications such as the sodium–glucose transport protein 2 (SGLT2) inhibitor dapagliflozin or empaglifozin may be used.⁴ However, these medications may also be useful for reducing heart failure hospitalization in all patients with HFpEF, including those who do not have diabetes mellitus.³

While nitrates and phosphodiesterase-5 inhibitors are often used in the management of patients with heart failure with reduced ejection fraction (HFrEF), these medications have not been shown to be beneficial in patients with HFpEF.³

Implantable Devices

Some patients with heart failure may be candidates for implantable devices such as cardiac resynchronization therapy (CRT) or implantable cardioverter-defibrillator (ICD).³ For patients with associated coronary artery disease, revascularization procedures may be advised.³

Monitoring Side Effects, Adverse Events, Drug-Drug Interactions

Beta Blockers

Beta-blocker common side effects include bradycardia, hypotension, fatigue, dizziness, nausea, constipation, and sexual dysfunction.⁸ Bronchospasm is another possible side effect, and patients with a history of respiratory disease such as asthma should be monitored carefully.⁸ Beta blockers may also exacerbate the symptoms associated with Raynaud disease.⁸ Because beta blockers affect heart rate and blood pressure, these parameters should be monitored closely.⁸ There is also a risk of heart block.⁸

ACE Inhibitors

ACE inhibitors may have side effects including dry cough, dizziness, hypotension, increased BUN and creatinine, syncope, and hyperkalemia.⁹ Less commonly, angioedema can occur and is potentially life-threatening, so patients should be educated and monitored appropriately and the ACE inhibitor discontinued if angioedema occurs.⁹ Patients should also be monitored for cough, because this side effect can decrease medication adherence.⁹

There are multiple contraindications to the use of ACE inhibitors, including absolute contraindications (hypersensitivity reaction with previous ACE inhibitor use, pregnancy) and relative contraindications (patients with abnormal renal function, aortic valve stenosis, or hypovolemia).⁹ Monitoring BP, potassium, and BUN and creatinine may be indicated due to these possible side effects.⁹ Because diuretics can also lead to hypotension, these medications can be discontinued prior to initiating ACE inhibitor therapy to avoid additive effects.⁹

ARBs

ARBs rates of side effects are low.¹⁰ While cough and angioedema are possible side effects, the rate of these are much lower with ARBs than with ACE inhibitors.¹⁰ These medications are also contraindicated in pregnancy, as well as in patients who have bilateral renal artery stenosis or hypotension due to heart failure.¹⁰

Using ARBs in combination with an ACE inhibitor leads to additive effects with regard to hypotension, hyperkalemia, and renal impairment, and patients should be monitored closely when ACE inhibitors and ARBs are given simultaneously.¹⁰ Additionally, because these medications lower blood pressure, BP should be monitored.¹⁰

ARNI in HFpEF: Sacubitril/Valsartan

ARNI sacubitril/valsartan is in a different class but is typically used in place of ACE inhibitors or ARBs in patients who have previously tolerated ACE inhibitors or ARBs.¹¹ Side effects are similar to the side effects of ACE inhibitors and ARBs and include hypotension, hyperkalemia, renal impairment, cough, and angioedema.¹¹ Symptomatic hypotension may occur more often with the use of an ARNI than with the use of ACE inhibitors or ARBs.³

Valsartan Contraindications

Sacubitril/valsartan is also contraindicated in patients who are pregnant, those who are hypersensitive to sacubitril/valsartan, or those who have experienced angioedema with ACE inhibitor or ARB administration.¹¹ This medication should not be given to patients with diabetes who take aliskiren.¹¹ Monitoring BP, potassium, and renal function is also important.¹¹ This medication inhibits the breakdown of BNP, so NT-proBNP levels should be monitored.¹¹

MRA Spironolactone in HFpEF

Common side effects of MRA spironolactone include hyperkalemia and the non-electrolyte hormonal effects such as gynecomastia in men and menstrual irregularities in women.¹² Liver toxicity as evidenced by elevated ALT and AST is a rare side effect, and the medication should be discontinued if this occurs.¹²

Due to the possible side effect of hyperkalemia, this medication is contraindicated in patients who have hyperkalemia, patients who are at an increased risk of developing hyperkalemia, or patients with renal impairment.¹² Monitoring potassium and renal function is important, especially in patients who are also taking ACE inhibitors or ARBs, due to the additive effects of these medications.¹²

SGLT-2 Inhibitors for HFpEF

SGLT-2 inhibitors that may be used especially within the context of comorbid diabetes mellitus (DM), common side effects include genital mycotic infections, nasopharyngitis, urinary tract infections, back pain, influenza, dyslipidemia, constipation, discomfort during urination, and pain in an extremity.¹³ There is the rare side effect of necrotizing fasciitis of the perineum. If this occurs, the patient will be managed with broad-spectrum antibiotics and surgical debridement and the medication should be discontinued.¹³

Contraindications include concurrent use with another SGLT-2 inhibitor or hypersensitivity reaction to the medication.¹³ Because this medication is given within the context of comorbid DM, blood glucose and hemoglobin A1c should be monitored.¹³ Additionally, volume status, renal function, and symptoms of hypoglycemia should be assessed.¹³

Digoxin

Digoxin, which may be used for rate control of comorbid AF, include side effects of nausea, vomiting, anorexia, and visual changes.¹⁴ Digoxin toxicity can also occur when serum concentration is greater than 2 ng/ml.¹⁴ Arrhythmias can occur within the context of digoxin toxicity.¹⁴ Many contraindications exist for the use of digoxin, including acute myocardial infarction, ventricular fibrillation, hypersensitivity to the medication.¹⁴

Digoxin should also be used with caution in patients with renal impairment, AV block, and thyroid disease.¹⁴ Digoxin also interacts with many medications, such as macrolide antibiotics, azole antifungals, loop diuretics, so careful analysis of drug-drug interactions should occur.¹⁴ Due to the potential for toxicity, digoxin levels should be monitored with medication changes or changes in clinical status.¹⁴

Statins

Common side effects of statin medications, used to address comorbid hyperlipidemia, include myopathy, rhabdomyolysis, and hepatotoxicity.¹⁵ Statins are contraindicated in pregnancy and in patients who have liver disease or increased liver enzymes.¹⁵ Some statins are substrates of CYP3A4 and drug-drug interactions can occur with medications that inhibit this enzyme, so the potential for drug-drug interactions should be assessed carefully.¹⁵ Baseline liver function should be assessed, but regular monitoring of liver function is no longer recommended unless there are clinical signs or symptoms of liver toxicity.¹⁵ Typically, lipid panels are performed at baseline and then again in 6 to 12 weeks to assess for efficacy of the statin.¹⁵

Anticoagulants

In anticoagulants, bleeding is the main risk.¹⁶ There are also absolute contraindications (active bleeding, coagulopathy, major trauma) and relative contraindications (gastrointestinal bleeding, low-risk surgery).¹⁶ Monitoring requirements vary based on medication, but routine monitoring is not typically required for direct oral anticoagulants that may be used within the context of atrial fibrillation management.¹⁶ If bleeding is suspected, testing such as CBC and aPTT, may be performed.¹⁶ Reversal agents vary based on medication and may be used in cases of toxicity.¹⁶

Complications of HFpEF

A variety of complications affecting multiple body systems can occur due to heart failure.¹⁷ These heart failure complications include arrhythmias (especially AF), thromboembolism (including stroke, pulmonary embolism, or deep venous embolism), gastrointestinal complications such as hepatic dysfunction due to congestion, musculoskeletal complications such as muscle wasting, and respiratory complications such as pulmonary congestion.¹⁷

Cardiovascular complications that occur specifically as heart failure with preserved ejection fraction (HFpEF) progresses include changes to cardiac reserve and rhythm, stiffening of the ventricles, and endothelial dysfunction, among others.¹⁸ Pulmonary complications of HFpEF include pulmonary hypertension. Pulmonary hypertension is associated with high mortality and morbidity.¹⁹

HFpEF Guidelines

A comprehensive overview of HFpEF guidelines can be found in the 2022 AHA/ACC/HFSA guidelines for the management of heart failure.³

HFpEF ICD 10 Codes

Here is the ICD 10 code for HFpEF:

References

1. Hajouli S, Ludhwani D. Heart failure and ejection fraction. In: StatPearls. NCBI Bookshelf version: 2022. Accessed September 8, 2022.

2. Malik A, Brito D, Vaqar S, et al. Congestive heart failure. In: StatPearls. NCBI Bookshelf version: 2022. Accessed September 8, 2022.

3. Heidenreich P, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol. 2022:e263–e421.

4. Borlaug B. Evaluation and management of heart failure with preserved ejection fraction. Nat Rev Cardiol. 2020:559-573.

5. Dunlay S, Roger V, Redfield M. Epidemiology of heart failure with preserved ejection fraction. Nat Rev Cardiol. 2017:591-602.

6. Pieske B, Tschöpe C, de Boer R, et al. How to diagnose heart failure with preserved ejection fraction: the HFA-PEFF diagnostic algorithm: a consensus recommendation from the Heart Failure Association (HFA) of the European Society of Cardiology (ESC). Eur J Heart Fail. 2019:391-412. doi: 10.1093/eurheartj/ehz641

7. Webb J, Jackson T, Claridge S, Sammut E, Behar J, Carr-White G. Management of heart failure with preserved ejection fraction. Practitioner. 2015:21-23.

8. Farzam K, Jan A. Beta blockers. In: StatPearls. NCBI Bookshelf version: 2022. Accessed September 14, 2022.

9. Goyal A, Cusick A, Thielemier B. ACE inhibitors. In: StatPearls. NCBI Bookshelf version: 2022. Accessed September 14, 2022.

10. Hill R, Vaidya P. Angiotensin II receptor blockers (ARBs). In: StatPearls. NCBI Bookshelf version: 2022. Accessed September 14, 2022.

11. Nicolas D, Kerndt C, Reed M. Sacubitril/valsartan. In: StatPearls. NCBI Bookshelf version: 2022. Accessed September 14, 2022.

12. Patibandla S, Heaton J, Kyaw H. Spironolactone. In: StatPearls. NCBI Bookshelf version: 2022. Accessed September 14, 2022.

13. Padda I, Mahtani A, Parmar M. Sodium-glucose transport protein 2 (SGLT2) inhibitors. In: StatPearls. NCBI Bookshelf version: 2022. Accessed September 14, 2022.

14. David M, Shetty M. Digoxin. In: StatPearls. NCBI Bookshelf version: 2022. Accessed September 21, 2022.

15. Sizar O, Khare S, Jamil R, et al. Statin medications. In: StatPearls. NCBI Bookshelf version: 2022. Accessed September 14, 2022.

16. Umerah C, II M. Anticoagulation. In: StatPearls. NCBI Bookshelf version: 2022. Accessed September 14, 2022.

17. Watson R, Gibbs C, Lip G. ABC of heart failure. Clinical features and complications. BMJ. 2000:236-239.

18. Borlaug B. The pathophysiology of heart failure with preserved ejection fraction. Nat Rev Cardiol. 2014:507-515.

19. Lai Y, Wang L, Gladwin M. Insights into the pulmonary vascular complications of heart failure with preserved ejection fraction. J Physiol. 2019:1143-1156. doi: 10.1113/JP275858

Author Bio

Anna Courant is a medical writer and nurse practitioner.

Updated: 03/29/2023

The post HFpEF: Heart Failure with Preserved Ejection Fraction appeared first on The Cardiology Advisor.

High sensitivity CRP tests can determine slight changes to CRP levels within the CRP normal range, which would otherwise be missed by standard tests.^1,3 Hs-CRP tests can help identify more specific issues and chronic inflammation over the long term.² Due to this, high hs-CRP results can be a good early indicator of cardiovascular disease (CVD) and atherosclerosis in otherwise asymptomatic patients.^4,5

Relevant Measures & Metrics

Levels of CRP in blood plasma is measured in milligrams of the protein per liter of plasma (expressed as mg/L). In blood plasma from healthy patients, the baseline median concentration of CRP is approximately 1 mg/L but may be lower. In cases of acute illness, levels can increase to 300 mg/L or higher, which is readily detectable with a standard CRP test.¹

Small increases in the baseline levels of CRP, typically to between 1 and 3 mg/L, that are only detectable with a high sensitivity CRP test are early signs of certain diseases, especially cardiovascular conditions.^1,4  When hs-CRP is referred to, it usually indicates small measurements that fall into this range. Higher baseline concentrations of CRP indicate higher risk of cardiovascular incident, with hs-CRP levels over 3 mg/L representing the highest risk.¹

Presentation & Causes of Elevated High Sensitivity CRP

Higher hs-CRP test results are often found among patients at risk of cardiovascular incidents that have no prior history of CVD.¹ It also indicates the patient’s risk of atherosclerosis.⁵ This typically takes the form of minor increases to the baseline level of the patient’s CRP that remain consistent over time. These increases suggest that the patient is experiencing systemic inflammation.¹

Elevated high sensitivity CRP results are frequently observed prior to cases of myocardial infarction, stroke, peripheral arterial disease, and sudden cardiac death in otherwise healthy people.^1,4 They are also indicative of recurring incidents and death in patients with acute or stable coronary conditions across most other measures of coronary health (eg, LDL cholesterol, blood pressure, etc.).¹

This is because systemic inflammation is strongly implicated in increased risk of various cardiovascular conditions, and may make recovery from incidents more difficult.³ While hs-CRP is a generally reliable marker of systemic inflammation, it is unclear whether CRP plays a role in causing or worsening this systemic inflammation or is only produced in response to it.¹ That CRP contributes to atherosclerotic plaque and clot formation suggests that it should be viewed as a risk factor.⁶

Symptoms of chronic inflammation can include chronic ulcers, chronic abscess cavities, and fibrosis.⁷ However, these symptoms will not necessarily indicate that a patient should receive high sensitivity CRP tests as the low levels of CRP visible in these tests can have subtler impacts. The value of an hs-CRP test, therefore, partly rests in detecting cardiovascular risk in otherwise healthy/asymptomatic patients.⁴

Diagnostic Workup

High sensitivity CRP tests are most often done for people who are in a high-risk demographic group for CVD, such as men over 50 and women over 60.⁸ They may also be carried out as part of several types of biochemical assay to test LDL, triglycerides, and other common measures of cardiovascular health to give a more complete picture of the patient’s risks.⁹

There is no single standard technique used for hs-CRP tests. Immunonephelometry and immunoturbidimetry are both common assay types used.¹⁰ The more sensitive assays used in hs-CRP tests include immunolatex, an immunonephelometry technique.^1,5,10 The main distinction between the standard and more sensitive nephelometry assays lie in the degrees of sample dilution and calibration.¹

The most optimal results can be achieved by averaging hs-CRP test results from two blood serum samples taken two weeks apart. If one of the samples shows a level higher than 10 mg/L, this suggests that infection or some other acute cause of inflammation is present. In this case, discard the sample and perform another hs-CRP test two weeks later.¹

Differential Diagnosis

Although high sensitivity CRP tests are most often used as a measure of cardiovascular health, CVD and atherosclerosis are not the only disorders that trigger a CRP response.¹¹ Other conditions, such as asthma, migraine, diabetes, and metabolic syndrome, are thought to be influenced by the levels of systemic inflammation identified by hs-CRP tests.^12,13,14,15 Therefore, other tests and visible symptoms indicative of each of these conditions should be considered in cases of elevated hs-CRP results.

High Sensitivity CRP Treatment & Management

As noted above, tracking changes in high sensitivity CRP test results from a patient’s baseline can help predict future risk of CVD and atherosclerosis in otherwise healthy patients. It can be a useful predictor to guide therapeutic decisions, particularly as part of a broader battery of tests tracking other risk factors.^1,4

Elevated hs-CRP results can also predict difficulty recovering from prior CVD incidents and slow remission of lasting conditions such as hypertension. It has been suggested that lower baseline hs-CRP levels predict more effective hypertension remission when treated with dietary interventions, independent of any other known predictive factors.¹⁵ It therefore follows that hs-CRP tests could form part of a management plan for hypertensive patients.

Determining inflammatory status with high sensitivity CRP may also prove valuable in preventing first time cardiovascular incidents among patients with existing atherosclerosis diagnoses. Interventions that selectively reduce or limit inflammation can reduce risk of cardiovascular events in such cases even if LDL is already effectively controlled.¹⁶

References

1. Back JL. Cardiac injury, atherosclerosis, and thrombotic disease. In: McPherson A, ed. Henry’s Clinical Diagnosis and Management by Laboratory Methods. 14^th ed. Elsevier; 2022:267-275.

2. Luan Y, Yao Y. The clinical significance and potential role of C-reactive protein in chronic inflammatory and neurodegenerative Diseases. Front Immunol. 2018;9:1302. doi: 10.3389/fimmu.2018.01302

3. Helal I, Zerelli L, Krid M, et al. Comparison of C-reactive protein and high-sensitivity C-reactive protein levels in patients on hemodialysis. Saudi J Kidney Dis Transpl. 2012;23(3):477-83.

4. Bassuk SS, Rifai N, Ridker PM. High-sensitivity C-reactive protein: Clinical importance. Curr Probl Cardiol. 2004;29(8):439-93.

5. Oh SW, Moon JD, Park SY. Evaluation of fluorescence hs-CRP immunoassay for point-of-care testing. Clin Chim Acta. 2005;356(1-2):172-7. doi: 0.1016/j.cccn.2005.01.026

6. Castro AR, Silva SO, Soares SC. The use of high sensitivity C-reactive protein in cardiovascular disease detection. J Pharm Pharm Sci. 2018;21(1):496-503. doi: 10.18433/jpps29872

7. Stephenson TJ. Inflammation. In: Cross S, ed. Underwood’s Pathology. 7^th ed. Elsevier; 2019:159-76.

8. Gulati M, Merz NB. Cardiovascular disease in women. In: Libby P, ed. Braunwald’s Heart Disease. 12^th ed. Elsevier; 2022:1710-22.

9. Hoogeveen RC, Ballantyne CM. Residual cardiovascular risk at low LDL. Clin Chem. 2021;67(1):143-153. doi: 10.1093/clinchem/hvaa252

10.Moutachakkir M, Hanchi AL, Barou A, Boukhira A, Chellak S. Immunoanalytical characteristics of C-reactive protein and high sensitivity C-reactive protein. Ann Biol Clin (Paris). 2017;75(2):225-9. doi: 10.1684/abc.2017.1232

11.Soeki T, Sata M. Inflammatory biomarkers and atherosclerosis. Int Heart J. 2016;57(2):134-9. doi: 10.1536/ihj.15-346

12. Kilic H, Karalezli A, Hasanoglu HC, Erel O, Ates C. The relationship between hs-CRP and asthma control test in asthmatic patients. Allergol Immunopathol (Madr). 2012;40(6):362-7. doi: 10.1016/j.aller.2011.10.002

13.Tanik N, Celikbilek A, Metin A, Gocmen AY, Inan LE. Retinol-binding protein-4 and hs-CRP levels in patients with migraine. Neurol Sci. 2015;36(10):1823-7. doi: 10.1007/s10072-015-2262-6

14. Sinha SK, Nicholas SB, Sung JH, et al. Hs-CRP is associated with incident diabetic nephropathy: Findings from the Jackson Heart Study. Diabetes Care. 2019;42(11):2083-9. doi: 10.2337/dc18-2563

15. Carbone F, Elia E, Casula M, et al. Baseline hs-CRP predicts hypertension remission in metabolic syndrome. Eur J Clin Invest. 2019;49(8):13128. doi: 10.1111/eci.13128

16. Libby P. Inflammation in atherosclerosis-No longer a theory. Clin Chem. 2021;67(1):131-42. doi: 10.1093/clinchem/hvaa275

Author Bio

Martyn Bryson is a medical writer living in Philadelphia, Pennsylvania. They have over a decade of experience as a writer and editor covering a wide range of health and wellness topics.

The post HS-CRP: High Sensitivity CRP (C-reactive Protein) appeared first on The Cardiology Advisor.

Introduction

An implantable cardioverter defibrillator (ICD) continuously monitors the heartbeat and delivers an electric ICD shock, when needed, to restore a regular heart rhythm. They are used for (1) the primary prevention of sudden cardiac death in individuals with increased risk of life-threatening ventricular tachycardia (VT) or ventricular fibrillation (VF), and (2) the secondary prevention of sudden cardiac death in individuals with previous sustained VT, VF, or who were resuscitated due to likely VT or VF.¹

An implantable cardioverter defibrillator also is used in cardiac resynchronization therapy, bradycardia pacing, and hemodynamic monitoring.^2,3,4

ICD Indications

An implantable cardioverter defibrillator is used to prevent ventricular arrhythmia-related sudden cardiac death. As primary prevention, ICDs are used in patients at high risk for ventricular arrhythmia and sudden cardiac arrest who do not have experience with these conditions. As secondary prevention, ICDs are used in patients with prior episodes of sudden cardiac arrest, sustained ventricular tachycardia (VT), and syncope caused by ventricular arrhythmia.¹

ICD shock therapy is not indicated for individuals who do not have a reasonable expectation of survival with an acceptable functional status for at least one year, even if they otherwise meet ICD implantation criteria. It is also not indicated in patients with ventricular tachyarrhythmias due to a completely reversible disorder in the absence of structural heart disease, as well as individuals with VF or VT that is amenable to surgical or catheter ablation where their risk of sudden cardiac death is normalized after successful ablation. Placement of an implantable cardioverter defibrillator should be delayed for active infections or acute medical problems; they can be bridged with a wearable cardioverter-defibrillator.

ICD indications include:

• Prior myocardial infarction and reduced left ventricular function (though not for VT or VF limited to the first 48 hours after an acute myocardial infarction)^5,6
• Non-sustained ventricular tachycardia due to prior MI, LVEF of 40% or less, and inducible, sustained VT or ventricular fibrillation (VF) at electrophysiological study⁷
• Prior sudden cardiac arrest due to VT/VF⁸
• Unstable VF¹
• Stable sustained VT not due to reversible causes¹
• Unexplained syncope with inducible sustained monomorphic VT¹
• Non-ischemic heart disease with LVEF of 35% or less, despite guideline-directed management and therapy¹
• Non-ischemic cardiomyopathy with previous sudden cardiac arrest due to VT/VF, hemodynamically unstable VT, or stable sustained VT, not due to reversible causes¹
• Left ventricular systolic dysfunction⁹
• Severe, dilated cardiomyopathy (LVEF less than 36)¹⁰
• Congestive heart failure (LVEF less than 35)¹¹
• Cardiac sarcoidosis with sustained VT or previous sudden cardiac arrest, or LVEF of 35% or less¹²
• Neuromuscular disorders for primary and secondary prevention¹³
• Cardiac channelopathies (high-risk long QT syndrome, catecholaminergic polymorphic ventricular tachycardia, Brugada syndrome, short QT syndrome)¹⁴

Device Overview & Selection Options

Two types of ICDs are currently available: transvenous (TV-) ICD and subcutaneous (S-) ICD. The first available type of implantable cardioverter defibrillator was TV-ICD. This device is implanted through the venous system ending in the chambers of the heart. TV-ICDs consist of a pulse generator, sensing/pacing electrodes, and defibrillation coils. The pulse generator contains a microprocessor that analyzes the cardiac rhythm and controls the delivery of the therapy, a memory component that stores electrocardiographic data, a high-voltage capacitor, and the battery.¹⁵

An electrode is transvenously placed at the endocardium of the right ventricular apex. Dual chamber ICDs have additional electrodes placed in the right atrium. Biventricular ICDs have a third electrode placed transcutaneously in a branch of the coronary sinus, or surgically on the epicardium of the left ventricle. Defibrillation coils are positioned on the right ventricular electrode. In most ICDs, current flows from the distal defibrillation coil simultaneously to the pulse generator and the proximal defibrillation coil. TV-ICDs can deliver multiple therapies when ventricular arrhythmia is detected, including anti-tachycardia pacing, low-energy cardioversion, and high-energy defibrillation.¹⁵

• TV-ICDs have a considerable rate of major complications at the time of implantation (e.g., hemorrhage, infection, pneumothorax, cardiac perforation, and death) and after implantation (e.g., inappropriate device therapy, endocarditis, vessel occlusion, valvular damage, lead dislodgement, and malfunction).¹⁶
• S-ICDs are a newer, less invasive version of ICDs that can avoid some of the complications arising from TV-ICDs because they don’t require venous access. S-ICDs show comparable sensitivity to TV-ICDs in arrhythmia detection, improve specificity, and lower rates of inappropriate shocks compared to TV-ICDs.¹⁷

S-ICDs comprise a pulse generator placed subcutaneously over the left thorax and a single subcutaneous lead placed along the left side of the sternum. The lead includes a single high-voltage, low-impedance shock coil, and two low-voltage, high-impedance sensing electrodes. Three distinct sensing vectors are available: proximal ring of electrode to pulse generator, distal tip of electrode to generator, and, distal tip of electrode to proximal ring of electrode.

The device is controlled by a programmer console that programs all S-ICD diagnostics, including therapy and post-shock pacing activation, conditional shock VT and shock VF activation zone, stored arrhythmic events, shock therapies, battery status, and shock coil integrity.¹⁶ S-ICDs are approved for treatment of ventricular arrhythmias in patients who do not have any of the following:¹⁶

• Symptomatic bradycardia
• Incessant ventricular tachycardia
• Spontaneous, frequently recurring VT that is reliably terminated with antitachycardia pacing

S-ICDs are contraindicated in patients that require permanent pacing, as it is unable to deliver bradycardia pacing, biventricular pacing, or anti-tachycardia pacing. S-ICDs are only able to provide limited post-shock pacing.¹⁸

ICD Shock: Patient and Special Populations Considerations

The use of ICDs as primary and secondary therapy of ventricular arrhythmias is well-established. Certain populations that tend to be under-represented in clinical trials require special consideration.

Older patients have an increased risk of complications, particularly pneumothorax and lead dislodgement.¹⁹ They are also more likely to have multiple comorbidities that could affect post-implantation survival.

ICDs are common in patients with continuous flow left ventricular assist devices (LVAD). However, there is no apparent mortality benefit associated with ICDs in this patient population.²⁰ Given considerable morbidity and complications involving ICDs and lack of randomized trials, use of ICDs in patients with LVADs require special consideration.

Pediatric patients at increased risk for sudden cardiac arrest due to dilated cardiomyopathy, hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, long or short QT syndrome, Brugada syndrome, catecholaminergic polymorphic VT, and congenital heart disease, require special consideration because of structural heart defects, small size and future growth. For pediatric patients, S-ICDs are particularly suitable to avoid complication due to the small venous access.²¹

ICD Shock: Monitoring & Post-implantation Management

Traditional follow-up of implantable cardioverter defibrillator patients includes in-person visits every three months. Scheduled in-person approaches generate a large number of non-actionable visits and enormous clinic workload. Remote patient monitoring (RPM) collects near continuous data from ICDs for automatic cloud-based analysis and then to the clinic, without the need for connection with clinic or patient action. RPM reduces the number of non-actionable in-person evaluations without compromising detection of at-risk patients.²²

ICDs are programmed to detect arrhythmias in the VF zone, with rates faster than 180/min to 200/min. Unfortunately, not all electrograms that meet the diagnostic criteria of VF zone are VF or ventricular arrhythmias. These are the events that trigger inappropriate ICD shock. Supraventricular tachycardias, including sinus tachycardias, atrial fibrillation and atrial flutter are accountable for more than 90% of inappropriate ICD shocks.²³

Technical causes of inappropriate ICD shocks include faulty components, lead fractures, magnetic interference, oversensing of electrical noise, myopotentials and T-waves, and double counting QRS complexes.¹⁵ Certain patients are at higher risk for inappropriate ICD shocks. Those include patients with atrial fibrillation, tobacco use, diastolic hypertension and non-ischemic heart disease.⁹ Although ICD therapy provides life-saving strategies in the case of sudden cardiac arrest, ICD shocks, both appropriate and inappropriate, are associated with increased mortality.^9,24 ICD shocks adversely affect mental and physical well-being. Strategies developed to reduce incidence of ICD shock involve:⁹

• Antitachycardia pacing, replacing shock as safe and effective therapy for fast ventricular tachycardia (>200 bpm)²⁵
• ICD programming
• More stringent arrhythmia detection algorithms
• Dual-chamber ICDs with detection of atrial and ventricular arrhythmias: in theory, but no data exists to support that dual-chamber ICDs reduce rate of inappropriate shocks
• Antiarrhythmic medication
• Catheter ablation

References

1. Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death. Circulation. 2018;138(13):e210-e271.

2. Wilkoff BL, Fauchier L, Stiles MK, et al. 2015 HRS/EHRA/APHRS/SOLAECE expert consensus statement on optimal implantable cardioverter-defibrillator programming and testing. Ep Europace. 2016;18(2):159-183.

3. Raj LM, USA U of SC USC Center for Body Computing, Keck School of Medicine, Los Angeles, CA, Saxon LA. Haemodynamic Monitoring Devices in Heart Failure: Maximising Benefit with Digitally Enabled Patient Centric Care. Arrhythmia Electrophysiol Rev. 2018;7(4):1.

4. Gill J. Implantable cardiovascular devices: current and emerging technologies for remote heart failure monitoring. Cardiol Rev. 2022;Publish Ahead of Print.

5. Moss AJ, Hall WJ, Cannom DS, et al. Improved Survival with an Implanted Defibrillator in Patients with Coronary Disease at High Risk for Ventricular Arrhythmia. New Engl J Medicine. 1996;335(26):1933-1940.

6. Moss AJ, Zareba W, Hall WJ, et al. Prophylactic Implantation of a Defibrillator in Patients with Myocardial Infarction and Reduced Ejection Fraction. New Engl J Medicine. 2002;346(12):877-883.

7. Buxton AE, Lee KL, Fisher JD, Josephson ME, Prystowsky EN, Hafley G. A Randomized Study of the Prevention of Sudden Death in Patients with Coronary Artery Disease. New Engl J Medicine. 1999;341(25):1882-1890.

8. Investigators A versus ID (AVID). A Comparison of Antiarrhythmic-Drug Therapy with Implantable Defibrillators in Patients Resuscitated from Near-Fatal Ventricular Arrhythmias. New Engl J Medicine. 1997;337(22):1576-1584.

9. Borne RT, Varosy PD, Masoudi FA. Implantable Cardioverter-Defibrillator Shocks: Epidemiology, Outcomes, and Therapeutic Approaches. Jama Intern Med. 2013;173(10):859-865.

10. Kadish A, Dyer A, Daubert JP, et al. Prophylactic Defibrillator Implantation in Patients with Nonischemic Dilated Cardiomyopathy. New Engl J Medicine. 2004;350(21):2151-2158.

11. Bardy GH, Lee KL, Mark DB, et al. Amiodarone or an Implantable Cardioverter–Defibrillator for Congestive Heart Failure. New Engl J Medicine. 2005;352(3):225-237.

12. Schuller JL, Zipse M, Crawford T, et al. Implantable Cardioverter Defibrillator Therapy in Patients with Cardiac Sarcoidosis. J Cardiovasc Electr. 2012;23(9):925-929.

13. Anselme F, Moubarak G, Savouré A, et al. Implantable cardioverter-defibrillators in lamin A/C mutation carriers with cardiac conduction disorders. Heart Rhythm. 2013;10(10):1492-1498.

14. Corrado D, Link MS, Schwartz PJ. Implantable defibrillators in primary prevention of genetic arrhythmias. A shocking choice? Eur Heart J. Published online 2022.

15. Gehi AK, Mehta D, Gomes JA. Evaluation and Management of Patients After Implantable Cardioverter-Defibrillator Shock. Jama. 2006;296(23):2839-2847.

16. Rhyner J, Knight BP. The Totally Subcutaneous Implantable Defibrillator. Cardiol Clin. 2014;32(2):225-237.

17. Gold MR, Theuns DA, Knight BP, et al. Head‐To‐Head Comparison of Arrhythmia Discrimination Performance of Subcutaneous and Transvenous ICD Arrhythmia Detection Algorithms: The START Study. J Cardiovasc Electr. 2012;23(4):359-366.

18. Raja J, Guice K, Oberoi M, et al. Shock without wires: A look at subcutaneous implantable cardioverter-defibrillator (ICD) compared to transvenous ICD for ventricular arrhythmias. Curr Prob Cardiology. Published online 2021:100927.

19. Lim WY, Prabhu S, Schilling RJ. Implantable Cardiac Electronic Devices in the Elderly Population. Arrhythmia Electrophysiol Rev. 2019;8(2):143-146.

20. Alvarez PA, Sperry BW, Pérez AL, et al. Implantable Cardioverter Defibrillators in Patients With Continuous Flow Left Ventricular Assist Devices: Utilization Patterns, Related Procedures, and Complications. J Am Hear Assoc Cardiovasc Cerebrovasc Dis. 2019;8(14):e011813.

21. Friedman DJ, Tully AS, Zeitler EP. Subcutaneous and Transvenous ICDs: an Update on Contemporary Questions and Controversies. Curr Cardiol Rep. 2022;24(8):947-958.

22. Varma N, Love CJ, Michalski J, Epstein AE, TRUST Investigators. Alert-Based ICD Follow-Up A Model of Digitally Driven Remote Patient Monitoring. Jacc Clin Electrophysiol. 2021;7(8):976-987.

23. Daubert JP, Zareba W, Cannom DS, et al. Inappropriate Implantable Cardioverter-Defibrillator Shocks in MADIT II Frequency, Mechanisms, Predictors, and Survival Impact. J Am Coll Cardiol. 2008;51(14):1357-1365.

24. Moss AJ, Greenberg H, Case RB, et al. Long-Term Clinical Course of Patients After Termination of Ventricular Tachyarrhythmia by an Implanted Defibrillator. Circulation. 2004;110(25):3760-3765.

25. Wathen MS, DeGroot PJ, Sweeney MO, et al. Prospective Randomized Multicenter Trial of Empirical Antitachycardia Pacing Versus Shocks for Spontaneous Rapid Ventricular Tachycardia in Patients With Implantable Cardioverter-Defibrillators. Circulation. 2004;110(17):2591-2596.

Author Bio

Ivana Celic, PhD, is a biomedical scientist and freelance medical and scientific writer. Her research interests include genome plasticity, cancer, aging, neurodegenerative disease and infertility. She actively participates in laboratory research and scientific writing and presentations.

The post Implantable Cardioverter Defibrillator (ICD) Shock appeared first on The Cardiology Advisor.

Presentation and Causes of Mitral Stenosis

Mitral stenosis (MS), also known as mitral valve stenosis, is a condition in which the opening between the left atrium and left ventricle of the heart, also known as the mitral valve orifice, is narrowed.¹ This condition is a type of valvular heart disease.¹ The narrowing of the mitral valve orifice can be caused by a number of issues, including infective endocarditis, mitral calcifications, congenital heart defects, and rheumatic heart disease.¹

Rheumatic heart disease mitral stenosis is the most common type of mitral stenosis. Symptomatic MS typically presents 20 to 40 years after the initial episode of rheumatic fever due to recurrent acute carditis that occurs in these patients.^1,2 In rheumatic heart disease, damage to the heart likely occurs because of a cross-reactive immune response that targets heart tissues while also targeting the streptococcal antigen that can be present during these infections.²

When the mitral valve heals after these recurrent episodes of inflammation associated with rheumatic heart disease, it also thickens. This leads to mitral stenosis and other associated changes within the heart over time.³ In developed countries such as the United States, the estimated incidence of rheumatic disease is 1 in 100,000.¹

Narrowing of the mitral valve orifice caused by MS creates an increase of pressure in the left atrium and the pulmonary vasculature.¹ This increase in pressure can then lead to sequelae such as pulmonary hypertension, increased size of the left atrium, atrial fibrillation, and heart failure.¹

Diagnostic Workup

The diagnostic workup of mitral stenosis includes noninvasive approaches (for example, auscultation, electrocardiogram [ECG], chest imaging, echocardiogram and exercise echocardiogram) and invasive approaches (for example, cardiac catheterization).¹

Because enlargement of the left atrium may be present in patients with MS, ECG findings may be consistent with left atrial enlargement.⁴ An increased P-wave area of greater than 24 ms x mv measured from ECG lead II typically indicates that atrial enlargement associated with mitral stenosis is present.⁴ The most common chest radiograph findings associated with mitral valvular disease include increased central density, enlargement in transverse diameter, widening of the carina, straightening of the left border, and others.⁵

However, the primary mode of evaluation for MS is echocardiography, because it allows for a detailed assessment of cardiac anatomy and hemodynamics in patients with mitral stenosis.³ Mitral stenosis grading is based on echocardiographic criteria and includes the Wilkins score, which assesses leaflet mobility, thickness, calcification, and subvalvular thickening, and the Padial score, which specifically grades mitral valve leaflet thickening.¹ The Wilkins score is reported as Grades 1 to 4 with Grade 1 having the best outcomes.¹

Echocardiography findings that are consistent with rheumatic disease include the presence of a commissural fusion, “fish mouth” appearance of the mitral valve orifice, leaflet thickening, and shortening and fusion of the chordae tendineae.² Occasionally, cardiac CT scanning or cardiac MRI may also be performed if echocardiography imaging quality is poor or to assess for associated coronary artery disease.³

Exercise echocardiography may be a helpful part of the diagnostic workup because it can unmask clinically or hemodynamically severe mitral stenosis in patients who report that they are asymptomatic at rest but have findings consistent with severe MS based on echocardiographic evaluation.²

Finally, diagnostic cardiac catheterization allows for direct measurement of pressures within the heart, which may be helpful in guiding selection of appropriate interventions.³ Diagnostic cardiac catheterization may also be performed if an assessment of associated coronary artery disease is needed.³

Differential Diagnosis of Mitral Stenosis

The differential diagnosis for mitral stenosis includes obstructive lesions such as left atrial myxoma and endocarditis.^1,2 Additionally, if the diagnosis is mitral stenosis, etiologies of MS should be differentiated.² These etiologies include rheumatic heart disease, mitral annular calcification, radiation valvulitis, prior surgery involving the mitral valve, congenital disease, and systemic inflammatory disorders.²

Relevant Measures & Metrics

Normally, the mitral valve area is 4 to 6 cm², and increased left atrial pressure typically develops when that area is less than 2cm². In fact, so long as the mitral valve orifice area is larger than 1.5 cm², patients are typically asymptomatic.³

Accordingly, measures for classifying the severity of mitral stenosis have been adapted from the ACC/AHA 2020 Valve Guidelines and include measurement of the mitral valve area ≤1.5 cm², diastolic pressure half-time ≥150 ms, and elevated pulmonary artery systolic pressure (PASP) >50mm Hg, in severe cases of MS.¹

Mitral Stenosis Complications & Risks

As mentioned above, mitral stenosis due to rheumatic heart disease is typically asymptomatic for decades after the initial episode of rheumatic fever.¹ Indeed, mitral stenosis itself is a complication of rheumatic fever and rheumatic heart disease, so appropriate medical management of Group A streptococcus pharyngitis with antibiotics is an important mode of prevention of the complication of MS.³

When symptoms of mitral stenosis do develop, the disease can progress quickly to complications such as pulmonary hypertension.¹ Another complication of mitral stenosis is atrial fibrillation.² Death can occur within three years in patients experiencing pulmonary hypertension.¹ Other most common causes of death related to MS are heart failure, abnormal valve anatomy and resultant turbulent blood flow across it, and thromboembolic complications.³

Management strategies for mitral stenosis include medical therapies (for example, diuretics and beta blockers for symptomatic relief) and interventions.² The procedure of choice for the management of MS is the percutaneous mitral balloon valvuloplasty, and eligibility is based on the echocardiography-determined Wilkins score discussed above.²

There are several contraindications to this procedure, including mitral valve area greater than 1.5cm², thrombus in the left side of the heart, mitral regurgitation that is more than mild, severe bi-commissural calcification, absence of commissural fusion, severe concomitant valve disease, or concomitant coronary artery disease requiring surgery.³ Surgical approaches are also available and include commissurotomy, mitral valve replacement, and mitral valve repair.²

Mitral Stenosis ICD 10 Codes

Here are ICD 10 codes relevant to mitral stenosis, with insufficiency or otherwise:

References

1 .Shah S, Sharma S. Mitral stenosis. In: StatPearls. NCBI Bookshelf version. StatPearls Publishing: 2022. Accessed August 30, 2022.

2. Harb S, Griffin B. Mitral valve disease: a comprehensive review. Curr Cardiol Rep. 2017;19(73): 73.

3. Wunderlich N, Dalvi B, Ho S, Küx H, Siegel R. Rheumatic mitral valve stenosis: Diagnosis and treatment options. Curr Cardiol Rep. 2019;21(3):14. doi: 10.1007/s11886-019-1099-7

4. Zeng C, Wei T, Zhao R, Wang C, Chen L, Wang L. Electrocardiographic diagnosis of left atrial enlargement in patients with mitral stenosis: the value of the P-wave area. Acta Cardiol. 2003;58(2):139-41. doi: 10.2143/AC.58.2.2005266

5. Sultana H, Rahman M, Begum M, et al. Chest radiography in the evaluation of mitral valvular disease and its correlation with echocardiography. Mymensingh Med J. 2021;30(2):292-300.

Author Bio

Anna Courant is a nurse practitioner and writer.

Updated: 03/28/2023

The post Mitral Stenosis appeared first on The Cardiology Advisor.

In both adults and children with hypertension, nitroprusside infusions are used to reduce blood pressure instantly. This medication is also used to treat acute heart failure and to decrease bleeding following surgery. Sodium nitroprusside (SNP) gained FDA approval for treating severe hypertension in 1974. It became widely used as a fast-acting antihypertensive agent and is clinically used for hypertensive crises, heart failure, cardiac and vascular surgery, pediatric surgery, and other indications.

A potent, fast-acting, and titratable vasodilator, SNP is still used in certain difficult clinical situations, though it has been replaced by newer agents due to its adverse effects and toxicity.¹

FDA-authorized Sodium Nitroprusside Indication

• Acute heart failure with decompensation¹
• Acute hypertensive emergencies
• Perioperative hypotension induction (to reduce blood loss)
• Reduce bleeding during surgery²

Off-label Nitroprusside Uses

• Acute preload decrease in valvular aortic stenosis patients
• Decreasing afterload in acute mitral regurgitation
• Acute ischemic stroke is associated with hypertension. The American Heart Association suggests that blood pressure not be reduced after at least 24 hours after an ischemic stroke (unless it is over 220/120 mm Hg), as it could worsen the ischemic injury.
• Elevated cardiac output in high SVR and cardiogenic shock¹

Emerging Applications for Nitroprusside

• Prevention and treatment of “no-reflow” in percutaneous coronary intervention
• Treatment of schizophrenia symptoms¹

Vasodilator Drugs List

• Alprostadil IV
• Corlopam
• Deponit
• Fenoldopam
• Glyceryl trinitrate transdermal
• Hydralazine
• Loniten
• Minitran
• Minodyl
• Minoxidil
• Minoxidil HTN
• Nipride RTU
• Nitrocine
• NitroDur
• Nitropress
• Nylidrin
• Papaverine
• ParaTime SR
• Prostin VR Pediatric
• Sodium Nitroprusside
• Transdermal Nitroglycerin³

Drug Class Profile

Vasodilators Mechanism of Action

Vasodilator agents, such as natriuretic peptides and nitric oxide, are antihypertensive agents. Vasodilators often dilate or prevent constriction of the blood vessels, which increases blood flow to different organs.

Numerous vasodilators bind to receptors on blood vessel endothelial cells, which then stimulate calcium release. Calcium triggers the nitric oxide synthase enzyme and transforms L-arginine to NO. It diffuses out of the endothelial cells and into the vascular smooth muscle cells.

Comparing nitroprusside vs nitroglycerin, they are both vasodilators, but nitroprusside is a potent arterial and venous vasodilator, while nitroglycerin is more of a venodilator.

Phosphoglycerate kinase (GTP), which catalyzes the chemical reaction, is activated and converted to cGMP by NO. Then, cGMP turns on an enzyme called myosin-light chain phosphatase, which removes a single phosphate from myosin and actin filaments. The dephosphorylation of myosin and actin filaments permits the relaxation of vascular smooth muscle.⁴

Vasodilators Mechanism of Action by Class

Each vasodilator class has a different mechanism of action:⁴

• Angiotensin-converting enzyme or ACE inhibitors
  • These inhibitors prevent angiotensin I from converting to angiotensin II, which is a strong vasoconstrictor.
• Angiotensin Receptor Blockers (ARBs)
  • These receptor blockers prevent angiotensin II from binding to its receptor.
• Nitrates
  • These increase the amount of nitric oxide in vascular smooth muscle cells, which causes vasodilation. Nitrates dilate veins more than arteries and decrease preload.
• Calcium Channel Blockers
  • These block calcium channels in the cardiac and smooth muscles, which causes decreased muscle contractility and vasodilation.
• Minoxidil
  • This directly relaxes arteriolar smooth muscle minimally affecting the vein. Cyclic adenosine monophosphate may mediate its effects.
• Hydralazine
  • The exact mechanism for Hydralazine is still unknown.
• Beta blockers
  • Nebivolol and carvedilol are third-generation β-adrenoreceptor antagonists. They have additional endothelium-dependent vasodilating properties.

Pharmacokinetics & Pharmacodynamics

• Angiotensin-converting enzyme (ACE) Inhibitors
  • ACE inhibitors prevent the conversion of angiotensin-I to angiotensin-II and are most effective when renin production is increased. Since ACE is identical to kininase-II, which inactivates the potent endogenous vasodilator bradykinin, ACE inhibition causes a reduction in bradykinin degradation.
• Minoxidil
  • Treatment with minoxidil, a potassium channel opener, is reserved for patients with moderately severe to severe hypertension.
• Hydralazine
  • Hydralazine is chiefly used to treat severe hypertensive emergencies, primary pulmonary and malignant hypertension, and severe preeclampsia.
• Beta Blockers
  • Nebivolol and carvedilol are third generation β-adrenoreceptor antagonists. They have additional endothelium-dependent vasodilating properties.⁵

Vasodilator Warnings & Precautions

After the initiation of vasodilators, the patient’s blood pressure and heart rate must be monitored to prevent possible adverse events. Administrators should also check antinuclear antibody titers and anti-histone antibody levels if the patient is on hydralazine and develops symptoms similar to those of the lupus virus.⁴

Vasodilator Adverse Effects & Events

• ACE inhibitors
  • ACE inhibitors can cause angioedema, dry cough, teratogenicity, hyperkalemia, and hypotension.
• ARBs
  • ARBs can cause hyperkalemia, hypotension, decrease GFR, and teratogenicity.
• Nitrates
  • Can cause reflex tachycardia, headache, flushing, and orthostatic hypotension.
• Calcium Channel Blocker
  • Calcium Channel Blockers can cause gingival hyperplasia, dizziness, flushing, peripheral edema, AV block (with Non-dihydropyridines), and constipation.
• Hydralazine
  • Hydralazine can cause compensatory tachycardia, headache, angina, SLE-like symptoms (in slow acetylators), and fluid retention.
• Beta Blockers
  • Beta-blockers can cause bradycardia, dizziness, headaches, nausea, hypotension, and metabolic abnormalities.⁵

Vasodilators Contraindications

• ACE inhibitors⁴
  • ACE inhibitors are hypotensive agents but are not advised as a treatment for patients who are pregnant or who have a history of angioedema or hereditary angioedema.
• ARBs
  • ARBs are teratogens and should not be used in pregnant patients.
• Nitrates
  • Nitrates decrease preload, so the administration of nitrates would be contraindicated in a person having an inferior Myocardial infarction (right ventricular infarction).
• Calcium Channel Blocker
  • severe hypotension, hypersensitivity.
• Hydralazine
  • CAD or angina (it can cause compensatory tachycardia), mitral valve rheumatic heart disease
• Beta Blockers
  • Bradycardia, severe chronic obstructive pulmonary disease, hypotension, cardiogenic shock, and a high degree of atrioventricular block.

Drug Specific Profile

Nitroprusside Mechanism of Action

Sodium nitroprusside interferes with both the influx and the intracellular activation of calcium to cause arterial and venous relaxation. Nitroprusside, which is water-soluble salt sodium, is composed of ferrous iron complexed with nitric oxide and five cyanide ions.

As a prodrug, SNP interacts with erythrocyte sulfhydryl groups (as well as albumin and other proteins) to form nitric oxide. When nitrate oxide binds to vascular smooth muscle, it stimulates intracellular cGMP-mediated activation of protein kinase G and subsequent inactivation of myosin light chains.

This leads to vascular smooth muscle relaxation. As a result of this signaling cascade, both arteries and veins experience peripheral vasodilation (with slightly more selectivity for veins).¹

Nitroprusside Pharmacokinetics & Pharmacodynamics

• Half-life of the parent drug
  • 2 minutes, metabolite (thiocyanate): 3 days or more in individuals who have hyponatremia or poor renal function.
• Onset of action
  • < 2 minutes
• Duration
  • 1 to 10 minutes
• Metabolism
  • 100% in blood. The ferrous ion in nitroprusside molecules reacts with sulfhydryl compounds in RBCs. Then, cyanide is released and metabolized to thiocyanate in the liver and kidneys.
• Metabolites
  • Inactive thiocyanate
• Excretion
  • Metabolites (predominantly thiocyanate) are secreted primarily via urine
• Dialyzable
  • Yes⁶

Nitroprusside Warnings & Precautions

Sodium nitroprusside should not be directly injected, because it requires dilution prior to infusion. Another risk is the possible occurrence of hypotension, leading to irreversible ischemic injury or death.

Therefore, treatment requires appropriate monitoring equipment and experienced personnel. Other precautions must be taken as cyanide toxicity may occur because of the accumulation of cyanide ion.⁶

Nitroprusside Adverse Events

• Cardiovascular:
  • Bradycardia
  • Tachycardia
  • Flushing
  • Palpitations
  • Severe hypotension
  • Electrocardiographic changes
  • Substernal chest pain
  • Shortness of breath
• Central Nervous System:
  • Headache
  • Dizziness
  • Increased intracranial pressure
  • Apprehension
  • Restlessness
• Dermatologic:
  • Diaphoresis
  • Skin rash
  • Local skin irritation with erythematous streaking
• Endocrine/Metabolic:
  • Hypothyroidism
• Gastrointestinal:
  • Abdominal pain
  • Nausea
  • Vomiting/retching
• Hematologic/Oncologic:
  • Decreased platelet aggregation
  • Methemoglobinemia
• Musculoskeletal:
  • Muscle twitching¹

Nitroprusside Contraindications

• Treatment of compensatory hypertension, such as that present in arteriovenous malformations or aortic coarctation
• SNP should not be administered to patients with known insufficient cerebral perfusion for the purpose of inducing controlled perioperative hypotension.
• Low systemic vascular resistance and acute heart failure, such as septic shock
• Vitamin B12 deficiency or related disease states
• Due to their complementary cGMP-mediated mechanisms of action, SNP and phosphodiesterase inhibitors like sildenafil, tadalafil, or vardenafil should not be used at the same time.
• Known hypersensitivity to nitroprusside or any other component of the formulation¹

Nitroprusside Interactions

Drugs that may interact with Nitroprusside include medications that help lower your blood pressure.

Patients who are also taking antihypertensive medications, such as hydralazine or hexamethonium, are often sensitive to the hypotensive effect of sodium nitroprusside. The dosage needs to be adjusted downward accordingly.⁷

Nitroprusside Administration & Dosage

Adult and pediatric administration of nitroprusside sodium is conducted by injectable solution.⁶

• Nitropress
  • 25mg/mL (50mg/2mL vial) (Nitropress)
• Nipride RTU
  • 0.2mg/mL (20mg/100mL 0.9% NaCl)
  • 0.5mg/mL (50mg/100mL 0.9% NaCl)

Nitroprusside Hypertensive Crisis

Cases of hypertensive crisis are indicated for immediate blood pressure (BP) decrease during a hypertensive crisis. The initial infusion rate should be 0.3 mcg/kg/min and the administrator should assess blood pressure for at least 5 minutes before adjusting the dosage to attain the target blood pressure. The infusion rate should not exceed 10 mcg/kg/min.

The dose may be titrated upward until the desired effect is achieved, the maximum recommended infusion rate (10 mcg/km/min) is reached, or the systemic BP cannot be reduced further without risking the perfusion of vital organs.⁶

Controlled Hypotension During Surgery

Cases of hypotension during surgery are indicated for controlled hypotension to lessen bleeding. The initial infusion rate should be 0.3 mcg/kg/min and the administrator should monitor the patient’s BP for at least 5 minutes before attempting a higher or lower dose to elicit the desired BP, but should not exceed 10 mcg/kg/min.

The dose may be titrated upward until the desired effect is achieved, they reach the maximum recommended infusion rate (10 mcg/km/min), or systemic BP cannot be lowered any further without risking the perfusion of vital organs.⁶

Nitroprusside Considerations for Patients & Special Populations

Older adults may be especially sensitive to the drug’s hypotensive effects, so special caution should be taken when it is used with this population.⁸

Nitroprusside Monitoring

During the infusion of nitroprusside sodium, continuous blood pressure monitoring is preferable via an arterial line in an intensive care unit for appropriate dose titration.

References

1. Holme MR, Sharman T. Sodium Nitroprusside. In: StatPearls. StatPearls Publishing, Treasure Island (FL); 2022. PMID: 32491419.

2. Nitroprusside. DrugBank Online. Published June 13, 2005. Updated November 8, 2022. Accessed November 9, 2022.

3. Jacob D. Vasodilators: Drug class, uses, side effects, drug names. RxList. Published November 9, 2021. Accessed October 23, 2022.

4. Hariri L, Patel JB. Vasodilators. In: StatPearls. Treasure Island (FL): StatPearls Publishing; Published January 2022. Updated August 2022 2022. Accessed October 25, 2022.

5. Kirsten R, Nelson K, Kirsten D, Heintz B. Clinical pharmacokinetics of vasodilators. Clinical pharmacokinetics. 1998 Jun;34(6):457-82. DOI: 10.2165/00003088-199834060-00003

6. Nipride RTU, Nitropress (nitroprusside sodium) dosing, indications, interactions, adverse effects, and more.

7. Product Monograph: Sodium Nitroprusside Injection. Kirkland, Québec: Pfizer Canada Inc.; 2017

8. Sodium Nitroprusside. Sodium Nitroprusside, an Overview, ScienceDirect Topics.

Author Bio

Sydney Murphy, M.S., is the Associate Editor of HealthDay Physicians Briefing and a freelance science writer based in New York City. You can follow her on Twitter @SydneyLiz_Murph.

The post Nitroprusside appeared first on The Cardiology Advisor.

Patients and physicians typically have two treatment choices for obstructive coronary artery disease: percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG). Both treatments have demonstrated efficacy in treating the condition, but there are significant distinctions between them.

Coronary artery disease (CAD) is extremely common in heart failure patients, accounting for two-thirds of all instances. Percutaneous coronary intervention, a series of minimally invasive procedures is used to open clogged coronary arteries, is often used in heart failure patients with CAD and has increased significantly, as it has been linked to improved outcomes in multiple observational studies.¹

CABG is another commonly performed operation, with approximately 200,000 procedures performed in the United States each year. However, CABG is a complex and high-risk operation that carries significant risks.²

CABG vs PCI Imaging

Advancements in imaging techniques, including computed tomography, magnetic resonance imaging, intravascular ultrasound, and optical coherence tomography, have improved the detection of patients’ needs for PCI vs CABG interventions. Accurate diagnosis, risk assessment, and appropriate choice of treatment are of utmost importance, because coronary artery anomalies (prevalent in 1% of the general population), ischemia-related symptoms, and arrhythmias lead to an increased risk of sudden cardiac death.³ There are currently many diagnostic methods being developed to improve the accuracy of differential diagnosis of such conditions.

Though researchers have recorded many patterns in the presentation of conditions needing PCI vs CABG, research has also shown a lack of awareness of some atypical, high-risk electrocardiogram (ECG) patterns that may need treatment with the primary PCI method. Up to 10% to 25% of acute coronary syndrome (ACS) patients needing immediate reperfusion treatment may have abnormal ECG rhythms. This varied, high-risk patient group is a challenge for doctors and paramedics, particularly in prehospital care.

Selection

Non-ST-elevation myocardial infarction (NSTEMI) is a large contributor to mortality rates of patients discharged from the hospital after diagnosis of multivessel coronary artery disease. NSTEMI patients are often elderly, comorbid, and have a significant risk of multivessel coronary artery disease (MVD), which is linked to poor clinical outcomes. Unfortunately, there is a current lack of treatment strategies for MVD in NSTEMI, especially treatments related to PCI.⁸

When comparing treatment outcomes for NSTEMI and MVD in PCI vs CABG, patients with three-vessel or left main disease have shown a lower incidence of death, stroke, myocardial infarction, or revascularization with CABG treatment compared with those who underwent PCI. But, in further research, CABG treatment has resulted in no comparative mortality benefit and has been associated with the patient’s higher incidence of stroke. Though overall, PCI appears to be a viable alternative to CABG in a large proportion of patients with NSTEMI and MVD, the lack of comparative data still leaves unanswered questions.⁸

Multivessel PCI has been increasingly used as the revascularization strategy in acute myocardial infarction (AMI) and shock. Hospitals that use multivessel PCI more, however, especially among patients with STEMI, tend to have worse outcomes than those that do not. These results could suggest harm caused by this strategy, and according to researchers, there appears to be an urgency to change practice and improve outcomes in this high-risk AMI population.⁹

In other cases of patients with multivessel coronary artery disease (MVCAD) who have gone through CABG or PCI treatment, mortality rates have been shown to go down with CABG treatment more substantially than with PCI.¹⁰

PCI vs CABG Complications

Though CABG has traditionally been the primary intervention for multivessel CAD with associated left ventricular systolic dysfunction (LVSD) for many years, PCI in patients with chronic and acute heart failure with reduced ejection fraction (HFrEF), as well as heart failure with preserved ejection fraction (HFpEF), has recently been introduced.¹ There are also currently multiple medications available for HFrEF management.¹²

PCI or CABG treatment carries a high risk of periprocedural complications, for which there are a number of predictors. The general characteristics of patients were examined in a study in Krakow, Poland, including concomitant diseases, past cardiovascular procedures, gender and age according to PCI of SVG and IMA.¹³

According to this and previous research, the most serious adverse events that may occur with CABG are death, stroke, bleeding requiring further surgery, peri-operative myocardial infarction, cardiac arrhythmias, and deep sternal wound infection. It is therefore important to discuss these possible risks with a patient during the consent process.²

The greatest differences in the incidence of periprocedural complications (because of the similarity of PCIs performed on internal mammary arteries compared to native coronary arteries), were noticed in patients undergoing PCIs of saphenous vein grafts (SVGs). These included an increased rate of all periprocedural complications, no-reflows, and perforations.

Risk of periprocedural complications are often limited to more specific factors: these include clinical presentation of CAD, TIMI flow before PCI, use of thrombectomy, and gender. Furthermore, a patient is considered more at risk of complications if they have comorbidities such as diabetes, kidney failure, or hypertension.¹³

Monitoring

Awareness of potential concerns, as well as thorough attention to equipment positioning and patient monitoring, can help to reduce the likelihood of difficulties and allow for rapid treatment if dangers arise. Today, there are devices that can be used in conjunction with artificial intelligence techniques as an effective form of monitoring patients with heart diseases.

Implementing technology could help reduce the number of visits to hospitals and improve patients’ quality of life. There are often no symptoms until a heart attack occurs in patients with heart disease, therefore emphasis on the increased use of remote health diagnosis and monitoring systems to predict, prevent, and monitor heart emergencies is needed.¹⁴

References

1. Parikh PB, Bhatt DL, Bhasin V, Anker SD, Skopicki HA, Claessen BE, Fonarow GC, Hernandez AF, Mehran R, Petrie MC, Butler J. Impact of percutaneous coronary intervention on outcomes in patients with heart failure: JACC state-of-the-art review. Journal of the American College of Cardiology. 2021 May 18;77(19):2432-47. 10.1016/j.jacc.2021.03.310

2. Hussain SM, Harky A. Complications of coronary artery bypass grafting. International journal of medical reviews. 2019 Mar 15;6(1):1-5. 10.29252/IJMR-060101

3. Kastellanos S, Aznaouridis K, Vlachopoulos C, Tsiamis E, Oikonomou E, Tousoulis D. Overview of coronary artery variants, aberrations and anomalies. World journal of cardiology. 2018 Oct 26;10(10):127. 10.4330/wjc.v10.i10.127

4. Tzimas G, Antiochos P, Monney P, Eeckhout E, Meier D, Fournier S, Harbaoui B, Muller O, Schläpfer J. Atypical electrocardiographic presentations in need of primary percutaneous coronary intervention. The American journal of cardiology. 2019 Oct 15;124(8):1305-14. 10.1016/j.amjcard.2019.07.027

5. Alizadehsani R, Abdar M, Roshanzamir M, Khosravi A, Kebria PM, Khozeimeh F, Nahavandi S, Sarrafzadegan N, Acharya UR. Machine learning-based coronary artery disease diagnosis: A comprehensive review. Computers in biology and medicine. 2019 Aug 1;111:103346. 10.1016/j.compbiomed.2019.103346

6. Abdar M, Książek W, Acharya UR, Tan RS, Makarenkov V, Pławiak P. A new machine learning technique for an accurate diagnosis of coronary artery disease. Computer methods and programs in biomedicine. 2019 Oct 1;179:104992.

7. Pastore MC, Mandoli GE, Contorni F, Cavigli L, Focardi M, D’Ascenzi F, Patti G, Mondillo S, Cameli M. Speckle tracking echocardiography: Early predictor of diagnosis and prognosis in coronary artery disease. BioMed Research International. 2021 Feb 2;2021. 10.1155/2021/6685378

8. Baumann AA, Mishra A, Worthley MI, Nelson AJ, Psaltis PJ. Management of multivessel coronary artery disease in patients with non-ST-elevation myocardial infarction: a complex path to precision medicine. Therapeutic Advances in Chronic Disease. 2020 Jun;11: 10.1177/2040622320938527

9. Khera R, Secemsky EA, Wang Y, Desai NR, Krumholz HM, Maddox TM, Shunk KA, Virani SS, Bhatt DL, Curtis J, Yeh RW. Revascularization practices and outcomes in patients with multivessel coronary artery disease who presented with acute myocardial infarction and cardiogenic shock in the US, 2009-2018. JAMA Internal Medicine. 2020 Oct 1;180(10):1317-27.  10.1001/jamainternmed.2020.3276

10. Mulukutla SR, Gleason TG, Sharbaugh M, Sultan I, Marroquin OC, Thoma F, Smith C, Toma C, Lee JS, Kilic A. Coronary bypass versus percutaneous revascularization in multivessel coronary artery disease. The Annals of Thoracic Surgery. 2019 Aug 1;108(2):474-80. 10.1016/j.athoracsur.2019.02.064

11. Hu CS, Wu QH, Hu DY, Tkebuchava T. Treatment of chronic heart failure in the 21st century: a new era of biomedical engineering has come. Chronic Diseases and Translational Medicine. 2019 Jun 1;5(02):75-88. 10.1016/j.cdtm.2018.08.005

12. Marti CN, Fonarow GC, Anker SD, Yancy C, Vaduganathan M, Greene SJ, Ahmed A, Januzzi JL, Gheorghiade M, Filippatos G, Butler J. Medication dosing for heart failure with reduced ejection fraction—opportunities and challenges. European journal of heart failure. 2019 Mar;21(3):286-96. 10.1002/ejhf.1351

13. Januszek RA, Dziewierz A, Siudak Z, Rakowski T, Dudek D, Bartuś S. Predictors of periprocedural complications in patients undergoing percutaneous coronary interventions within coronary artery bypass grafts. Cardiology Journal. 2019;26(6):633-44. CJ.a2018.0044/50024

14. Otoom AF, Abdallah EE, Kilani Y, Kefaye A, Ashour M. Effective diagnosis and monitoring of heart disease. International Journal of Software Engineering and Its Applications. 2015 Jan;9(1):143-56. 10.14257/ijseia.2015.9.1.12

Author Bio

Sydney Murphy is the Associate Editor of HealthDay Physicians Briefing and a freelance science writer based in New York City. You can follow her on Twitter @SydneyLiz_Murph.

The post PCI vs CABG appeared first on The Cardiology Advisor.

Stent thrombosis, also known as abrupt vessel closure, occurs when an implanted coronary stent causes a thrombotic occlusion.¹ Often, this can lead to myocardial infarction. Although it occurs in about 0.5% of patients that undergo a coronary stent procedure, it is a severe complication that has a mortality rate of up to 45% and a recurrence rate of up to 20% within 5 years of the first episode.^{2, 3}

Nonadherence to dual antiplatelet therapy (DAPT) is the most common of acute stent thrombosis causes.⁴ The premature discontinuation of the DAPT within 6 months of a coronary stent implantation is associated with an increased risk of stent thrombosis.⁵ 

The high-risk population of abrupt vessel closure involves patients with diabetes mellitus or renal insufficiency. Moreover, the Duke jeopardy score, the final stent’s minimal luminal diameter, and the characteristics of the preprocedural thienopyridine administration have been shown to be involved in stent thrombosis development.¹

Other predictors include ongoing inflammation and the development of neoatherosclerosis, both of which delay healing after stent implantation.⁶

Stent Thrombosis Classification

Different types of this complication can be classified regarding the type of underlying stent (stent material), clinical scenario, and timing after initial stent placement.¹

• Underlying stent category classifications — Stent thrombosis as bare-metal stent, a first-generation drug-eluting stent (DES), and a second-generation DES
• Clinical scenario classification — Symptomatic or clinically silent
• Timing classification — Early abrupt vessel closure occurs 30 days after the initial placement, late-state stem thrombosis occurs between 1 and 12 months after the initial placement, and very late abrupt vessel closure occurs after 1 year of the initial placement

Diagnostic Workup & Differential Diagnosis

A provider should first evaluate the patient’s history, focusing on the date of the stent surgery, as most cases occur within the first 30 days of a coronary stent implantation. Later, the individual should also be evaluated through physical examination, electrocardiogram, echocardiogram, and cardiac enzymes.¹

Stent Thrombosis vs Restenosis

The most common differential diagnosis is restenosis. While stent thrombosis is an acute occlusion that causes an acute coronary syndrome, restenosis is a slow and progressive process that involves the narrowing of the stent lumen due to the growth of biologically fibrous neointima around the stem, resulting in anginal symptoms.³

Stent Thrombosis Management

Management is based on nonpharmacotherapy and pharmacotherapy. Nonpharmacotherapy may involve aspiration thrombectomy, angioplasty, and additional stent implantation. Pharmacotherapy may involve the optimization of the applied antiplatelet therapy.

Nonpharmacotherapy

When an angina occurs as a consequence of stent thrombosis, the patient immediately needs an aspiration thrombectomy or angioplasty to restore the patency of the occluded vessel.¹ In some cases, an additional stent must be placed, although it should be avoided as much as possible since every additional centimeter of stent implantation increases the risk of subsequent abrupt vessel closures.¹

Coronary imaging, such as intravascular ultrasound (IVUS) or optical coherence tomography, helps identify the mechanisms of abrupt vessel closure, like malapposition and underexpansion, which should be treated with dilation by balloon angioplasty. The IVUS can also identify uncovered struts, which must be treated with aspiration thrombectomy plus more potent antiplatelet therapy. If the imagining indicates an in-stent neoatherosclerosis, the patient may require additional stent implantation.⁷

Pharmacotherapy

Dual antiplatelet therapy with aspirin and ticlopidine is currently recommended for patients undergoing stent implantation, which has a lower prevalence of stent thrombosis than therapy with aspirin alone or aspirin plus warfarin.⁵

Patients must be evaluated for confirmation of adherence to the prescribed antiplatelet therapy.⁷ In the case of therapy inefficacy, the therapy may be modified by replacing the drugs used. For example, prasugrel or ticagrelor may replace clopidogrel as more potent options.⁶

Complications

Complications may lead to myocardial infarction, cardiogenic shock, or death.¹ Due to poor prognosis, prevention is highly important. Main prevention measures are to ensure the patient adheres to the dual antiplatelet therapy, choose an adequate stent size, and identify the expansion characteristics.⁴

Monitoring

Within the first 24 hours of a percutaneous coronary intervention, patients need dynamic monitoring. This procedure includes continuous monitoring of vital signs and the electrophysiologic activity of the heart.

Cardiac enzymes, such as troponin, may take time to increase with stent thrombosis.⁸ A finding of angina pectoris, or symptoms such as chest pain or shortness of breath, is a sign to act and treat the patient even if cardiac enzymes are still negative.⁸

Although less likely, abrupt vessel closure can occur at a late-stage post percutaneous coronary intervention. The outpatient follow-up includes monitoring for chest pain and shortness of breath, which can be signs. Particularly, patients with diabetes mellitus and renal failure are at higher risk of developing late stent thrombosis.³

References

1. Modi K, Soos MP, Mahajan K. Stent Thrombosis. In: StatPearls. NCBI Bookshelf version. StatPearls Publishing: 2022, June 19. Accessed October 7, 2022.

2. Moukarbel GV. Coronary stent thrombosis and mortality: Does the relationship stand the test of time? Journal of the American Heart Association. 2022;11(7):e025341. doi:10.1161/JAHA.122.025341

3. Gori T, Polimeni A, Indolfi C, et al. Predictors of stent thrombosis and their implications for clinical practice. Nature Reviews Cardiology. 2019;16(4):243-256. doi:10.1038/s41569-018-0118-5

4. Levine GN, Bates ER, Blankenship JC, et al. 2011 ACCF/AHA/SCAI guideline for percutaneous coronary intervention. Circulation. 2011;124(23):e574-e651. doi:10.1161/CIR.0b013e31823ba622

5. Kirtane AJ, Stone GW. How to minimize stent thrombosis. Circulation. 2011;124(11):1283-1287. doi:10.1161/CIRCULATIONAHA.110.976829

6. Cutlip DE. Stent thrombosis management. Cardiac Interventions Today. May/June 2015. Accessed September 20, 2022.

7. Ong DS, Jang IK. Causes, assessment, and treatment of stent thrombosis—intravascular imaging insights. Nature Reviews Cardiology. 2015;12(6):325-336. doi:10.1038/nrcardio.2015.32

8. Ge J, Yu H, Li J. Acute coronary stent thrombosis in modern era: Etiology, treatment, and prognosis. Cardiology. 2017;137(4):246-255. doi:10.1159/000464404

Author Bio

Francina Agosti is a freelance science and medical writer based in Canada. She holds a PhD in neuroscience and has worked in academia for 10 years. Now she writes scientific and medical articles for digital outlets and works as a scientific consultant for biotech and biopharma companies.

The post Stent Thrombosis appeared first on The Cardiology Advisor.

Since the 1960s, coronary artery disease (CAD) has been the leading cause of death in the United States, and myocardial perfusion imaging (MPI) agents have been researched and developed to aid in early diagnosis and treatment planning. A myocardial perfusion imaging test is used to assess the blood flow through the heart muscle and is useful in patients experiencing chest discomfort. It is commonly known as a nuclear stress test.

When the heart doesn’t receive enough oxygen-rich blood, CAD symptoms and signs develop. Reduced blood flow to the heart in cases of CAD can result in angina, shortness of breath, and even a heart attack if blood flow is completely blocked. Fatal circumstances can be prevented by using MPI for early detection of such risks.¹

MPI using single photon emission computed tomography (SPECT) and, more recently, positron emission tomography (PET) have diagnostic and prognostic value for the management of patients with known or suspected CAD.¹ MPI can now be customized to the patient and clinical question at hand due to the fundamental changes in the acquisition, processing, and interpretation the new technology has brought to MPI.

The key principles for the use of a myocardial perfusion imaging test include performing the appropriate MPI test on the appropriate patient at the appropriate time. Another main principle incorporates patient comfort and convenience, cost, and especially image quality and radiation dose. Appropriate use of a myocardial perfusion imaging test is eased by appropriate use criteria.²

Myocardial Perfusion Imaging Diagnostic Workup

Widely used to diagnose and treat patients with known or suspected CAD, MPI using SPECT provides vital data on myocardial perfusion and function. The development of camera systems using solid-state crystals and novel collimator designs tailored for cardiac imaging has resulted in significant advancements in SPECT imaging.³ The main part of a SPECT system is the detector, which gathers the photon events, interprets the photon energy and position of detection, and produces data for subsequent image reconstruction.²

While maintaining high diagnostic accuracy, solid-state tomographic camera systems have allowed for significantly shorter imaging sessions and lower radiation doses. Fast or low-dose MPI has been made possible by improved photon sensitivity, and early dynamic imaging has emerged as a method for evaluating myocardial blood flow with SPECT.³ A SPECT detector’s performance is primarily determined by its sensitivity, energy resolution, and spatial resolution.²

Although MPI with SPECT has traditionally been the clinical diagnostic tool, PET MPI has seen growth over the past 20 years due to improved image quality that produces higher diagnostic accuracy than SPECT. Furthermore, routine quantification of myocardial blood flow (MBF) and myocardial flow reserve (MFR) in absolute units is done by dynamic PET imaging of the tracer distribution process from the time of tracer administration to tracer accumulation in the myocardium. Over MPI alone, MBF and MFR incrementally enhance the accuracy of diagnosis and prognosis. MPI, MBF, and MFR may be acquired simultaneously in some circumstances without added expense, radiation exposure, or processing time.¹

Based on recent developments in PET, cardiac-specific SPECT with dynamic image acquisition has also sparked research into the creation and validation of SPECT MBF imaging protocols.¹ PET and SPECT are particularly suited for molecular imaging because of their high sensitivity and well-established quantitative methodologies. Molecular imaging, as opposed to the detection of “defects” in MPI, is primarily based on “hot-spot” imaging.⁴ The development of hybrid SPECT/CT systems and general-purpose solid-state camera systems has also raised the possibility of significant clinical applications in cardiac imaging.³

A thorough understanding of the artifacts that can appear during the acquisition and processing of image data is necessary for accurate interpretation of SPECT/CT myocardial perfusion imaging studies, as well as working knowledge of possible abnormalities. Incorrect alignment of the raw SPECT/CT image datasets and patient motion are two factors that can cause artifacts to propagate onto the final images.⁵

To further understand CAD, it is also possible to combine MPI and cardiac CT angiography into one test to examine the anatomy and physiology of the coronary arteries as well as the structure and composition of plaque. However, further clinical studies are necessary to establish the added value of a combined assessment of biology by molecular imaging as well as anatomy and physiology.⁴ With a significant reduction in radiation exposure and procedure costs, hybrid imaging modalities allow for evaluation of myocardial perfusion and coronary artery calcium (CAC) quantification as a part of the same examination.⁶

Population Considerations

MPI can now be customized to the patient and clinical question.² A well-validated index of atherosclerosis known as the CAC score is used to classify asymptomatic patients at an intermediate risk of developing CAD. To improve the diagnostic and prognostic power of radionuclide cardiac imaging, coronary perfusion data may be combined with anatomical data from CAC measurements. The addition of a CAC score may change the classification of MPI scans.⁶

The risk of cardiovascular disease in patients with chest pain varies significantly. Acute angina is associated with changes in electrocardiography (ECG) or an increase in cardiac enzymes in patients with atypical chest pain. The evaluation of atypical chest pain can be difficult because ECG results can be negative in a large number of patients with ischemic heart disease (IHD) who are experiencing chest pain. An MPI SPECT scan is a method used to increase the speed and accuracy of acute coronary syndrome (ACS) diagnosis. It can also be used to determine long-term prognosis.⁷

Differential Diagnosis for Myocardial Perfusion Imaging

The majority of patients with ischemia in non-obstructive coronary artery disease (INOCA) exhibit coronary microvascular dysfunction (CMD), which is linked to poor outcomes and abnormal MPI. CMD is also hardly identified by routine coronary angiography, as seen in nearly 60% to 70% of women and 30% of men undergoing diagnostic coronary angiography. A new non-invasive method to evaluate CMD is the coronary angiography-derived index of microvascular resistance (caIMR).⁸

IMR, independent of hemodynamic perturbations, enables direct and repeatable quantitative measurement of the minimal microcirculatory resistance in a particular coronary artery territory. IMR’s use in clinical practice is constrained by the need for a dedicated pressure-temperature sensor wire and hyperemic agents, which add to the complexity of the procedure. An offline evaluation of the microcirculatory system without the use of specialized wires or hyperemic agents has been proposed for the novel angiographic index known as caIMR.⁸

In patients with ST-segment elevation myocardial infarction (STEMI) and myocardial infarction with non-obstructive coronary arteries (MINOCA), caIMR has been shown to have a positive correlation with invasive IMR and to provide predictive implications for abnormal results. However, the value of the prognosis of caIMR-derived CMD in INOCA patients is still unknown.⁸

Relevant Measures & Metrics

In order to identify regional myocardial ischemia and infarction as the underlying cause of patient symptoms, radiolabeled tracer imaging in tandem with physiologic (exercise) or pharmacological (vasodilator) stress has proven to be an effective combination. These imaging biomarkers are frequently used to guide medical and interventional therapies intended to alleviate symptoms and lower the risk of serious adverse cardiac events like myocardial infarction (MI), heart failure, and death from cardiovascular causes.¹

A noninvasive myocardial perfusion imaging test is used as a gatekeeper test before invasive coronary angiography in North America, Europe, and many other industrialized nations, helping to restrict the costs and risks of embolic stroke and MI to patients who need interventional treatment after receiving an image-guided diagnosis.¹

Myocardial Perfusion Scan Risks & Complications

A risk of using MPI is radiation exposure to the patient and staff performing the scan. Clinically, stress-only imaging with a solid-state camera system enables the lowest total radiation exposure with current tomographic MPI (1 mSv). Stress-only MPI can cut patient radiation exposure by up to 60% and significantly cut radiation exposure for staff as well.³

References

1. Klein R, Celiker-Guler E, Rotstein BH, et al. PET and SPECT tracers for myocardial perfusion imaging. Seminars in Nuclear Medicine. 2020 (Vol. 50, No. 3, pp. 208-218). WB Saunders.

2. Dorbala S, Ananthasubramaniam K, Armstrong IS, et al. Single photon emission computed tomography (SPECT) myocardial perfusion imaging guidelines: instrumentation, acquisition, processing, and interpretation. Journal of Nuclear Cardiology. 2018;25(5):1784-1846.

3. Slomka PJ, Miller RJH, Hu L, Germano G, et al. Solid-state detector SPECT myocardial perfusion imaging. Journal of Nuclear Medicine. 2019;60(9):1194-1204.

4. Sadeghi MM. Beyond perfusion imaging. Journal of Nuclear Cardiology. 2022;29(4):1485-1486.

5. Dvorak RA, Brown RKJ, Corbett JR. Interpretation of SPECT/CT myocardial perfusion images: common artifacts and quality control techniques. RadioGraphics. 2011;31(7):2041-2057.

6. Zampella E, Assante R, Acampa W. Myocardial perfusion imaging and CAC score: Not only a brick in the wall. Journal of Nuclear Cardiology. 2021:1-3.

7. Taban Sadeghi M, Mahmoudian B, Ghaffari S, et al. Value of early rest myocardial perfusion imaging with SPECT in patients with chest pain and non-diagnostic ECG in emergency department. The International Journal of Cardiovascular Imaging. 2019;35(5):965-971.

8. Liu L, Dai N, Yin G, et al. Prognostic value of combined coronary angiography-derived IMR and myocardial perfusion imaging by CZT SPECT in INOCA. Journal of Nuclear Cardiology. 2022:1-8.

Author Bio

Sydney Murphy is the Associate Editor of HealthDay Physicians Briefing and a freelance science writer based in New York City. You can follow her on Twitter @SydneyLiz_Murph.

The post Stress Myocardial Perfusion Imaging appeared first on The Cardiology Advisor.

History & Epidemiology

Ventricular arrhythmia is a condition where the pumping of the heart ventricles is abnormal. Ventricular arrhythmias produce a broad range of conditions, from premature ventricular complex to ventricular fibrillation. The clinical presentations can vary, from lack of symptoms to cardiac arrest.¹

The term “arrhythmia” was introduced in 1872 by the German physiologist Rudolph Heidenhain² and has been used since.

The development of ventricular arrhythmias depends on factors such as familial history, genetic variants, heart conditions, and even certain medications.¹ People with advanced heart disease are at risk for ventricular arrhythmias, especially in the elderly population.³

Ventricular arrhythmias cause about 300,000 deaths per year in the US, accounting for almost half of deaths from cardiac causes.⁴ Cases of ventricular arrhythmias can be lethal, as when presenting with ventricular fibrillation or when caused by myocardial infarction.⁵

Ventricular arrhythmias are unusual in children but can show in patients with congenital heart disease. The incidence of ventricular arrhythmia increases with age, peaking in the middle decades of life, the same age for incidence of structural heart diseases. However, idiopathic ventricular arrhythmias can occur at any age. Men suffer more frequently from ventricular arrhythmias than women since ischemic heart disease is more prevalent in men, and ischemia predisposes for ventricular arrhythmias.⁶

Presentation & Diagnosis of Ventricular Arrhythmia

The most common, easily detectable symptoms of ventricular arrhythmias are palpitations, light-headedness, syncope, and chest pain. Based on clinical presentation, however, ventricular arrhythmias be categorized as hemodynamically stable or unstable.⁷

• Hemodynamically stable arrhythmias show no symptoms or minimal ones, such as palpitation.
• Hemodynamically unstable ventricular arrhythmias can present with a presyncope, syncope, or sudden cardiac death or cardiac arrest.

There are specific etiologies of ventricular arrhythmias⁸:

• Idiopathic ventricular arrhythmia without structural heart disease can present with right ventricular outflow tract tachycardia, left ventricular outflow tract tachycardia, or left posterior fascicular ventricular tachycardia.
• Ischemic cardiomyopathy mainly shows monomorphic ventricular tachycardia but can also be seen with polymorphic ventricular tachycardia, and a ventricular tachycardia storm may occur.
• Nonischemic cardiomyopathy, where polymorphic ventricular tachycardia is more common than monomorphic ventricular tachycardia, and the myocardial scar is more commonly localized to the epicardium or mid-myocardium than the endocardium.
• Arrhythmogenic right ventricular dysplasia, in which an electrocardiogram may show right ventricular dilation with systolic dysfunction, and an electrophysiologic study typically demonstrates reduced endocardial voltage indicative of scar.
• Hypertrophic cardiomyopathy, which mainly presents with nonsustained or polymorphic ventricular tachycardia or ventricular fibrillation. Murmur caused by outflow tract obstruction and bisferiens pulse are common signs.
• Genetic arrhythmia syndromes are diagnosed with a long QT syndrome, Brugada syndrome, catecholaminergic polymorphic VT, early repolarization syndrome, or (rarely) with a short QT syndrome.

Ventricular Arrhythmia Diagnostic Workup

For a diagnosis, the health provider should start with a physical examination looking for hypotension, tachypnea, signs of diminished perfusion (including a reduced level of consciousness, pallor, and diaphoresis), high jugular venous pressure, Cannon A waves when the atria are in sinus rhythm, and variation in the intensity of first heart sound (S1) produced by loss of atrioventricular synchrony. The patient may also be affected by a particular mental status involving signs of anxiety, agitation, and/or lethargy.⁶

If signs of ventricular arrhythmia appear during physical examination, an electrocardiogram (ECG) is required for confirmation. Laboratory studies to measure electrolyte levels, including calcium, magnesium, and phosphates, may also be necessary, in combination with cardiac troponin I enzymes, concentration levels of which would determine myocardial ischemia. A toxicology screen is recommended if there is a suspicion that recreational or therapeutic drug consumption, such as cocaine or methadone, could be causing ventricular arrhythmia.⁶

Differential Diagnosis

Common symptoms that can be confused with other pathologies include exercise intolerance, chest pain, dyspnea, presyncope, and syncope.

When performing an ECG, it is difficult to differentiate a ventricular arrhythmia presenting a complex tachycardia from supraventricular tachycardia. Some criteria on the 12-lead ECG that define ventricular arrhythmia include the absence of an RS complex in the precordial leads, an RS interval of greater than 0.1 seconds in any precordial lead, and atrioventricular dissociation with or without fusion, with or without capture beats. If the differentiation from supraventricular tachycardia is still uncertain after the 12-lead ECG, it is preferable to assume ventricular arrhythmia.⁸

Management of Ventricular Arrhythmias

The management of ventricular arrhythmia principally depends on the patient’s hemodynamic status and clinical condition.

Nonpharmacotherapy for Ventricular Arrhythmia Treatment

When sustained ventricular tachycardia is present, the patient requires urgent conversion to sinus rhythm. If hemodynamically unstable with monomorphic ventricular tachycardia, the patient should be immediately treated with synchronized direct-current cardioversion. Unstable polymorphic ventricular tachycardia should be treated with immediate defibrillation.⁶

Pharmacotherapy for Ventricular Arrhythmia Treatment

In hemodynamically stable patients with monomorphic ventricular tachycardia and normal left ventricular function, restoration of sinus rhythm is typically achieved with intravenous procainamide or beta blockers such as amiodarone or sotalol. If the left ventricular function is impaired, amiodarone (or lidocaine) is preferred. When pharmacological therapy is unsuccessful, sedation and synchronized cardioversion should be applied.⁸

If the patient shows runs of polymorphic ventricular tachycardia punctuated by sinus rhythm with QT prolongation, magnesium sulfate, isoproterenol, pacing, or a combination should be used. Also, the administration of phenytoin and lidocaine may help.⁶

Ventricular Arrhythmia Treatment: Side Effects, Adverse Events, Drug-Drug Interactions

Amiodarone is particularly associated with long-term adverse effects such as pulmonary, thyroid, cardiac, skin, and ocular toxicities.¹⁰ Moreover, its chronic administration has been associated with complex medication interactions,¹ including with fingolimod and certain drugs to treat hepatitis C, such as ledipasvir and sofosbuvir.

If untreated, malignant ventricular arrhythmia can result in serious adverse events, such as syncope, sudden cardiac arrest, and death.

Ventricular Arrhythmia ICD 10 Codes

Here are the ICD 10 codes relevant to ventricular arrhythmia:

References

1. Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death. A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Circulation. 2018. 138:e272–e391. doi: 10.1161/CIR.0000000000000549

2. Anderson ME, Antzelevitch C, Balser JR, et al. Basis and Treatment of Cardiac Arrhythmias. Springer; 2006. doi: 10.1007/3-540-29715-4

3. Tan NY, Roger VL, Killian JM, et al. Ventricular arrhythmias among patients with advanced heart failure: A population-based study. J Am Heart Assoc. 2022; 11:e023377. doi: 10.1161/JAHA.121.023377

4. Foth C, Gangwani MK, Alvey H. Ventricular tachycardia. In:StatPearls: NCBI Bookshelf version. StatPearls Publishing; 2022. Updated 2021 Aug 11.

5. Sattler SM, Skibsbye L, Linz D, et al. Ventricular arrhythmias in first acute myocardial infarction: Epidemiology, mechanisms, and interventions in large animal models. Front Cardiovasc Med. 2019; 6:158. doi: 10.3389/fcvm.2019.00158. eCollection 2019.

6. Compton SJ. Ventricular tachycardia. Medscape. Updated Dec 2017. Accessed Sept 28, 2022.

7. Zipes DP, Camm AJ, Borggrefe M, et al. ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: A Report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death). J Am Coll Cardiol.2016; 48(5); e247-e346. doi: 10.1016/j.jacc.2006.07.010

8. Dresen WF, Ferguson JD. Ventricular arrhythmias. Cardiol Clinics. 2018 Feb;36(1):129-139. doi: 10.1016/j.ccl.2017.08.007.

9. Jons C, Sogaard P, Behrens S, et al. The clinical effect of arrhythmia monitoring after myocardial infarction (BIO-GUARD|MI):study protocol for a randomized controlled trial. Trials. 2019; 20:563. doi: 10.1186/s13063-019-3644-5

10. Doyle JF, Ho KM. Benefits and risks of long-term amiodarone therapy for persistent atrial fibrillation: A meta-analysis. Mayo Clin Proc. 2009;84(3):234-242. DOI: 10.1016/S0025-6196(11)61140-3

Author Bio

Francina Agosti is a freelance science and medical writer based in Canada. She holds a PhD in neuroscience, and she worked in academia for 10 years. Now she writes scientific and medical articles for digital magazines, and she also works as a scientific consultant for biotech and biopharma companies.

Updated: 03/29/2023

The post Ventricular Arrhythmia appeared first on The Cardiology Advisor.

Wide complex tachycardia (WCT) is a general term describing a group of conditions that present with an accelerated heart rhythm, specifically a heart rate of more than 100 beats per minute (bpm) and a QRS duration of more than 120 milliseconds. WCT can be loosely divided into 2 types: ventricular tachycardia (VT) and supraventricular WCT (SWCT).^1,2

Ventricular Tachycardia

Ventricular tachycardia is the most common type of wide complex tachycardia. It is defined as a sequence of 3 or more ventricular beats with a frequency greater than 100 bpm. Ventricular tachycardia can be further classified as nonsustained or sustained, depending on the arrhythmia duration.

Nonsustained ventricular tachycardia refers to an arrhythmia with a duration of less than 30 seconds. Sustained ventricular tachycardia describes an arrhythmia lasting more than 30 seconds or one during which the patient experiences hemodynamic instability in less than 30 seconds. Ventricular tachycardia usually manifests as a heart rate ranging from 100 bpm to 200 bpm; in most patients with ventricular tachycardia, the heart rate exceeds 170 bpm.^1,3,4

Supraventricular Tachycardia

Supraventricular wide complex tachycardia, a relatively rare form of WCT, is defined as any WCT that does not originate in the ventricles. There are many possible variations of supraventricular wide complex tachycardia, but there are 4 main types⁵: 

• Aberrant conduction;
• Ventricle pre-excitement via accessory pathway conduction;
• QRS duration prolongation due to metabolic abnormalities; and 
• Rapid ventricular pacing.

Historical Background

The evolution in understanding tachycardia and other arrhythmias, including ventricular arrhythmias, is closely related to the history of electrocardiography. The string galvanometer, created in 1901, was the first tool to effectively measure electrical activity from the body’s surface, and its use led to rapid development in the study of tachycardia and related heart conditions.⁶ 

For most of the 20th century, the roving electrode was the primary means of mapping electrical activity in the heart, but it was reliable only for strictly regular forms of arrhythmia. The first intentional activation and stopping of tachycardias occurred in experimental and clinical demonstrations conducted in the 1960s.⁶

In the late 1970s, systems were developed that enabled measurements to be made simultaneously from multiple electrical positions. As a result of these innovations, arrhythmias could be measured with greater accuracy, and more types could be defined. Clinical data accumulated since that time have informed current approaches to the management of wide complex tachycardia.⁶

Epidemiology

Wide complex tachycardia is a major contributor to sudden cardiac death.⁴ Approximately 80% of WCT cases are due to ventricular tachycardia,^1,7 and this estimate may be even higher given the difficulty in gathering accurate data.⁷ In the United States, ventricular tachycardia alone accounts for approximately 50% of cardiac deaths and 15% of all-cause deaths. Ventricular tachycardia that progresses to ventricular fibrillation (VF) often results in sudden death.⁴ 

The most common subtype of supraventricular wide complex tachycardia is aberrant conduction. In aberrant conduction, supraventricular electrical impulses are conducted through the ventricle tissues. Aberrant conduction accounts for approximately 15% of WCT cases.⁸

Etiology & Wide Complex Tachycardia Risk Factors

Distinguishing between the many possible causes of wide complex tachycardia is key to establishing a differential diagnosis of wide complex tachycardia and determining appropriate wide complex tachycardia treatment. Some of the most common causes of WCT include: 

• Acute myocardial infarction^3,4,7
• Inflammatory disease of the heart³
• Infectious disease of the heart³
• Ischemic heart disease^3,4
• Structural heart disease³
• Electrolyte imbalances, such as hyperkalemia^3,7 
• Side effects of return of spontaneous circulation (ROSC), resuscitation⁷
• Pacemaker-mediated tachycardia⁷
• Overdose or toxicity of certain illicit drugs, such as cocaine⁷
• Effects of digitalis poisoning^3,7

Wide complex tachycardias most commonly occur in people older than 35 years, and they generally occur more frequently in men. Other key risk factors contributing to wide complex tachycardias include a history of heart conditions. Regarding ventricular tachycardia in particular, a history of structural heart disease is a strong indicator, especially in a patient with a prior myocardial infarction. Structural heart disease also increases the risk of WCT in children.^3,4,9,10

Triggering Agents for Supraventricular Tachycardia

Among people considered to be at increased risk for wide complex tachycardia, the following are believed to be triggering agents for supraventricular wide complex tachycardia: 

• Caffeine¹¹
• Alcohol consumption¹¹
• Stress¹¹
• Certain medications⁹ 

A history of using medications specifically known to have proarrhythmic effects also may be a risk factor and can narrow down the possible causes of WCT.⁹

Prognosis

The prognosis of wide complex tachycardia varies depending on the mechanisms underlying the condition. Urgent wide complex tachycardia treatment is required for any patient with hemodynamic instability. Because many patients with WCT are hemodynamically stable, however, identification of the specific type of WCT in an individual patient is essential to improve prognosis.^7,12

Ventricular & Supraventricular Tachycardia Prognosis

As previously noted, sustained ventricular tachycardia in particular contributes significantly to cases of sudden cardiac death.⁴ Nonsustained ventricular tachycardia has been linked to long-term increases in the risk of death, but this risk typically disappears after associated conditions have been identified and addressed.¹³ Mortality risk associated with supraventricular wide complex tachycardia varies depending on the type, but it is generally not fatal.¹²

Sustained ventricular tachycardia can lead to fainting and possibly cardiac arrest. Because at any time ventricular tachycardia can also degenerate into ventricular fibrillation — which can be fatal in a matter of minutes — urgent treatment of sustained ventricular tachycardia is warranted.^13,14 

Wide Complex Tachycardia Diagnosis & Presentation

Wide complex tachycardia can cause a wide range of visible symptoms. People who are unstable due to the condition may present with⁷: 

• Hypotension
• Pulmonary edema
• Reduced body temperature
• Altered mental status
• Unusual pallor

In stable patients, persistent chest pain is common and may occur in conjunction with shortness of breath, nausea, and dizziness.⁷

Patients with WCT may also be asymptomatic or only present with relatively mild symptoms such as palpitations or slight lightheadedness, especially in cases of hemodynamically stable, nonsustained ventricular tachycardia.⁹

Medical History

Medical history is a key indicator of wide complex tachycardia, with a history of myocardial infarction, coronary artery disease, and/or congestive heart failure found to be predictive of ventricular tachycardia. Use of antiarrhythmic drugs and pacemakers is also known to cause WCT.⁷

Diagnostic Wide Complex Tachycardia Workup/Physical Examination

The standard first step to confirm a diagnosis of any type of wide complex tachycardia is use of a 12-lead electrocardiogram (ECG) or another imaging method, such as cardiac magnetic resonance imaging (MRI).^4,7

Further testing varies depending on prior results, symptoms, and medical history. Treadmill stress tests are used in cases of symptoms related to exercise or ischemic heart disease. Ambulatory ECG may be used for patients who have experienced fainting and palpitations but had no arrhythmia detected by the first ECG.^4,7

Differential Diagnosis of Wide Complex Tachycardia

Certain other conditions need to be differentiated from tachycardias and may manifest with similar visible symptoms.

Differential Diagnosis with Bradycardia

Bradycardia, a condition in which the heart rate slows to fewer than 60 bpm, is known to cause¹⁵: 

• Chest pain,
• Fainting,
• Lightheadedness,
• Dizziness, and
• Confusion

Because a differential diagnosis of wide complex tachycardia from bradycardia can be accomplished once a patient’s heart rate has been measured, clinical problems usually arise only in the most urgent situations.¹⁵

Differential Diagnosis with Noncardiac Conditions

Certain noncardiac conditions may also symptoms similar to those of wide complex tachycardia and can be more difficult to quickly produce a differential diagnosis from cardiac problems. For example, insufficient delivery of oxygen to vital organs due to anemia, hemoglobin malfunction, or respiratory issues may trigger symptoms similar to those associated with cardiac events, including¹⁰:

• Dizziness,
• Fainting, and
• Chest pain

Seizures and other brain conditions may cause an increased heart rate and changes to consciousness similar to those seen in patients with primary tachycardias. Some medications and stimulants, such as anticholinergic and antihypertensive agents, can result in similar symptoms, especially in the setting of overdose.¹⁰

Wide Complex Tachycardia ICD 10 Codes

These are the relevant ICD 10 codes for wide complex tachycardia.

Challenges

The key challenge presented by wide complex tachycardia is the need to quickly and accurately identify and treat the specific type of condition in a potential emergency situation. This ability is critical to preserving the patient’s life, especially when there is a history of serious heart conditions.

References

1. Alblaihed L, Al-Salamah T. Wide complex tachycardias. Emerg Med Clin North Am. 2022:40(4):733-753. doi:10.1016/j.emc.2022.06.010

2. Kashou AH, Noseworthy PA, DeSimone CV, Deshmukh AJ,  Asirvatham SJ, May AM. Wide complex tachycardia differentiation: a reappraisal of the state-of-the-art. J Am Heart Assoc. 2020;9(11):e016598. doi:10.1161/JAHA.120.016598

3. Watson KT. Abnormalities of cardiac condition and cardiac rhythm. In: Hines RL, Jones SB, eds. Stoetling’s Anesthesia and Co-Existing Disease. 8th ed. Elsevier Inc; 2022:155-186.

4. Koplan BA, Stevenson, WG. Ventricular tachycardia and sudden cardiac death. Mayo Clin Proc. 2009;84(3):289-297. doi:10.1016/S0025-6196(11)61149-X

5. Kashou AH, Evenson CM, Noseworthy PA, et al. Differentiating wide complex tachycardias: a historical perspective. Indian Heart J. 2021;73(1):7-13. doi:10.1016/j.ihj.2020.09.006

6. Janse MJ, Rosen MR. History of arrhythmias. In: Kass RE, Clancy CE, eds. Basis and Treatment of Cardiac Arrhythmias. Springer; 2006;1-39. 

7. Garmel GM. Wide complex tachycardias: understanding this complex condition: part 1 – epidemiology and physiology. West J Emerg Med. 2008;9(1):28-39.

8. Katritsis DG, Brugada J. Differential diagnosis of wide QRS tachycardias. Arrhythmia & Electrophysiol Rev. 2020;9(3):155-160. doi:10.15420/aer.2020.20

9. Lam P, Saba S. Approach to the evaluation and management of wide complex tachycardias. Indian Pacing Electrophysiol J. 2002;2(4):120-126.

10. Marill KA. Tachydysrhythmias. In: Adams JG, Barton ED, Collings JL, DeBlieux PMC, Gisondi MA, Nadel ES, eds. Emergency Medicine. 2nd ed. Saunders; 2013:497-513.e2.

11. Medi C, Kalman JM, Freedman SB. Supraventricular tachycardia. Med J Aust. 2009;190(5):255-260. doi:10.5694/j.1326-5377.2009.tb02388.x 

12. McGill TD, Kashou AH, Deshmukh AJ, LoCoco S, May AM, DeSimone CV. Wide complex tachycardia differentiation: an examination of traditional and contemporary approaches. J Electrocardiol. 2020;60:203-208. doi:10.1016/j.jelectrocard.2020.04.006 

13. Stevenson WG, Zeppenfield K. Ventricular arrhythmias. In: Libby P, Bonow RO, Mann DL, Tomaselli GF, Bhatt DL, Solomon SD, eds. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine.12th ed. Elsevier, Inc; 2022:1288-1311. 

14. Ventricular fibrillation. American Heart Association. Updated November 15, 2022. Accessed November 29, 2022.

15. Kusumoto FM, Schoenfield MH, Barrett C, et al. 2018 ACC/AHA/HRS guideline on the evaluation and management of patients with bradycardia and cardiac conduction delay: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Circulation. 2019;140(8):16(9):e382-e482. doi:10.1161/CIR.0000000000000628

Author Bio

Martyn Bryson, a medical writer and editor living in Philadelphia, Pennsylvania, has more than a decade of experience covering a wide range of health and wellness topics.

The post Wide Complex Tachycardia appeared first on The Cardiology Advisor.

History & Epidemiology

Wolff Parkinson White syndrome, or WPW syndrome, is a condition that occurs when an extra electrical pathway in the heart causes a rapid heartbeat leading to congenital pre-excitation of the heart. In some cases, conduction through this accessory pathway leads to malignant tachyarrhythmias.¹ In a normal heart, electricity is conducted from the atria to the ventricles through the atrioventricular (AV) node.¹

The hallmark finding of Wolff Parkinson White syndrome is the electrocardiographic (ECG) finding of the delta wave.¹ Many patients are asymptomatic making epidemiological tracking a challenge. The estimated prevalence of WPW syndrome in the general population is 0.1 to 0.3%.¹

Wolff Parkinson White Syndrome Diagnosis & Presentation

Because some Wolff Parkinson White syndrome patients never develop an arrhythmia, these patients may be asymptomatic and have a normal physical exam.¹ Symptomatic patients typically present with cardiovascular symptoms such as palpitations, presyncope, or syncope due to tachyarrhythmia.²

Patients who are symptomatic may also present with chest pain, dyspnea, and even sudden cardiac death (SCD).¹ SCD typically occurs due to ventricular fibrillation.

Patients who previously experienced arrhythmia may have learned of their condition if an ECG was performed and exhibited the hallmark delta wave ECG finding associated with Wolff Parkinson White syndrome.¹ Patients may also discuss a family history of WPW syndrome.

Diagnostic Workup of Wolff Parkinson White Syndrome

The initial diagnostic workup for Wolff Parkinson White syndrome includes the surface ECG.¹ ECG findings that are associated with Wolff Parkinson White syndrome include a short PR interval (<120 ms), prolonged QRS complex (>120 ms), and QRS morphology that includes a slurred delta wave.¹

WPW syndrome is split into type A and type B based on the direction of the dominant QRS deflection in lead V1 of the ECG.³ In Type A the QRS complex is typically upright with a negative delta wave in lead I.

In Type B the QRS complex and delta wave are typically negative in lead V1 while lead I shows a positive delta wave. Occasionally, patients may not present with this hallmark ECG pattern because some accessory pathway activity may be concealed.¹

Further diagnostic workup may be done to identify higher risk patients, which are those patients who are at greater risk of SCD.¹ Noninvasive methods for risk stratification include Holter monitoring, exercise treadmill testing, and echocardiography.² When noninvasive testing is insufficient, electrophysiologic (EP) studies may also be performed.

WPW Syndrome Differential Diagnosis

The differential diagnosis for Wolff Parkinson White syndrome is broad and includes acute events such as myocardial infarction, structural disease such as congenital abnormality or hypertrophy, and other conduction abnormalities such as regular narrow complex tachycardia, irregular narrow complex tachycardia, and regular wide complex tachycardia.¹

Management of Wolff Parkinson White Syndrome

Nonpharmacotherapy for WPW Syndrome

Wolff Parkinson White syndrome patients who are asymptomatic typically do not require immediate treatment.¹ Evaluation by a cardiologist or electrophysiologist can help to identify higher risk, asymptomatic patients. These higher risk patients are candidates for catheter ablation of the accessory pathway and preventive antiarrhythmic treatment as further described below.

WPW syndrome patients who are symptomatic are typically treated with catheter ablation.¹ Catheter ablation is the first-line treatment because it is less invasive than surgical ablation.

Pharmacotherapy for WPW Syndrome

Medical management is reserved for those who are poor candidates for catheter ablation and include flecainide and propafenone, among other medications.¹

Patients with an acute episode of tachyarrhythmia are managed according to the 2010 American Heart Association guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care algorithm.¹

Avoiding AV node blocking medications such as calcium channel blockers and beta blockers is essential as these medications can exacerbate symptoms.¹

Monitoring Side Effects, Adverse Events, Drug-Drug Interactions

Catheter ablation procedures carry the risk of adverse events including the commonly cited AV block.⁴ Other serious complications include death, esophageal perforation, heart block requiring a pacemaker, stroke, phrenic nerve injury, and vascular access complications.⁵

Vascular access complications such as arteriovenous fistula, aneurysm, and retroperitoneal bleeding more commonly impact surgery recovery and occur in 2 to 4% of cases.⁵ Due to this broad range of possible complications, patients should be thoroughly informed of the risks prior to the procedure.

Medical management may include antiarrhythmic medications such as flecainide and propafenone. Both of these medications are part of the sodium channel blocker class 1C group of antiarrhythmic medications and therefore have similar profiles.⁶

When using for ventricular arrhythmia prophylaxis, flecainide dosage is 100 to 400 mg taken orally at 8 or 12-hour intervals.⁷ The dose may need to be adjusted for patients with renal disease.

The main adverse effects are cardiac toxicity and an increased incidence of mortality which can occur due to the medication’s proarrhythmic effects. Flecainide is contraindicated with known hypersensitivity to flecainide, structural heart disease, and documented second or third-degree AV block, among others.⁷

The medication should be used with caution in patients who have myocardial dysfunction, heart failure, QT prolongation, electrolyte abnormalities, and those with a pacemaker. Flecainide interacts with many medications, and a thorough evaluation of drug-drug interactions should be performed with its use.

Significant interactions occur between flecainide and ritonovir, cisapride, despiramine, dronedarone, quinidine, saquinavir, and tipranavir.⁷

In addition to a sodium channel blocker profile, propafenone, also has beta blocking and calcium channel blocking activity which worsens its toxicity profile.⁶ As with flecainide, drug-drug interactions are common, and a thorough assessment of possible drug-drug interactions is necessary.

Patients with suspected sodium channel blocker toxicity should receive immediate ECG evaluation.⁶ Management of toxicity includes administration of sodium bicarbonate and management of hypotension, seizures, and extracorporeal membrane oxygenation (ECMO) in refractory cases.⁶

Drugs to avoid in Wolff Parkinson White syndrome are AV node blocking medications such as adenosine, calcium channel blockers, and beta blockers because these medications can exacerbate the associated arrhythmias.¹

Wolff Parkinson White Syndrome ICD 10 Code

Here is the ICD 10 code relevant to Wolff Parkinson White syndrome, or pre-excitation:

References

1. Chhabra L, Goyal A, Benham MD. Wolff Parkinson White syndrome. In: StatPearls. NCBI Bookshelf version. StatPearls Publishing: 2022. Accessed July 14, 2022.

2. Rao AL, Salerno JC, Asif IM, Drezner JA. Evaluation and management of Wolff Parkinson White in athletes. Sports Health. 2014;6(4):326-332.

3. Narula OS. Wolff Parkinson White syndrome. Circulation. 1973;47:872-887.

4. Cohen M, Triedman J. Guidelines for management of asymptomatic ventricular pre-excitation. Circ Arrhythm and Electrophysiol. 2014;7(2):187–189. doi:10.1161/CIRCEP.114.001528.

5. Ghzally Y, Ahmed I, Gerasimon G. Catheter ablation. In StatPearls. NCBI Bookshelf version. StatPearls Publishing: 2021. Accessed July 14, 2022.

6. Dokken K, Fairley P. Sodium channel blocker toxicity. In StatPearls. NCBI Bookshelf version. StatPearls Publishing: 2022. Accessed July 14, 2022.

7. Arunachalam K, Alzahrani T. Flecainide. In StatPearls. NCBI Bookshelf version. StatPearls Publishing: 2021. Accessed July 14, 2022.

Author Bio

Anna Courant is a nurse practitioner and writer.

Updated: 03/29/2023

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