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Sunday, April 3, 2011

Heart failure guidelines : strategies for implementation

A 50-year-old man is evaluated during a routine follow-up office visit for heart failure, which was diagnosed 1 year ago. A stress test at the time of diagnosis was negative for ischemia. At his most recent evaluation 4 months ago, an echocardiogram showed left ventricular enlargement and hypertrophy, a left ventricular ejection fraction of 40%, and no significant valvular disease. An electrocardiogram was unchanged, showing left ventricular hypertrophy but no evidence of previous myocardial infarction. The patient is currently asymptomatic, and his medications are hydrochlorothiazide and lisinopril.

On physical examination, heart rate is 85/min and blood pressure is 135/85 mm Hg. There is no jugular venous distention or peripheral edema. The lungs are clear. There is a soft S4 but no murmur.

Which of the following medications should be added to the patient's regimen?
A Carvedilol
B Digoxin
C Diltiazem
D Losartan
E Spironolactone

Key Points
* An angiotensin-converting enzyme inhibitor and a β-blocker are indicated in all patients with systolic heart failure, including asymptomatic patients with low ejection fractions.
* Spironolactone and digoxin are not indicated in patients with asymptomatic systolic heart failure.

Answer and Critique (Correct Answer = A)

Treatment with an angiotensin-converting enzyme (ACE) inhibitor and a β-blocker is indicated for all patients with any degree of systolic heart failure, including this asymptomatic patient with a low ejection fraction, because treatment with both agents has been shown to reduce morbidity and mortality.

Losartan, an angiotensin-receptor blocker (ARB), is an acceptable alternative in a patient who cannot tolerate an ACE inhibitor, but there is no benefit to adding an ARB to an ACE inhibitor. Calcium-channel blockers are indicated in patients with heart failure who have hypertension or angina that is not adequately controlled with an ACE inhibitor or β-blocker. First-generation calcium-channel blockers, such as nifedipine, diltiazem, and verapamil, cause a reactive increase in sympathetic activity in response to peripheral vasodilatation and negative inotropic effects, whereas second-generation calcium-channel blockers, such as amlodipine, are more vasoselective, less cardiodepressant, and do not appear to have a deleterious effect on outcome in patients with heart failure. Spironolactone and digoxin are not indicated for patients with asymptomatic systolic heart failure. Spironolactone reduces mortality in patients with severe symptomatic heart failure (New York Heart Association class III or IV) and a left ventricular ejection fraction ≤35%. Digoxin alleviates symptoms and reduces hospitalizations related to heart failure, but has not been shown to reduce mortality.

1. O’Connor CM. The new heart failure guidelines: strategies for implementation. Am Heart J. 2007;153:2-5. [PMID: 17394896]

Systolic Heart Failure

A 58-year-old man is evaluated in the office for a 3-month history of shortness of breath with exertion. He has a 10-year history of hypertension and type 2 diabetes mellitus but no history of coronary artery disease. His medications are extended-release metoprolol, aspirin, metformin, and atorvastatin.

On physical examination, blood pressure is 165/92 mm Hg and heart rate is 88/min. Jugular venous pressure is 10 cm H2O. Bibasilar crackles are present, cardiac rhythm is regular, and an S3 is present. Electrocardiogram shows normal sinus rhythm and left ventricular hypertrophy. Laboratory test results include potassium of 4.2 meq/L and creatinine of 1.0 mg/dL. An echocardiogram is ordered, and furosemide is prescribed.

The patient returns the following week with resolution of his symptoms. His blood pressure at this visit is 130/78 mm Hg, his heart rate is 65/min, jugular venous pressure is 4 cm H2O, lungs are clear, and the S3 is absent. The echocardiogram shows left ventricular hypertrophy, reduced systolic function, and inferior wall hypokinesis.

Which of the following is the most appropriate medication change at this time?
A Change metoprolol to carvedilol
B Start digoxin
C Start lisinopril
D Start spironolactone

Key Point
Angiotensin-converting enzyme inhibitors are indicated for all patients with systolic heart failure, regardless of ejection fraction or functional status, barring contraindications.

Answer and Critique (Correct Answer = C)

Angiotensin-converting enzyme inhibitors are indicated for all patients with systolic heart failure, regardless of the level of the ejection fraction or functional status unless there are contraindications (including hyperkalemia, acute renal failure, or a history of angioedema).

Sustained-release metoprolol and carvedilol are both approved for heart failure treatment in the United States. Currently, there is no definitive evidence indicating whether one is better than the other for the treatment of heart failure. Digoxin improves symptoms and reduces hospitalizations for patients with heart failure but is not indicated for patients with asymptomatic heart failure in the absence of other indications (such as rate control for atrial fibrillation). Spironolactone is indicated for patients with heart failure who have severe symptoms (New York Heart Association class III or IV).

1. Dagenais GR, Pogue J, Fox K, Simoons ML, Yusuf S. Angiotensin-converting-enzyme inhibitors in stable vascular disease without left ventricular systolic dysfunction or heart failure: a combined analysis of three trials. Lancet. 2006;368:581-8. [PMID: 16905022]

Acute Myocarditis

A 26-year-old woman is hospitalized because of a 7-day history of increasing shortness of breath. Two weeks ago, she had flu-like symptoms of fever, muscle aches, and chest pain, which have since resolved. She does not take any medications.

On physical examination, temperature is 37 °C (98.6 °F), blood pressure is 120/79 mm Hg, and heart rate is 100/min and regular. The lungs are clear. Cardiac examination shows a normal S1 and S2. Echocardiogram shows normal-sized ventricles, decreased systolic function (left ventricular ejection fraction, 40%) that is global and most severe in the anterior wall, and no significant valvular abnormalities. Coronary angiography discloses no evidence of coronary artery disease.

Which of the following is the most appropriate next step in treating this patient?
A Azithromycin
B Enoxaparin
C Ibuprofen
D Lisinopril
E Prednison

Key Point
Therapy for acute myocarditis generally consists of standard care for heart failure tailored to the severity of the myocarditis.

Answer and Critique (Correct Answer = D)

This patient's presentation, including a viral prodrome, chest pain, symptoms and findings of heart failure in the absence of significant coronary artery disease, is consistent with acute myocarditis, which can range in presentation from asymptomatic to acute cardiogenic shock. Wall motion abnormalities on echocardiography can be regional or global during acute myocarditis. There is no specific treatment for acute myocarditis other than supportive care and the usual treatment for heart failure, including an angiotensin-converting enzyme inhibitor such as lisinopril, in the absence of contraindications.

The patient's normal blood pressure is not consistent with a serious infection, such as sepsis, and in the absence of other, more concrete evidence for infection, antibiotics are not indicated. The results of the coronary angiography rule out acute coronary syndrome, and therefore enoxaparin is not indicated. Although myocarditis is characterized by inflammation, there is no proven role for ibuprofen or corticosteroids for treatment.

1. Magnani JW, Dec GW. Myocarditis: current trends in diagnosis and treatment. Circulation. 2006;113:876-90. [PMID: 16476862]

Heart Failure

A 68-year-old woman is hospitalized with palpitations and shortness of breath. She has a history of hypertension and chronic atrial fibrillation, and her medications are furosemide, candesartan, and warfarin. On physical examination, the heart rate is 120/min with an irregularly irregular rhythm, and blood pressure is 130/80 mm Hg with no evidence of pulsus paradoxus. She has an elevated jugular venous pressure with normal x and y descent, crackles in both lungs, and marked lower extremity edema. Echocardiography shows left ventricular hypertrophy, an ejection fraction of 70%, and no significant valvular disease.

After intravenous diuretics are begun, the patient's symptoms improve, and the crackles and peripheral edema resolve. Her heart rate is now 99/min, and her blood pressure is 120/75 mm Hg.

Which of the following is the most likely primary mechanism of her heart failure?
A Constrictive pericarditis
B Diastolic dysfunction
C Systolic dysfunction
D Valvular disease

Key Point
The diagnosis of diastolic heart failure is generally made when signs and symptoms of systolic heart failure are present but the echocardiogram shows a normal left ventricular ejection fraction and an absence of significant valvular abnormalities.

Answer and Critique (Correct Answer = B)

This patient has a history and echocardiographic findings consistent with diastolic dysfunction. She has hypertension, which predisposes to the development of left ventricular hypertrophy and associated impaired ventricular relaxation.

Although she presented with evidence of heart failure, the echocardiogram demonstrated normal systolic function and no significant valvular abnormalities that could account for the heart failure. Therefore, systolic dysfunction and valvular disease are unlikely. Constrictive pericarditis is also unlikely in the absence of pulsus paradoxus, normal x and y descent, and no echocardiographic evidence of constrictive pericarditis, such as pericardial thickening or abrupt posterior motion of the ventricular septum in early diastole with inspiration.

The primary treatment goals in patients with diastolic heart failure are to treat the underlying cause (if possible), manage any potentially exacerbating factors, and optimize diastolic filling by slowing the heart rate with β-blockers. To date, there have been no medications shown to reduce morbidity and mortality in patients with diastolic dysfunction.

1. Chinnaiyan KM, Alexander D, Maddens M, McCullough PA. Curriculum in cardiology: integrated diagnosis and management of diastolic heart failure. Am Heart J. 2007;153:189-200. [PMID: 17239676]

Friday, April 1, 2011


A 38-year-old man is hospitalized with palpitations and dyspnea. He has no significant medical history and does not take any medications. He has a 20-pack-year smoking history and drinks alcohol daily. He does not use illicit drugs.

On physical examination, temperature is 36.9 °C (98.5 °F), blood pressure is 120/80 mm Hg, and heart rate is 115/min. Jugular venous pressure is normal. The lungs are clear. Cardiac examination shows an irregularly irregular rhythm. There is trace edema at both ankles.

Laboratory Studies
Hemoglobin 14 g/dL
Mean corpuscular volume 101 fL
Aspartate aminotransferase 55 U/L
Alanine aminotransferase 45 U/L
Thyroid-stimulating hormone 4.5 μU/mL

Electrocardiogram shows normal voltage, normal axis, and atrial fibrillation. Echocardiogram shows dilated ventricles with normal wall thickness and severely decreased systolic function (left ventricular ejection fraction, 15%). The patient is started on lisinopril, carvedilol, and warfarin. Later in the hospital course, he spontaneously converts to normal sinus rhythm, he feels well, and has a blood pressure of 105/75 mm Hg and a heart rate of 63/min. Electrocardiogram confirms normal sinus rhythm.

Which of the following is the most likely type of cardiomyopathy in this patient?
A Alcoholic
B Amyloid
C Hypertrophic
D Ischemic

Key Point
Alcoholic cardiomyopathy is a dilated cardiomyopathy.

Answer and Critique (Correct Answer = A)

This patient likely has alcoholic cardiomyopathy, which generally occurs after many years of heavy alcohol consumption, although it may also occur after a short period of heavy consumption. Typically, both ventricles are dilated and globally hypokinetic. The patient reports that he drinks alcohol daily, and his laboratory test results suggest chronic alcohol use (macrocytosis) and possibly an acute episode of heavy alcohol use (mild elevation of aminotransferases, new-onset atrial fibrillation). In addition to medical therapy for heart failure, therapy for alcoholic cardiomyopathy must include total abstinence from alcohol. Abstinence may reverse the cardiomyopathy in patients with less advanced disease.

Cardiac amyloidosis results in increased left ventricular wall thickness due to deposition of amyloid, and, as a result, typically presents with restrictive cardiomyopathy, which is characterized by diastolic rather than systolic dysfunction. On echocardiography, ventricular chambers are typically small with thick walls, and the atria are dilated. Because increased left ventricular wall thickness is caused by infiltration of the myocardium rather than hypertrophy, the electrocardiographic voltage is generally low.

Hypertrophic cardiomyopathy is characterized by inappropriate, marked, and asymmetric hypertrophy of the left ventricle. The hypertrophy usually involves the interventricular septum, although there is a wide range of severity and location of hypertrophy, hemodynamic consequences, and symptoms. The left ventricular cavity is small, unlike the cavity in this patient.

Ischemic cardiomyopathy is often, but not invariably, associated with symptomatic coronary artery disease. The electrocardiogram may show evidence of previous infarction and the echocardiogram typically shows focal, not global, hypokinesis.

1. Piano MR. Alcoholic cardiomyopathy: incidence, clinical characteristics, and pathophysiology. Chest. 2002;121:1638-50. [PMID: 12006456]

Premature Ventricular Contractions

A 33-year-old man is evaluated in the office for palpitations. He reports intermittent symptoms that do not correlate with any particular activity. He is only mildly disturbed by the palpitations but wants to have his heart evaluated. His medical history is unremarkable, and he takes no medications. His physical examination and electrocardiogram also are unremarkable. A 24-hour electrocardiogram shows a normal sinus rhythm with 3004 total premature ventricular contractions in 24 hours. An echocardiogram shows a structurally normal heart. Thyroid function studies and electrolyte levels are normal.

Which of the following is the most appropriate treatment for this patient?
A Atenolol
B Flecainide
C Radiocatheter ablation
D Reassurance

Key Point
In healthy adults, premature ventricular contractions are common and are not a cause for concern.

Answer and Critique (Correct Answer = D)

n healthy adults, premature ventricular contractions at rest are common and are not a cause for concern. Even very frequent premature ventricular contractions on a 24-hour electrocardiogram are not of concern in the absence of underlying structural heart disease. This otherwise healthy patient needs reassurance. Suppression of premature ventricular contractions is indicated only in patients with severe and disabling symptoms, which may include palpitations, fatigue, and lightheadedness. In these patients, β-blockers are the safest initial choice. Antiarrhythmic agents such as flecainide are associated with more side effects and thus are a second-line option for patients who continue to have debilitating symptoms despite β-blocker therapy. Catheter ablation of premature ventricular contractions is feasible; however, because of the technical demands of the procedure and its variable success rate, it is reserved for the most refractory cases.

1. Ng GA. Treating patients with ventricular ectopic beats. Heart. 2006;92:1707-12. [PMID: 17041126]

Asymptomatic Atrial Fibrillation

A 56-year-old man is evaluated in the office during a routine physical examination. He has no cardiovascular complaints. His medical history is unremarkable.

On physical examination, heart rate is approximately 90/min and irregularly irregular, and blood pressure is 130/78 mm Hg. Except for the abnormal cardiac rhythm, the remainder of the examination is unremarkable.

The electrocardiogram demonstrates atrial fibrillation with a heart rate of 92/min. The chest radiograph is unremarkable. Laboratory test results, including assessment of thyroid function, are normal. The patient is not aware of the abnormal rhythm or its duration.

In addition to heart rate control, which of the following would be most appropriate for this patient?
A Aspirin
B Clopidogrel
C Direct-current cardioversion
D Warfarin

Key Point
Aspirin is sufficient thromboembolic risk protection in patients with asymptomatic atrial fibrillation and no risk factors for stroke.

Answer and Critique (Correct Answer = A)

This patient with asymptomatic atrial fibrillation has no risk factors for stroke; therefore, aspirin would be sufficient thromboembolic risk protection. The CHADS2 score is used to assess stroke risk in patients with atrial fibrillation. The CHADS2 score assigns 1 point each for the presence of congestive heart failure, hypertension, age 75 years or older, and diabetes mellitus and 2 points for a history of stroke or transient ischemic attack. This patient's CHADS2 score is 0; therefore, risk of stroke is low and anticoagulation other than aspirin is not necessary.

Cardioversion is recommended primarily for patients with symptoms related to atrial fibrillation or patients with hemodynamic deterioration due to the loss of sinus rhythm. There are no data to suggest that conversion to sinus rhythm improves survival; cardioversion is therefore not indicated in this patient. If the patient's symptoms progressed to a point at which cardioversion would be indicated, anticoagulation with warfarin would be required first because of the potential of having an atrial clot that could embolize upon the restoration of sinus rhythm. Clopidogrel has not been demonstrated to be effective thromboprophylaxis for patients with atrial fibrillation. The combination of clopidogrel and aspirin has been shown to worsen outcomes in patients with atrial fibrillation by increasing the risk of bleeding.

1. Go AS, Fang MC, Singer DE. Antithrombotic therapy for stroke prevention in atrial fibrillation. Prog Cardiovasc Dis. 2005;48:108-24. [PMID: 16253651]