MOC Questions_1

Cardiology Review® OnlineAugust 2007
Volume 24
Issue 8

Preparing for the American Board of Internal Medicine Maintenance of Certification

The following questions can assist candidates for the Maintenance of Certification Exam in Cardiovascular Disease prepare for this test. We hope you find this helpful and welcome your feedback.


What can be said about the presence of peripheral arterial disease?

1. At a routine office visit, a 67-year-old man describes exertional leg (right calf) discomfort. He notes no diabetes or hypertension but does have a former (35 pack-year) smoking history. On physical exam you note a blood pressure of 160/90 mm Hg, a heart rate of 88 bpm, and a respiratory rate of 16 bpm. He has no jugular venous distention (JVD) or hepatojugular reflux (HJR). His lungs are clear bilaterally. You detect an S4; no murmur is detected despite provocative maneuvers. He has good femoral pulses. However, the dorsalis pedis pulses are difficult to palpate bilaterally. No ischemic changes are present on the lower extremities. You obtain blood pressures, in the supine position, in his brachial artery, doralis pedis, and posterior tibial arteries on both sides (right: 146, 96, and 92 mm Hg, respectively; left 155, 94, and 91 mm Hg, respectively).

  1. The patient has severe arterial obstructive disease.
  2. The patient has moderate arterial obstructive disease.
  3. The patient has mild arterial obstructive disease.
  4. The patient has no arterial obstructive disease and requires no intervention.
  5. The patient may have spinal cord or orthopedic issues.

2. What drug decreases the serum level of cyclosporin?

  1. Phenytoin
  2. Erythromycin
  3. Diltiazem
  4. Verapamil
  5. Cimetidine

The next step should be:

3. A 61-year-old previously healthy gentleman is admitted to the intensive care unit after a 4-day history of upper respiratory tract infection with now sudden onset of shortness of breath and mental status changes. When you see him he is unresponsive. His blood pressure is 80/50 mm Hg and his heart rate is 123 bpm. He is not breathing on his own and is rapidly intubated. Electrocardiogram reveals a sinus tachycardia with diffuse ST elevations. He has JVD to the angle of the jaw and bibasilar rales. He has no murmurs. No peripheral edema is present and his extremities are cool. A pulmonary artery catheter is placed, revealing a central venous pressure of 17 mm Hg, pulmonary artery pressure 60/30 mm Hg, and a pulmonary capillary wedge pressure of 26 mm Hg with a cardiac output 2.8 L/min. He is currently on norepinephrine, dopamine at 8 µg/kg/min, and a lasix infusion.

  1. Implantation of a left ventricular assist device.
  2. Initiation of intravenous levosimendan.
  3. Start intravenous nesiritide.
  4. Initiate ultrafiltration.
  5. Start intravenous dobutamine.

What cardiovascular complication is she most likely to subsequently develop?

4. You are asked to consult on a 45-year-old woman with chest tightness. She has had shortness of breath over a 1-year period of time that has not responded to antibiotics or inhalers. A chest computed tomography (CT) reveals only bilateral hilar lymphadenopathy. On exam, she has a blood pressure of 121/87 mm Hg, a heart rate of 125 bpm, and a respiratory rate of 25 bpm. She has diminished breath sounds bilaterally. A chest radiograph is unremarkable. A dobutamine stress echocardiogram is unremarkable except for baseline septal wall thickening and a right ventricular systolic pressure estimated at 25 mm Hg. No wall motion abnormalities are detected. Cardiac magnetic resonance imaging reveals discontinuous hyperenhancement within the myocardium in the septal, basilar anterior, anterolateral, and lateral walls, sparing the endocardium. In addition, T2-weighted imaging revealed subtle myocardial abnormalities in the same anatomic locations. The left ventricle was normal in size and shape, with mildly globally depressed function (left ventricular ejection fraction [LVEF] = 0.47).

  1. Myocardial ischemia.
  2. Pericardial tamponade.
  3. Conduction abnormality/heart block.
  4. Constrictive pericarditis.
  5. Pulmonary hypertension.

All of the following should be considered except:

5. A 51-year-old woman comes to your office with a history of an idiopathic dilated cardiomyopathy of 6 years duration. In the past 3 months, she has been hospitalized twice for acutely decompensated heart failure, the last time requiring inotrope-assisted diuresis. At that time, a biventricular pacemaker and an implantable cardiac defibrillator were implanted. Today, she reports continued dyspnea and fatigue when walking more than 50 feet. On exam, her heart rate is 92 bpm, blood pressure is 85/50 mm Hg, and respiratory rate is 28 bpm. She has JVD at 12 cm with positive HJR. She has bilateral rales, half way up in both lung fields. She has a laterally displaced point of maximal impulse, a II/VI holosystolic murmur at the apex radiating to the axilla, bilateral pitting edema to the knees, and warm extremities. She reports being compliant with her medical regimen, which includes carvedilol 25 mg twice a day, lisinopril 40 mg once a day, spironolactone 25 mg once a day, lasix 80 mg twice a day, metolazone 5 mg once a day, and dioxin 0.125 mg once a day. Laboratory results included: hematocrit 12.5 mg/dL, sodium 129 meq/dL, blood urea nitrogen 35 mg/dL, and creatinine 1.1 mg/dL. An echocardiogram, unchanged from 1 year ago, reveals biventricular heart failure with an LVEF of 20% to 25%. She has moderate mitral regurgitation and tricuspid insufficiency. Her VO2 max on cardiopulmonary exercise testing was 11 mL/min/kg.

  1. Addition of amlodipine for enhanced rate control.
  2. Admission for intravenous diuretics.
  3. Consideration of inotrope or vasodilator-assisted diuresis.
  4. Evaluation for left ventricular assist device implantation.
  5. Evaluation for cardiac transplantation.

What would you recommend next?

6. You are asked to consult on a 38-year-old woman with breast cancer who is being treated with a chemotherapeutic regimen that includes anthracycline (200 mg/m2) and trastuzumab for a HER2+ tumor with metastases. Radionucleotide ventriculography revealed a baseline ejection fraction of 59%. On follow-up, her ejection fraction is now 49%. She is scheduled for trastuzumab.

  1. Do not initiate the trastuzumab.
  2. Substitute trastuzumab with a lower dose of anthracycline.
  3. Repeat radionucleotide ventriculography in 3 months and to reassess use of trastuzumab.
  4. Give trastuzumab and follow ejection fraction at 3 weeks.
  5. Consider alternative medical regimen.

What is the current recommendation of future pregnancies?

7. A 22-year-old woman presents to you for a second opinion. She was diagnosed with peripartum cardiomyopathy during which time her LVEF was 20%. A repeat echocardiogram, 1 year after delivery reveals an LVEF of 40%. She jogs 1 mile a day without shortness of breath.

  1. Allow pregnancy with serial echocardiograms every 3-6 weeks.
  2. Allow pregnancy but delivery at 33 weeks with cesarean section.
  3. Allow pregnancy but switch lisinopril to hydralazine/oral nitrates.
  4. Allow pregnancy, stop beta blocker, and switch lisinopril to hydralazine/oral nitrates.
  5. Caution against future pregnancy.

Interventions known to improve her 1-year survival include:

8. A 62-year-old woman is admitted to the hospital with acutely decompensated heart failure. Until recently, she had led a fit and active life but had noted increasing breathlessness and swollen ankles over the past 2 months. She now describes 4 pillow orthopnea without chest pain or palpitations. On exam, her blood pressure is 101/78 mm Hg, heart rate regular at 98 bpm, and respiratory rate is 18 bpm. She has JVD to the angle of the jaw and a holosystolic murmur, but otherwise the cardiac exam is benign. She has a positive fluid wave sign, bilateral pitting edema to the knees, and is warm to touch in her extremities.

  1. The use of intravenous diuretics only.
  2. Inotrope-assisted diuresis.
  3. Intravenous nesiritide-assisted diuresis.
  4. Ultrafiltration to euvolemia.
  5. Initiation of ACE inhibition when hemodynamically stable.

Prior to considering atrioventricular ablation, which of the following may be tried?

9. You are asked to see a 48-year-old man with an ischemic cardiomyopathy and a prior history of symptomatic heart failure with episodes of paroxysmal atrial fibrillation (PAF). He was placed on amiodarone 1 year ago but this was discontinued 2 months ago due to increasing shortness of breath and a high suspicion of pulmonary toxicity on CT scanning. During the past 2 weeks, however, he has had several episodes of PAF associated with shortness of breath and requiring acute administration of higher doses of diuretics. He is currently on an ACE inhibitor, beta blocker, mineralocorticoid inhibitor, and is euvolemic. Most recent laboratory analysis shows a potassium level of 4.2 meq/L and a creatinine of 1.0 mg/dL.

  1. Propofenone.
  2. Flecainide.
  3. Verapamil.
  4. Dofetilide.
  5. Ibutilide.

Which of the following has the least affect on her surgical risk?

10. A 67-year-old woman presents with severe valvular aortic stenosis.

  1. The presence of concomitant moderate aortic insufficiency.
  2. The presence of a 95% left anterior descending artery disease.
  3. The presence of left ventricular systolic dysfunction and ventricular thinning.
  4. The presence of atrial fibrillation (AF) with a dilated left atrium.
  5. An aortic valve area of 0.6 cm2.


1: B

The ankle-brachial artery index (ABI) can be employed at the bedside to help evaluate for the presence of peripheral vascular disease. The ABI is measured by placing the patient in a supine position for 5 min. It is calculated as the ratio of the highest lower extremity pressure to the highest brachial artery pressure. In the example, 96/155 on the right (ABI .62) and 94/155 on the left (ABI .61) indicates moderate disease on both sides. The normal ABI is 0.9-1.3. Mild peripheral artery disease is indicated by an ABI .71-.90, moderate from .41-.70 and severe if the ABI is < 0.4. An ABI > 1.0 suggest a poorly compressible artery.

Klein S, Hage JJ. Measurement, calculation, and normal range of the ankle-arm index: a bibliometric analysis and recommendation for standardization. Ann Vasc Surg. 2006;20:282-292.

Goessens BM, Visseren FL, Algra A, et al for the SMART Study Group. Screening for asymptomatic cardiovascular disease with noninvasive imaging in patients at high-risk and low-risk according to the European Guidelines on Cardiovascular Disease Prevention: the SMART study. J Vasc Surg. 2006;43(3):525-532.

Belch JJ, Topol EJ, Agnelli G, et al. Critical issues in peripheral arterial disease detection and management: a call to action. Arch Intern Med. 2003;163:884-892.

2: A

Cyclosporin has had a major impact on cardiac transplantation. Although therapeutic drug monitoring of cyclosporin is extremely useful because of the wide inter- and intraindividual pharmacokinetic variability after oral or intravenous administration, long-term use of cyclosporin requires careful monitoring of the blood (or plasma) concentrations because of significant drug interactions. The clearance of cyclosporin is increased by drugs including rifampin, isoniazid, phenytoin, and phenobarbital. Decrease clearance of cyclosporin is caused by drugs including erythromycin, detoconazole, diltiazem, verapamil and cimetidine.

Campana C, Regazzi MB, Buggia I, Molinaro M. Clinically significant drug interactions with cyclosporin. An update. Clin Pharmacokinet. 1996;30:141-179.

3: E

The patient is in primary cardiogenic shock, in the setting of a myocarditis, as evidenced by hypotension and hypoperfusion. An inotropic agent is urgently needed to augment myocardial stroke volume and thus cardiac output. The use of the inotropic agent may also decrease the need for norepinephrine and dopamine, both being used as vasopressor agents in this example. In the setting of cardiogenic shock without peripheral vasodilation, consideration may have been given to the use of nitroprusside, nitroglycerin, or nesiritide. Once hemodynamic stability has been obtained, in the absence of adequate diuresis, ultrafiltration may be considered. Levosimendan is a new calcium sensitizer that also opens K-ATP channels. Exciting evidence suggests that compared with other inodilators, it improves myocardial contractility without increasing oxygen requirements. However, limited data and experience is available for its use in the setting of myocarditis. In the event of ongoing hemodynamic instability, consideration should be given for implantation of a left ventricular assist device as a bridge to recovery or transplantation, assuming that the patient's underlying mental status is intact.

McGhie AI, Golstein RA. Pathogenesis and management of acute heart failure and cardiogenic shock: role of inotropic therapy. Chest. 1992; 102:626S-632S.

Frazier OH, Delgado RM 3rd, Scroggins N, et al. Mechanical bridging to improvement in severe acute “nonischemic, nonmyocarditis” heart failure. Congest Heart Fail. 2004;10:109-113.

Dubin A, Murias G, Sottile JP, et al. Effects of levosimendan and dobutamine in experimental acute endotoxemia: a preliminary controlled study. Intensive Care Med. 2007;33:485-494.

4: C

Sarcoidosis is a multisystem disease of unknown etiology that can affect virtually any organ. Most typically it afflicts the lungs, liver, skin, and eyes with infiltrating, noncaseating granulomas. While it may occur in the heart in as many as 25% to 50% of patients with systemic sarcoidosis, it clinically manifests in only 5%. Clinical cardiac sequelae range from asymptomatic conduction abnormalities to heart block and fatal ventricular arrhythmias.

Nandya C, Brunken RC, Tchou P, et al. Detecting cardiac involvement in sarcoidosis: a call for prospective studies of newer imaging techniques. Eur Respir J. 2007;29:418-422.

Grutters JC, van den Bosch JM. Corticosteroid treatment in sarcoidosis. Eur Respir J. 2006;28:627-636.

Doughan AR, Williams BR. Cardiac sarcoidosis. Heart. 2006;92:282-288.

5: A

The patient has had recurrent hospital admissions despite optimized medical therapy including angiotensin-converting enzyme (ACE) inhibition, ß-blockade, a mineralocorticoid antagonist, digoxin, and a biventricular pacemaker. She requires admission for acute stabilization with intravenous diuretics (and vasodilators or inotropes if necessary) but also immediate evaluation for left ventricular assist device implantation as bridging therapy for cardiac transplantation if she cannot be medically stabilized. Amlodipine has not proven beneficial for acutely decompensated patients.

Loebe M, Koerner MM, Lafuente JA, Noon GP. Patient selection for assist devices: bridge to transplant. Curr Opin Cardiol. 2003;18:141-146.

Deng MC, Smits JM, Packer M. Selecting patients for heart transplantation: which patients are too well for transplant? Curr Opin Cardiol. 2002;17:137-144.

Lund LH, Aaronson KD, Mancini DM. Validation of peak exercise oxygen consumption and the Heart Failure Survival Score for serial risk stratification in advanced heart failure. Am J Cardiol. 2005;95:734-741.

Packer M, O'Connor CM, Ghali JK, et al. Effect of amlodipine on morbidity and mortality in severe chronic heart failure. Prospective Randomized Amlodipine Survival Evaluation Study Group. N Engl J Med. 1996; 335:1107-1114.

6: D

Anthracyclines (doxorubicin, daunorubicin, epirubicin, aclarubicin and idarubicin) are useful in the treatment of lymphomas, breast cancer and soft tissue sarcomas but are cardiotoxic. Although the exact mechanism of the cardiac toxicity is unknown, it may be due to the appearance of free radicals and interference with the mitochondrial electron transport chain. Although the cardiotoxicity may sometimes be fatal, improvement in ejection fraction has been reported in up to 80% of patients. Histologic changes are observed at cumulative doxorubicin doses that do not cause an increase in the pre-ejection period/left ventricular ejection time ratio. Cardiac damage is related to total cumulative dose, with those receiving more than 400 mg/m2 being at significant risk. With concomitant underlying heart disease, an abnormal electrocardiogram, or radiation exposure and an LVEF > 50%, check the patient's LVEF 3 weeks after adriamycin administration.

Schwartz RG, McKenzie WB, Alexander J, et al. Congestive heart failure and left ventricular dysfunction complicating doxorubicin therapy. Seven-year experience using serial radionuclide angiocardiography. Am J Med. 1987;82(6):1109-1118.

Druck MN, Gulenchyn KY, Evans WK, et al. Radionuclide angiography and endomyocardial biopsy in the assessment of doxorubicin cardiotoxicity. Cancer. 1984;53;1667-1674.

Bristow MR, Manson JW, Billingham ME, et al. Doxorubicin cardiomyopathy: Evaluation by phonocardiography, endomyocardial biopsy, and cardiac catheterization. Ann Intern Med. 1978;88:168-175.

Keefe DL. Trastuzumab-associated cardiotoxicity. Cancer. 2002;95:1592-1600.

7: E

Peripartum cardiomyopathy (PPCM) is a rare and potentially lethal cardiac complication of pregnancy occurring in the final month of pregnancy through the first 5 months after birth. It is characterized by the development of left ventricular systolic dysfunction, usually with congestive heart failure, in previously healthy women with no other identifiable cause for heart failure. While the signs and symptoms are similar to dilated cardiomyopathy and difficult to distinguish during the pregnancy, early diagnosis and initiation of treatment are essential to optimize pregnancy and maternal outcomes. About half the patients with PPCM recover without complications. Persistence of disease after 6 months indicates an irreversible cardiomyopathy and portends worse survival.

Elkayam U, Tummala PP, Rao K, et al. Maternal and fetal outcomes of subsequent pregnancies in women with peripartum cardiomyopathy. N Engl J Med. 2001;344:1567-1571.

Pearson GD, Veille JC, Rahimtoola S, et al. Peripartum cardiomyopathy: National Heart, Lung, and Blood Institute and Office of Rare Diseases (National Institutes of Health) workshop recommendations and review. JAMA. 2000;283:1183-1188.

8: E

Randomized, placebo-controlled mortality studies showing benefit of intravenous diuretics, inotrope, or vasodilator assisted diuresis and ultrafiltration have not been performed. Only ACE inhibitors, ß-blockers, and mineralocorticoid inhibitors have been shown to improve long-term survival in chronic heart failure patients.

Costanzo MR, Guglin ME, Saltzberg MT, et al for the UNLOAD Trial Investigators. Ultrafiltration versus intravenous diuretics for patients hospitalized for acute decompensated heart failure. J Am Coll Cardiol. 2007; 49:675-683.

Cleland JG, Coletta A, Witte K. Practical applications of intravenous diuretic therapy in decompensated heart failure. Am J Med. 2006;119:S26-S36.

Aaronson KD, Sackner-Bernstein J. Risk of death associated with nesiritide in patients with acutely decompensated heart failure. JAMA. 2006;296:1465-1466.

Shin DD, Brandimarte F, De Luca L, et al. Review of current and investigational pharmacologic agents for acute heart failure syndromes. Am J Cardiol. 2007;99(2A):4A-23A.

9: D

In heart failure patients without prior PAF, more than 20% will subsequently developed PAF over then next 4 years. The prevalence of PAF in patients with HF varies from 10% to 30%. While rate and not rhythm control in the absence of left ventricular dysfunction has been advocated, we do not know which strategy is better for patients with heart failure who develop PAF. Many advocate an initial attempt at maintaining sinus rhythm if PAF onset is associated with severe hemodynamic deterioration. The cornerstone of anti-arrhythmic therapy in these patients is amiodarone or dofetilide. The Danish Investigations of Arrhythmia and Mortality on Dofetilide in Congestive Heart Failure (DIAMOND-CHF) study included 1518 patients with recent hospitalizations and NYHA class III/IV heart failure and an LVEF ≤ 35%. Dosage adjustments were based on creatinine clearance and QTc interval prolongation. Dofetilide did not adversely affect mortality and significantly reduced the risk of hospitalization for worsening heart failure. However, torsades de pointes was seen in more than 3% of patients. Class I anti-arrhythmic agents and calcium channel blockers are contraindicated in heart failure. Finally, when antiarrhythmic drugs are ineffective and patients remain highly symptomatic, transcatheter ablation of PAF in the left atrium may be a valuable alternative.

Pardaens K, Van Cleemput J, Vanhaecke J, Fagard RH. Atrial fibrillation is associated with a lower exercise capacity in male chronic heart failure patients. Heart. 1997;78:564-568.

Wang TJ, Larson MG, Levy D, et al. Temporal relations of atrial fibrillation and congestive heart failure and their joint influence on mortality: the Framingham Heart Study. Circulation. 2003;107:2920-2925.

Torp-Pedersen C, Moller M, Bloch-Thomsen PE, et al. Dofetilide in patients with congestive heart failure and left ventricular dysfunction. N Engl J Med. 1999;341:857-865.

10: E

Aortic valve replacement surgery risk is related to underlying ventricular function (especially if the ventricular wall has thinned with LV dilation), the presence of ischemia and the need for concomitant surgical revascularization, the presence of AF, and the presence of coexisting aortic insufficiency. Aortic valve area determines the severity of the disease, but not the surgical risk. The necessity for aortic valve replacement should be assessed via a risk-benefit analysis in this setting and include the nature of the patients underlying renal, pulmonary, and neurologic status.

Stout KK, Otto CM. Indications for aortic valve replacement in aortic stenosis. J Intensive Care Med. 2007;22:14-25.

Alsoufi B, Karamlou T, Slater M, et al. Results of concomitant aortic valve replacement and coronary artery bypass grafting in the VA population. J Heart Valve Dis. 2006;15:12-18.

ACC/AHA Task Force on Practice Guidelines; Society of Cardiovascular Anesthesiologists; Society for Cardiovascular Angiography and Interventions; Society of Thoracic Surgeons; Bonow RO, Carabello BA, Kanu C, et al. ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2006;114:e84-e231.

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