Answers

1: B

Isolated premature ventricular contractions (PVCs) are common after a myocardial infarction (MI). Frequent or complex PVCs in the post-MI period have been shown to signify increased mortality, especially in patients with reduced left ventricular function. The Cardiac Arrhythmia Suppression Trial (CAST) tested the hypothesis that suppression of asymptomatic or mildly symptomatic ventricular arrhythmias after acute MI with the Class IC antiarrhythmics encainide or flecainide would decrease mortality during long-term follow-up. The results from CAST showed that encainide and flecainide caused an increased cardiovascular mortality with a relative risk of 2.5. As a result, antiarrhythmic suppression of frequent or complex PVCs after an MI is no longer recommended.

Echt DS, Liebson PR, Mitchell LB, et al. Mortality and morbidity in patients receiving encainide, flecainide, or placebo. The Cardiac Arrhythmia Suppression Trial. N Engl J Med. 1991;21;324(12):781-788.

2: E

After an acute coronary syndrome (ACS), an aggressive lipid-lowering strategy with a statin has been proven to reduce future cardiovascular events. The Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis in Myocardial Infarction 22 (PROVE ITTIMI 22) study randomized more than 4000 hospitalized ACS patients to either pravastatin 40mg or atorvastatin 80 mg. Low-density lipoprotein cholesterol (LDL-C) decreased from a mean of 106 mg/dL in both groups to 95 mg/dL in the standard-dose pravastatin group and 62 mg/dL in the high-dose atorvastatin group. The primary composite end point of death, MI, unstable angina requiring hospitalization, revascularization, and stroke at a mean follow-up of 24 months was 26.3% in the standard-dose group versus 22.4% in the high-dose group. All-cause mortality was also reduced from 3.2% to 2.2%. This study, in addition to others, has led to the inclusion of the Class I recommendation that the "target LDL-C level after a STEMI should be substantially less than 100 mg/dL" in the 2004 American College of Cardiology/American Heart Association (ACC/AHA) guidelines on management of STEMI patients. Even in patients with normal LDL-C levels, early initiation of statin therapy has been proven to reduce cardiovascular events, presumably from their pleiotropic effects in addition to LDL-C lowering. Therefore the ACC/AHA guidelines also include the recommendation that "patients with LDL-C less than 100 mg/dL or unknown LDL-C levels should be prescribed statin therapy on hospital discharge."

Cannon CP, Braunwald E, McCabe CH, et al. Intensive versus moderate lipid lowering with statins after acute coronary syndromes. N Engl J Med. 2004;350(15):1495-1504.

3: B

The patient's electrocardiogram shows the classic characteristics of typical atrial flutter, with an inferiorly directed saw-tooth pattern. Typical atrial flutter is a macroreentrant arrhythmia that occurs in the right atrium with a counterclockwise activation. The circuit usually involves the isthmus that lies between the tricuspid annulus, the inferior vena cava, and the coronary sinus. The isthmus is readily accessible by an ablation catheter and provides an excellent target for radiofrequency ablation. Pulmonary vein isolation ablation is reserved for atrial fibrillation treatment and not for atrial flutter. Although there are no good controlled studies regarding risk of thromboembolism in these patients, anticoagulation is recommended. The flutter often is paradoxical and frequently degenerates into atrial fibrillation. The atrial flutter circuit frequently travels at a rate of approximately 300 beats per minute (BPM), and, depending on the amount of atrioventricular nodal blockade, the ventricular rate usually is 150, 100, or 75 BPM.

Wellens HJ. Contemporary management of atrial flutter. Circulation. 2002;106(6):649-652.

4: A

In 2007, the AHA published revised guidelines concerning who should receive antibiotic prophylaxis to prevent infective endocarditis (IE). These guidelines significantly reduced the number of conditions for which antibiotics were recommended. The revision was based on multiple factors, but specifically a lack of evidence that dental procedures cause a significant amount of IE cases compared with risks associated with daily activities. The investigators also concluded that even if antibiotic prophylaxis is 100% effective, it would prevent only an extremely small number of IE cases. Although prophylaxis was previously recommended for mitral valve disease with evidence of regurgitation, this is no longer the case.

Wilson W, Taubert KA, Gewitz M, et al. Prevention of Infective Endocarditis. Guidelines from the American Heart Association. Circulation. 2007;116(15):1736-1754.

5: D

This patient has long QT syndrome evidenced by her prolonged QT interval on electrocardiogram. Her tachyarrhythmia described as polymorphic ventricular tachycardia was torsade de pointes. The long QT syndrome is an acquired or congenital disorder of myocardial repolarization that can lead to sudden cardiac death. The most common causes of acquired QT prolongation are medications, such as Class III antiarrhythmics and fluoroquinolones, and electrolyte disorders, especially hypomagnesemia and hypokalemia. The congenital form is caused by a genetic mutation also leading to abnormal repolarization and a high risk of sudden cardiac death, especially in the young. Acute therapy of long QT and torsade de pointes includes removal of the offending agent if it is acquired, magnesium infusion, and increasing the heart rate. Increasing the heart rate serves to shorten the QT interval and can be achieved either through atrial pacing or isoproterenol infusion. Patients with the congenital form should be started on ß blockers, which have been proven to reduce arrhythmias, undergo genetic testing, have first-degree relatives evaluated, and be evaluated for insertion of an ICD to prevent sudden cardiac death.

Moss AJ. Long QT syndrome. JAMA. 2003;289(16):2041-2044.

Roden DM. Drug-induced prolongation of the QT interval. N Engl J Med. 2004;350(10):1013-1022.

6: C

Bicuspid aortic valve has been reported to occur in approximately 30% to 40% of cases of coarctation of the aorta. Although mitral stenosis, mitral regurgitation, and ventricular septal defects have also been associated with coarctation, these are much less common. Bicuspid aortic valve is a common cause of early-onset aortic stenosis, with frequent presentation in the fourth decade of life.

Brickner ME, Hillis LD, Lange RA. Congenital heart disease in adults. First of two parts. N Engl J Med. 2000;342(4):256-263.

7: D

Hypertrophic cardiomyopathy (HCM) is a genetic cardiac disorder that is the leading cause of sudden cardiac death (SCD) in young people. Four risk factors have been identified that increase the risk of SCD in these patients. These are massive left ventricular hypertrophy > 30 mm, history of HCM-related SCD in a first-degree relative, nonsustained ventricular tachycardia on Holter monitoring, and unexplained syncope not thought to be vasovagal. Outflow obstruction has not been shown to increase the risk of SCD independently. If any of these risk factors are present, then placement of an ICD for primary prevention should be further evaluated.

Maron BJ, McKenna WJ, Danielson GK, et al. American College of Cardiology/European Society of Cardiology clinical expert consensus document on hypertrophic cardiomyopathy. J Am Coll Cardiol. 2003;42(9):1687-1713.

8: B

Intraortic balloon pump counterpulsation devices are inserted through the femoral artery and are situated in the descending aorta just distal to the left subclavian artery. The balloon inflation is timed so that inflation, not deflation, occurs at the dicrotic notch of the arterial waveform, coinciding with closure of the aortic valve. Indications for placement include cardiogenic shock and mechanical complications of MI, such as mitral regurgitation. Contraindications include aortic insufficiency and aortic disease. By inflating during diastole, coronary blood flow is increased.

Stone GW, Ohman EM, Miller MF, et al. Contemporary utilization and outcomes of intra-aortic balloon counterpulsation in acute myocardial infarction: the benchmark registry. J Am Coll Cardiol. 2003;41(11):1940-1945.

9: E

Atrial fibrillation is the most common arrhythmia, increasing in incidence with increasing age. Embolic stroke is a devastating consequence, but one that can be prevented with anticoagulation. The CHADS2 score provides an algorithm for determining who needs anticoagulation based on the yearly risk of stroke. One point is assigned for congestive heart failure, hypertension, age > 75 years, and diabetes. A history of stroke is assigned 2 points. The yearly risk of stroke for scores of 0, 1, 2, 3, 4, 5, or 6 are 1.9%, 2.8%, 4.0%, 5.9%, 8.5%, 12.5%, and 18.2%, respectively. Based on this, our patient has a risk of 4% per year of stroke. Based on this, he should be started on warfarin. The AFFIRM trial showed that a strategy of rate control was equal to a strategy of maintaining sinus rhythm. Cardioversion can be performed safely without transesophageal echocardiogram if the onset of atrial fibrillation was less than 48 hours. Pulmonary vein isolation is effective 70% to 80% of the time.

Gage BF, Waterman AD, Shannon W, et al. Validation of clinical classification schemes for predicting stroke: results from the National Registry of Atrial Fibrillation. JAMA. 2001;285(22):2864-2870.

10: B

Cardiac tamponade occurs when the rapid accumulation of pericardial fluid causes equalization of intracardiac and intrapericardial pressures. Pulsus paradoxus is an exaggeration of the normal systolic fall in systemic blood pressure with inspiration. Normally this is less than 8 mm Hg, but in cardiac tamponade this fall is usually greater than 10 mm Hg. Echocardiogram is helpful in identifying tamponade physiology, especially early in the course of the disease. Collapse of the right ventricle is highly specific. A decrease in mitral inflow velocity during inspiration correlates with pulsus paradoxus.

Spodick DH. Acute cardiac tamponade. N Engl J Med. 2003;349(7):684-690.