Maintenance of Certification in Cardiology

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.

These questions were prepared by Hal A. Skopicki, MD, PhD.

Questions

A 46-year-old gentleman with aortic stenosis comes to your office noting dyspnea upon climbing 1 flight of stairs. He denies chest pain, palpitations or syncope. On exam, his blood pressure is 125/80 mm Hg, heart rate 88 beats per minute and respiratory rate is an unlabored 16 breaths per minute. He has no jugular venous distention (JVD). You note a delayed carotid upstroke that is decreased in volume. S₁ is normal, S₂ is physiologically split. No click is appreciated. An S₄ is present. He has a late peaking, II/VI systolic ejection murmur. You refer him for an echocardiogram that reveals a left atrium of 5.5 cm (upper limit of normal 4.5 cm), septal and posterior wall thicknesses of 1.3 cm (both upper limits of normal 1.0 cm), a left ventricular internal diastolic dimension of 6.6 cm (upper limit of normal of 5.5 cm) with moderate aortic stenosis, and a peak gradient of 30 m/sec with an aortic valve area of 1.1 cm². His left ventricular ejection fraction (LVEF) is 58%. Of the following choices, the next best step is:
1. Reevaluate in 12 months with a transthoracic echocardiogram.
2. Reevaluate in 6 months with a transthoracic echocardiogram.
3. Cardiac catheterization.
4. Cardiopulmonary exercise testing.
5. Referral for urgent surgery.

You are asked to lecture a group of medicine interns on the preoperative management of patients. All of the following are true, except:
1. Obtaining a preoperative resting 12-lead electrocardiogram (ECG) is a class I indication prior to all operations.
2. Noninvasive testing is not indicated for patients without clinical risk factors undergoing intermediate- risk noncardiac surgery.
3. Coronary revascularization before moderate risk noncardiac surgery is useful in patients with stable angina who have significant left main or major 3-vessel coronary artery disease (especially when LVEF is < 0.50) or 2-vessel disease with significant proximal left anterior descending stenosis and an LVEF < 0.50.
4. Coronary revascularization before noncardiac surgery is useful in patients with demonstrable ischemia on noninvasive testing, high-risk unstable angina or non–ST-segment elevation myocardial infarction (MI) or acute ST elevation MI.
5. ß blockers should be continued in patients who are receiving them to treat angina, symptomatic arrhythmias, or hypertension or initiated in patients undergoing vascular surgery who are at high cardiac risk owing to the finding of ischemia on preoperative testing.

Adequate secondary prevention in the management of cholesterol for patients with coronary vascular disease includes all the following except:
1. Goal low-density lipoprotein cholesterol (LDL-C) < 120 mg/dL and total cholesterol to < 200 mg/dL. If triglycerides are >200 mg/dL, non–high-density lipoprotein cholesterol should be < 130 mg/dL.
2. Initiating dietary therapy with a reduction in the intake of saturated fats.
3. Recommending the addition of plant stanol/sterols and viscous fiber to further lower LDL-C.
4. Encouraging increased consumption of omega-3 fatty acids in the form of fish or in capsule form is a level IIB indication.
5. With an acute cardiovascular or coronary event, further reduction of target LDL-C to < 70 mg/dL.

Prior to considering undergoing a heart transplantation for an idiopathic dilated cardiomyopathy (LVEF 25% with a maximal myocardial oxygen consumption of 11 mL/kg/min), one of your patients presents you with a list of potential medications that she will have to take to understand and include in her risk:benefit decision-making process. All of the following agents are matched with their mechanism of action and potential side effects except:
1. Cyclosporin (calcineurin inhibition)—hypertension, renal insufficiency, gingival hyperplasia, and hirsuitism.
2. Aziothioprine (antimetabolite)—Gastrointestinal (GI) complaints, liver failure, and bone marrow suppression.
3. Mycophenolate (antimetabolite inhibiting inosine monophosphate dehydrogenase)—GI complaints, viral infection, and leucopenia.
4. Sirolimus (macrolide antibiotic that inhibits cell cycle proliferation)—Pancytopenia, hyperlipidemia with hypertriglyceridemia.
5. Steroids (immunosuppressive and anti-inflammatory agents)—Hypertension, cataracts, myopathy, hirsutism, moon facies, buffalo hump, weight gain, and diabetes mellitus.

All of the following are true of dual-antiplatelet therapy with aspirin and clopidogrel except:
1. It lowers the risk of stent thrombosis and adverse cardiac events in patients who have undergone percutaneous coronary intervention.
2. It is more effective than aspirin alone at lowering the risk of atherothrombotic events in patients with stable cardiovascular disease or multiple risk factors.
3. It is associated with an increased risk of bleeding in the elderly (age >75 years) with acute coronary syndromes.
4. It may both safely and effectively reduce mortality and the occurrence of major adverse vascular events in patients presenting with acute MI.
5. Desensitization for clopidogrel-sensitive patients appears safe and highly effective in inducing a sustained remission for patients who require prolonged therapy after drug-eluting stents.

A patient with diabetes arrives at the emergency department with an acute inferior wall ST-elevation MI. Emergent cardiac catheterization 2 hours after the onset of chest pain reveals a 30% distal left main stenosis, 80% proximal left anterior descending (LAD) stenosis, 80% ostial left circumflex artery (LCx) stenosis, and a 95% mid right coronary artery (RCA) stenosis with thrombus. His LVEF is 35%. He is hemodynamically stable with a blood pressure of 110/60 mm Hg. Appropriate therapy could include all of the following except:
1. Urgent percutaneous coronary intervention (PCI) of the RCA, LCx, and LAD lesions.
2. PCI of the RCA followed by staged procedures for the LAD and LCx.
3. PCI of the RCA, placement of an intra-aortic balloon pump and coronary artery bypass graft surgery.
4. PCI of the RCA with follow-up nuclear perfusion study to consider staged procedures for the LAD and LCx.

Properties of the vulnerable atherosclerotic plaque may include:
1. Erosion of atherosclerotic plaque.
2. Rupture of the atherosclerotic plaque.
3. Calcium nodules within the periluminal area of the intima.
4. Local endothelial dysfunction.
5. Vasospasm.

A local internist refers a patient and includes an echocardiogram report noting a sinus venosus atrial septal defect. You should consider all of the following except:
1. Surgical closure if there is a pulmonary to systemic flow ratio of < 1.5 or less to prevent right ventricular dysfunction.
2. Surgical closure in patients with irreversible pulmonary vascular disease and pulmonary hypertension to forestall the need for cardiac transplantation.
3. Cardiac magnetic resonance imaging to look for partial anomalous drainage of the pulmonary veins.
4. Be reassured if the left-to-right shunting noted on prior echocardiograms begins to decrease.
5. Be reassured of the diagnosis if inverted P waves, signifying a junctional or low atrial rhythm, are present in the inferior leads.

Which of the following statements about endomyocardial biopsy is true?
1. In a 44-year-old man with cardiogenic shock, unexplained, new-onset heart failure of less than 2 weeks duration associated with a normal-sized left ventricle is a class II, level of evidence B, indication for endomyocardial biopsy.
2. In a 52-year-old woman, with new-onset heart failure of approximately 1 month duration, third degree heart block with a dilated left ventricle is a class I, level of evidence B indication for endomyocardial biopsy.
3. Unexplained atrial fibrillation is a class I, level of evidence B indication for endomyocardial biopsy.
4. Hypertrophic cardiomyopathy, believed to be due to a spontaneous mutation is a class I, level of evidence B indication for endomyocardial biopsy.
5. Suspected arrhythmogenic right ventricular (RV) dysplasia/cardiomyopathy is a class I, level of evidence B indication for endomyocardial biopsy

In patients with heart failure and systolic left ventricular dysfunction, an absolute contraindication (class III) for all angiotensin-converting enzyme (ACE)-inhibitor therapy includes:
1. An episode of angioedema in a patient on an ACE inhibitor for 4 months.
2. A history of hypotensive shock.
3. A serum creatinine of 2.1 mg/dL or greater.
4. Bilateral renal artery stenosis.
5. Cough exacerbated by recumbency.

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Answers

1: C

Echocardiography can underestimate the severity of aortic stenosis, especially if the Doppler beam is not perfectly parallel to the aortic stenosis jet. Similarly the echocardiogram may overestimate the presence of aortic stenosis, particularly in the presence of left ventricular dysfunction. In this case, your exam suggests severe aortic stenosis. The guidelines state that if a discrepancy exists between the physical exam and echocardiogram, cardiac catheterization should be performed. In clinical practice, a transesophageal transthoracic echocardiogram may be instructive and less invasive.

ACC/AHA 2006 Guidelines for the Management of Patients With Valvular Heart Disease: Executive Summary: A Report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines. Circulation. 2006;114(5):E84-231.

2: A

In emergent surgery, the need for surgery outweighs nearly all risk to proceed. However, preoperative resting 12-lead ECG is only recommended for patients with at least 1 clinical risk factor (history of ischemic heart disease, compensated or prior heart failure, cerebrovascular disease, diabetes mellitus, and renal insufficiency) undergoing vascular surgical procedures (level of evidence: IB) or for patients with known coronary heart disease, peripheral arterial disease, or cerebrovascular disease who are undergoing intermediate-risk surgical procedures (level of evidence: IC). It is not indicated in asymptomatic persons undergoing low-risk surgical procedures (level of evidence IIIB).

Noninvasive testing is not useful for patients without clinical risk factors undergoing intermediate-risk noncardiac surgery (level of evidence: IIIC). Coronary revascularization is indicated in situations with extensive unrevascularized coronary artery disease (CAD) with acute coronary syndromes (level of evidence: IA). It is not recommended that routine prophylactic coronary revascularization be performed in patients with stable CAD before noncardiac surgery (level of evidence: IIIB). ß blockers should be continued in patients who are receiving ß blockers to treat known cardiac conditions (level of evidence IC) or who may be at high cardiac risk based on preoperative testing (level of evidence: IB).

Fleisher LA, Beckman JA, Brown KA, et al. ACC/AHA 2007 Guidelines on Perioperative Cardiovascular Evaluation and Care for Noncardiac Surgery: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2007;116(17):1971-1996.

3: A

The target for LDL-C reduction is < 100 mg/dL. Dietary therapy should be encouraged with an intake of saturated fats less than 7% of a patient's total calories and the addition of plant stanol/sterols (2 g/d) and viscous fiber (>10 g/d) to further lower LDL-C. Daily physical activity and weight management can be an important component of cholesterol control in some patients. Encouraging increased consumption of omega-3 fatty acids in the form of fish or in capsule form is a level IIb indication. When a patient has a cardiovascular event despite an LDL-C < 70 mg/dL, it is reasonable to use pharmacologic therapy to reduce LDL-C further. Therapeutic options to reduce non–HDL-C include statins with more intense LDL-C–lowering therapy I (level Ib), niacin after LDL-C–lowering therapy (level IIa), or fibrate therapy, after LDL-C–lowering therapy (level IIa).

Smith SC Jr, Allen J, Blair SN, et al. AHA/ACC Guidelines for Secondary Prevention for Patients with Coronary and Other Atherosclerotic Vascular Disease: 2006 Update. Circulation. 2006;113(19):2363-2372.

4: D

Cyclosporin is believed to complex with ciclophilin to inhibit calcineurin responsible for the transcription of IL-2 and also in inhibits both lymphokine production and the function of effector T-cells. Aziothioprine is an older prodrug, converted in the body to the active metabolites 6-mercaptopurine and 6-thioinosinic acid, which inhibits purine synthesis. Its toxic effects may be increased with allopurinol. It is often being replaced by mycophenolate (CellCept), another antimetabolite immunosuppressant, which has decreased the incidence of acute rejection in solid transplants but is less toxic than aziothioprine. It is also now used for small-vessel vasculitides. Steroids are potent immunosuppressive and anti-inflammatory agents that are mainstays of therapy in acute rejection. They are believed to work through inhibition of the transcription factors, activator protein-1, and nuclear factor (NF)-B. Steroids are associated with the greatest number of side effects. In addition to those mentioned above, emotional lability, gastric ulcer, impaired wound healing, acne, skin fragility, hyperlipidemia, fluid retention, and osteopenia are prominent concerns. Sirolimus is a macrolide antibiotic that binds the FK 506 binding protein and inhibits the target of rapamycin kinase that is responsible for cell cycle proliferation in response to growth factors. It has been used in place of calcineurin inhibitors to treat rejection.

Kobashigawa JA, Patel JK. Immunosuppression for heart transplantation: where are we now? Nat Clin Pract Cardiovasc Med. 2006;3(4):203-212.

Lindenfeld J, Miller GG, Shakar SF, et al. Drug therapy in the heart transplant recipient. Part II: Immunosuppressive drugs. Circulation. 2004; 110(25):3858-3865.

Raichlin E, Bae JH, Khalpey Z, et al. Conversion to sirolimus as primary immunosuppression attenuates the progression of allograft vasculopathy after cardiac transplantation. Circulation. 2007;116(23):2726-2733.

5: B

Dual antiplatelet therapy has been shown to reduce stent thrombosis and adverse cardiac events. Several studies on suspected acute MI (left bundle branch block, STsegment elevation, or ST-segment depression) have found a significant reduction in the risk of reinfarction, stroke, and death in patients presenting with an acute MI with aspirin plus clopidogrel (9.2%) compared to the group given aspirin plus placebo (10.1%; 9% proportional risk reduction, 95% confidence interval [CI] 3%-14%, P = .002, data from the COMMIT study). All-cause mortality was also significantly lower in the aspirin-clopidogrel group than in the aspirin-placebo group (7.5% vs 8.1%; 7% proportional risk reduction, 95% CI 1%-13%, P = .03). Desensitization appears safe and highly effective in inducing a sustained remission in clopidogrel-sensitive patients who require prolonged dual antiplatelet therapy after placement of a drug-eluting stent. However, the CHARISMA study, which randomized more than 15,000 patients (> 45 years) with clinical cardiovascular disease or multiple cardiac risk factors to either aspirin plus placebo or aspirin plus clopidogrel, showed that clopidogrel added no significant benefit in preventing atherothrombotic events in patients with stable cardiovascular disease or multiple risk factors.

The Clopidogrel in Unstable Angina to Prevent Recurrent Events Trial Investigators. Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation. N Engl J Med. 2001;345(7):494-502.

Chen ZM, Jiang LX, Chen YP, et al. Addition of clopidogrel to aspirin in 45,852 patients with acute myocardial infarction: randomised placebocontrolled trial. Lancet. 2005;366(9497):1607-1621.

Sabatine MS, Cannon CP, Gibson CM, et al. Addition of clopidogrel to aspirin and fibrinolytic therapy for myocardial infarction with ST-segment elevation. N Engl J Med. 2005;352(12):1179-1189.

Mehta SR, Yusuf S. Short- and long-term oral antiplatelet therapy in acute coronary syndromes and percutaneous coronary intervention. J Am Coll Cardiol. 2003;41(4 suppl S):79S-88S.

Steinhubl SR, Berger PB, Mann JT 3rd, et al. Early and sustained dual oral antiplatelet therapy following percutaneous coronary intervention: a randomized controlled trial. JAMA. 2002;288(19):2411-2420.

Bhatt DL, et al. Clopidogrel and aspirin versus aspirin alone for the prevention of atherothrombotic events. N Engl J Med. 2006;354(16):1706-1717.

Schömig A, Neumann FJ, Kastrati A, et al. A randomized comparison of antiplatelet and anticoagulant therapy after the placement of coronaryartery stents. N Engl J Med. 1996;334(17):1084-1089.

Leon MB, Baim DS, Popma JJ, et al. A clinical trial comparing three antithrombotic-drug regimens after coronary-artery stenting. Stent Anticoagulation Restenosis Study Investigators. N Engl J Med. 1998; 339(23):1665-1671.

von Tiehl KF, Price MJ, Valencia R, et al. Clopidogrel desensitization after drug-eluting stent placement. J Am Coll Cardiol. 2007;50(4):2039-2043.

6: A

"Time is myocardium," and urgent revascularization of the culprit lesion is mandatory to acutely preserve at risk myocardium. However, the success of the initial procedure should not be compromised by revascularizing noninfarctrelated regions in the acute setting. The presence of significant left ventricular dysfunction during an acute MI, a time where a hyperdynamic and hypercontractile ventricle should be apparent, suggests a high-risk presentation. After successful percutaneous revascularization of the RCA, the clinical scenario is of a diabetic patient with significant 2-vessel disease (that includes a proximal LAD lesion) and a reduced LVEF. Although a greater survival benefit with surgical revascularization is suggested by the BARI study, the use of PCI is being evaluated in the ongoing, multicenter FREEDOM, CARDia, and SYNTAX trials.

Seven-year outcome in the Bypass Angioplasty Revascularization Investigation (BARI) by treatment and diabetic status. J Am Coll Cardiol. 2000;35(5):1122-1129.

Kip KE, Alderman EL, Bourassa MG, et al. Differential influence of diabetes mellitus on increased jeopardized myocardium after initial angioplasty or bypass surgery: bypass angioplasty revascularization investigation. Circulation. 2002;105(16);1914-1920.

Berry C, Tardif JC, Bourassa MG. Coronary heart disease in patients with diabetes: part II: recent advances in coronary revascularization. J Am Coll Cardiol. 2007;49(6):643-656.

Flaherty JD, Davidson CJ. Diabetes and coronary revascularization. JAMA. 2005;293(12):1501-1508.

Anastasiadis K, Moschos G. Diabetes mellitus and coronary revascularization procedures. Int J Cardiol. 2007;119(1):10-14.

Daemen J, Serruys PW. Optimal revascularization strategies for multivessel coronary artery disease. Curr Opin Cardiol. 2006;21(6):595-601.

7: E

Rupture of high-risk, vulnerable plaques is responsible for a significant portion of coronary thrombosis, unstable angina, acute MI, and sudden cardiac death. In addition to rupture, plaque erosion can also lead to occlusive thrombosis and acute coronary events. Endothelial dysfunction, plaque healing, and fibrocalcification also occurs. Targets for intervention include the endothelial dysfunction, modulation of cholesterol transport, and vascular remodeling. While vasospasm may occur, it is not felt to acutely initiate the cascade leading to plaque instability.

Libby P. Atherosclerosis: disease biology affecting the coronary vasculature. Am J Cardiol. 2006;98(12A):3Q-9Q.

Fuster V, Moreno PR, Fayad ZA, et al. Atherothrombosis and high-risk plaque: part I: evolving concepts. J Am Coll Cardiol. 2005;46(6):937-954.

Pucci A, Sheiban I, Formato L, et al. In vivo coronary plaque histology in patients with stable and acute coronary syndromes: relationships with hyperlipidemic status and statin treatment. Atherosclerosis. 2007;194(1): 189-195.

8: C

Atrial septal defects account for nearly 30% of all cases of adult congenital heart disease. Ostium secundum (presenting right-bundle branch block and right axis deviation) are most common. The presence of left-axis deviation occurs with ostium primum while inverted P waves, signifying a junctional or low atrial rhythm, are found with sinus venosus defects. With sinus venosus defects, partial anomalous drainage of the pulmonary veins may be present and their elucidation prior to surgery is helpful with surgical repair. Shunts with a flow ratio > 1.5 should be surgically closed to prevent RV failure. As the right ventricle fails, left-to-right shunting diminishes in magnitude and right-to-left shunt may actually occur. Once pulmonary hypertension becomes severe/irreversible, closure is contraindicated and a transplant evaluation should be performed.

Brickner ME, Hillis LD, Lange RA. Congenital heart disease in adults. First of two parts. N Engl J Med. 2000 Jan 27;342(4):256-263.

9: B

The latest guidelines suggest 2 scenarios that are class I, level of evidence B indications for endomyocardial biopsy: (1) new-onset heart failure of less 2 weeks' duration associated with a normal-sized or dilated left ventricle and hemodynamic compromise; and (2) new-onset heart failure of 2 weeks-to-3 months' duration associated with a dilated left ventricle and new ventricular arrhythmias, second- or thirddegree heart block, or failure to respond to usual care within 1 to 2 weeks. Endomyocardial biopsy may provide unique and clinically meaningful information and should be performed based on the ability to detect typical lymphocytic myocarditis (suggesting an excellent prognosis perhaps requiring supportive inotropic or mechanic assistance) and to detect giant cell and necrotizing eosinophilic myocarditis (which present with a more fulminant clinical course, requiring aggressive support and possibly urgent mechanical support). Therapy with combinations of immunosuppressive agents has been associated with improved outcomes in these cases. Endomyocardial biopsy is further indicated in the setting of unexplained, new-onset heart failure of 2 weeks'-to-3 months' duration associated with a dilated left ventricle and new ventricular arrhythmias, Mobitz type II second- or third-degree atrioventricular heart block, or failure to respond to usual care within 1 to 2 weeks to detect giant cell myocarditis.

Cooper LT, Baughman KL, Feldman AM, et al for the American Heart Association; American College of Cardiology; European Society of Cardiology; Heart Failure Society of America; and the Heart Failure Association of the European Society of Cardiology. The role of endomyocardial biopsy in the management of cardiovascular disease: a scientific statement from the American Heart Association, the American College of Cardiology, and the European Society of Cardiology. J Am Coll Cardiol. 2007;50(19):1914-1931.

10: A

Angiotensin converting enzyme inhibitors have consistently shown beneficial effects on mortality, morbidity, and quality of life in large-scale, prospective clinical trials and are a class IA indication in all stages of symptomatic heart failure resulting from impaired left ventricular systolic function. Bilateral renal artery stenosis is a strong, but relative, contraindication to the use of ACE inhibitors in patients with heart failure. Hypotension may occur due to a variety of causes and, once corrected, heart failure patients should almost always be rechallenged with an ACE inhibitor. Similarly, creatinine may be elevated for a variety of reasons and may improve with proper therapy or remain stable despite up-titration of ACE inhibitor therapy. In patients with intrinsic renal disease due to diabetes mellitus or hypertension, ACE inhibitor therapy may be salutory. Angioedema is a rare but potentially life-threatening adverse effect of ACE inhibitors that usually appears during the first weeks of treatment. However, late appearances have been described. Cross reaction with angiotensin receptor blockers is rare and these agents should be used with ACE inhibitors are not tolerated.

Ricketti AJ, Cleri DJ, Ramos-Bonner LS, Vernaleo JR. Hereditary angioedema presenting in late middle age after angiotensin-converting enzyme inhibitor treatment. Ann Allergy Asthma Immunol. 2007;98(4): 397-401.

Garcia-Pavia P, Tomas JM, Alonso-Pulpón L. Late-onset angioedema due to an angiotensin-converting enzyme inhibitor. Can J Cardiol. 2007;23(4): 315-316.

Flattery MP, Sica DA. Angiotensin-converting enzyme inhibitor-related angioedema: recognition and treatment. Prog Cardiovasc Nurs. 2007; 22(1):47-51.

Byrd JB, Adam A, Brown NJ. Angiotensin-converting enzyme inhibitor-associated angioedema. Immunol Allergy Clin North Am. 2006;26(4):725-737.