2 diabetes mellitus. He takes glyburide and pravastatin. His physical examination demonstrates a heart rate of 98/min

Transcription

1 Cardiology Board Review

2 Question 1 A 76-year-old man is evaluated for new-onset atrial fibrillation. He reports fatigue and decreased exercise tolerance for approximately 6 weeks, but otherwise feels well with no chest pain or palpitations. His medical history is pertinent for a 10-year history of hypertension treated with hydrochlorothiazide and type 2 diabetes mellitus. He takes glyburide and pravastatin. His physical examination demonstrates a heart rate of 98/min and a blood pressure of 162/88 mm Hg. The cardiac examination reveals an irregular rate with no murmur and an S1 of variable intensity. The lungs are clear to auscultation. The echocardiogram demonstrates left ventricular hypertrophy p y with normal left ventricular function and left atrial enlargement.

3 What is the most effective way to prevent stroke in this patient? A Aspirin therapy B Warfarin therapy with target INR of 2 to 3 C Cardioversion i and antiarrhythmic th i drugs for maintenance of sinus rhythm D Aspirin i combined with clopidogrel l

4 Risk factors for stroke in atrial fibrillation include prior embolic event or stroke, hypertension, advanced age, left ventricular dysfunction, coronary artery disease, and diabetes mellitus. The overall risk in patients with atrial fibrillation is determined using the CHADS2 score. This patient has a CHADS2 score of 3, which indicates that he has a high risk of stroke. Current guidelines mandate that unless there is a contraindication, warfarin should be administered to all patients with atrial fibrillation and risk factors for stroke (CHADS2 score of 1 or greater). The target intensity for anticoagulation is an INR between 2 and 3, a range that provides the best balance between efficacy and bleeding risk.

5 Although low-dose aspirin is appropriate therapy for patients with risk factors for coronary artery disease, aspirin offers only modest protection from stroke in atrial fibrillation, showing less consistency in its benefit compared to warfarin, probably because atrial clots are not rich in platelets. Antiarrhythmia therapy does not appear to prevent stroke; many patients continue to have asymptomatic episodes of atrial fibrillation and therefore remain at risk for stroke. The role of clopidogrel for stroke prevention in atrial fibrillation has not been determined. In addition, the combination of aspirin and clopidogrel increases the risk of life-threatening and other major bleeding as compared with aspirin i alone.

6 Question 2 A 64-year-old woman is evaluated in the emergency department 6 hours after the onset of severe ere crushing chest pain associated with diaphoresis, nausea, and vomiting. Her medical history is significant only for mild hyperlipidemia; her medications include atorvastatin and aspirin. Her blood pressure is 140/88 mm Hg, and her pulse rate is 88/min. The lungs are clear; she has no murmurs; examination of the abdomen and extremities is normal. Electrocardiogram shows a 3-mm ST-segment elevation in leads II, III, and avf, with occasional premature ventricular contractions. The hospital does not have cardiac catheterization facilities, and the patient is therefore given fibrinolytic therapy and transferred to another hospital's s intensive care unit. In transit, the chest pain resolves. The patient has two episodes of 6- to 10-beat ventricular tachycardia and stable hemodynamic parameters. Electrocardiogram now shows a <0.5-mV ST-segment elevation.

7 In addition to heparin and aspirin, which of the following approaches is the most appropriate next step? A Coronary angiography B Clopidogrel C β-blocker D Amiodarone E Dobutamine stress echocardiography

8 This patient has features of successful reperfusion after acute inferior ST-elevation myocardial infarction and may be treated medically until risk stratification is performed or recurrent ischemia or complications occur. Patients with depressed left ventricular systolic function by echocardiography are at high risk for ventricular tachyarrhythmias. Even the occurrence of asymptomatic nonsustained ventricular tachycardia within 48 hours of myocardial infarction should not change usual management consisting of aspirin, β-blockers,, angiotensin- converting-enzyme inhibitors, and statins. Evidence of successful fibrinolysis involves resolution of both chest pain and ST-segment elevation. The rapidity with which these resolve is directly related to early patency of the affected artery. Reperfusion arrhythmias, typically manifested as a transient accelerated idioventricular arrhythmia, usually do not require additional antiarrhythmic therapy

9 Immediate coronary angiography is not indicated unless recurrent rrent ischemia, persistent ST-segment elevation, or hemodynamic instability including congestive heart failure occurs. Clopidogrel may be added if indicated by stenting or significant additional evidence of atherosclerotic vascular disease. Dobutamine stress echocardiography to assess the heart for regions of myocardial viability and inducible ischemia can be performed after the patient has been stabilized and treated with initial medical management of myocardial infarction. If the patient can exercise, a limited exercise stress test may be the best option to assess cardiovascular risk. Predictors for future adverse events in post myocardial infarction patients include inability to exercise, exercise-induced ST-segment depression, failure to achieve 5 metabolic equivalents during treadmill testing, and failure to increase systolic blood pressure by 10 to 30 mm Hg during exercise.

10 Question 3 A 50-year-old asymptomatic man is evaluated during a routine follow-up 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, echocardiography showed left ventricular enlargement and hypertrophy, left ventricular ejection fraction of 40%, and no significant valvular disease. A 12-lead electrocardiogram was unchanged, showing left ventricular hypertrophy p y but no evidence of previous myocardial infarction. His current medications include 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. There is a soft S4 but no murmur, and the lungs are clear.

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

12 Treatment with an angiotensin-converting enzyme (ACE) inhibitor and a β-blocker is indicated for patients with all degrees of systolic heart failure, including asymptomatic patients, because treatment with both agents has been shown to reduce morbidity and mortality. Losartan, an angiotensin-receptor blocker (ARB), is an acceptable substitute 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 heart failure for the management of hypertension or angina not adequately controlled with an ACE inhibitor or β-blocker.

13 Early generation calcium-channel blockers, such as nifedipine, diltiazem, and verapamil, cause a reactive increase in sympathetic activity in response to peripheral vasodilation 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 asymptomatic systolic heart failure. Spironolactone reduces mortality in patients with severe symptomatic heart failure (New York Heart Association class III or IV) and left ventricular ejection fraction 35%. Digoxin alleviates symptoms and reduces hospitalizations ti related to heart failure, but has not been shown to reduce mortality.

14 Question 4 A72-year-old man is evaluated for lower extremity edema that has been worsening over the past 2 months. He notes 6 months of fatigue, a 9-kg (19.8 lb) weight gain, and dyspnea on exertion. He denies chest pain, palpitations, and syncope. He has long- standing intermittent arthralgias of his knees. He does not use tobacco but admits to occasional alcohol use. There is no history of hypertension or diabetes. Medications include indomethacin as needed for knee pain.

15 On physical examination he is in no acute distress. Pulse rate is 98/min, respiration rate is 20/min, and blood pressure is 141/82 mm Hg. Pulse oximetry on room air shows an oxygen saturation ti of 96%. Jugular veins are distended, increasing with inspiration. The lungs are clear. Heart sounds are normal with no evidence of murmur. An S4 gallop is present. Abdomen demonstrates a liver border 4 cm below the costal margin. Lower extremities show 2+ to 3+ pitting edema to the level of the knees.

16 12-lead electrocardiography shows diffuse low voltage and Q waves in leads V1 to V3. Chest radiograph shows normal heart size and clear lungs. Echocardiography shows moderate biatrial enlargement, a moderate to marked diffuse increase in left ventricular diastolic wall thickness with a small left ventricular cavity, normal regional and global left and right ventricular systolic function with an ejection fraction of 58%, restrictive filling without respiratory variation, and a small posterior pericardial effusion.

17 What diagnostic test is most appropriate to perform next? A Abdominal fat aspiration biopsy B Right and left heart hemodynamic catheterization C Nuclear perfusion stress test DE Endomyocardial di lbiopsy

18 This patient's clinical presentation suggests restrictive cardiomyopathy, and the results of diagnostic studies raise the suspicion of cardiac amyloidosis. Therefore, an abdominal fat aspiration biopsy to diagnose amyloidosis is the most appropriate test to perform next. This test is easily performed, is extremely safe, and is relatively sensitive. This patient's clinical presentation is consistent with heart failure. Examination findings indicative of right-sided heart failure include leg edema, jugular venous distention, and hepatomegaly. Echocardiography shows normal systolic function and confirms diastolic dysfunction with a restrictive filling pattern.

19 Common etiologies of diastolic dysfunction, such as hypertension, diabetes mellitus, and coronary or valvular heart disease are not readily apparent in this patient. The divergence between the electrocardiogram showing low voltage and the echocardiogram demonstrating a substantial increase in left ventricular wall thickness is the most obvious diagnostic clue to the etiology of diastolic dysfunction in this patient. These findings are most likely explained by a restrictive cardiomyopathy y from amyloidosis. It has been shown that if low voltage is present and interventricular septal thickness is greater than 1.98 cm, the diagnosis of cardiac amyloidosis can be made with a sensitivity of 72% and a specificity it of 91%. Clinically i ll significant ifi cardiac involvement is more common with primary amyloidosis (for example, plasma cell dyscrasia) and less common with secondary amyloidosis (for example, rheumatoid arthritis).

20 An endomyocardial biopsy of the right or left ventricle may be helpful in establishing the diagnosis of cardiac amyloidosis in unclear cases, particularly if the fat aspirate is negative. However, endomyocardial biopsy is invasive and carries greater risks as compared to an abdominal fat aspiration biopsy, and is therefore unwarranted as the next diagnostic test in this patient. A right and left heart hemodynamic catheterization can be crucial in the evaluation of patients with presumptive restrictive cardiomyopathy, particularly when constrictive pericarditis is possible. However, the lack of accentuated phasic respiratory variation in ventricular filling as noted on this patient's echocardiogram makes a diagnosis of constrictive pericarditis unlikely. In addition, the procedure is invasive and carries risks.

21 This patient has clinical signs of heart failure and an abnormal electrocardiogram demonstrating Q waves in the anterior leads. His risk factors for coronary artery disease include age and male gender. However, echocardiography shows no evidence of an anterior myocardial infarction. In addition, cardiac amyloidosis can display small or even absent R waves (i.e., Q waves) in the right precordial leads, simulating a myocardial infarction (a so-called pseudo-infarction pattern). Thus, a stress test for possible coronary artery disease would not be an appropriate p test to perform in this patient.

22 Question 5 A 78-year-old woman is evaluated for a 1-year history of progressively decreasing exercise tolerance. She has been in good health other than hypertension and osteoarthritis. Physical examination shows a regular pulse of 84/min, a respiration rate of 12/min, and blood pressure of 170/90 mm Hg. Carotid upstrokes are brisk, and her jugular venous pressure is 8 cm H2O. Her lungs are clear to percussion and auscultation. Her S1 is soft, and there is a physiologically y split S2. A grade 2/6 midsystolic murmur is present at the base with radiation to the apex but not to the carotids, and there is a grade 1/6 early diastolic decrescendo murmur at the left sternal border. There is no peripheral edema.

23 Which of this patient's physical examination findings are the most helpful for excluding severe aortic stenosis? A Blood pressure B Carotid upstroke C Second heart sound D Loudness of the murmur E Radiation of the murmur

24 Physical examination is helpful for defining the presence of heart valve disease but is less useful for evaluation of disease severity. In this elderly woman with symptoms that might be due to aortic stenosis, the presence of a systolic murmur on examination is concerning. The most helpful physical examination finding in this patient is a physiologically split S2, which has a specificity of 76% for excluding severe aortic stenosis. With severe stenosis, the stiff aortic valve leaflets do not snap shut, thus the aortic component of the S2 is absent. In addition, the physiologically split S2 rules out the delay in left ventricular ejection that is associated with severe stenosis.

25 About one-third of adults with severe aortic stenosis have systemic hypertension, so this finding does not exclude the diagnosis. In fact, concurrent hypertension and aortic stenosis double loads the left ventricle, resulting in increased wall stress and earlier symptom onset. In patients with hypertension, the increased stiffness of the peripheral vessels may mask the expected delay and decrease in carotid upstroke that is classically associated with severe aortic stenosis. The loudness of the murmur in aortic stenosis is only helpful when a grade 4/6 murmur (a palpable thrill) is present, because this finding is specific for severe valve obstruction. In the elderly, the murmur of aortic stenosis may radiate to the apex instead of to the carotids. In clinical practice, most physicians would obtain an echocardiogram in this patient t because aortic valve disease almost certainly is present, even if not yet severe. Echocardiography provides prognostic information in this setting

26 Mild aortic stenosis (aortic jet velocity <3 m/s, valve area >1.5 cm2) progression to symptoms occurs in only 8% of patients per year. Moderate aortic stenosis (jet velocity 3 4 m/s, valve area cm2), with an annual rate of symptom onset of about 17%. Severe stenosis (jet velocity >4 m/s, valve area <1.0 cm2), about 40% develop symptoms that prompt valve surgery within 1 year.

27

28 Question 6 A 72-year-old man is evaluated for bilateral leg pain and cramping after walking briskly up an incline. The pain is in the distal thigh and calf and is worse on the right side. He has no pain when walking downhill. The patient is a cigarette smoker with a 100 pack-year history; he has type 2 diabetes mellitus, hypertension, and heart failure. His medications are captopril, furosemide, atenolol, atorvastatin, insulin, and aspirin. On examination, the blood pressure is 146/68 mm Hg and pulse rate 82/min and regular. Cardiac examination reveals an S4. The lungs are clear. There is a right femoral artery bruit with diminished pulses and mild dependent rubor. Ankle-brachial index is 1.4.

29 What is the most likely cause of the patient's symptoms? A Ischemia with vascular calcification B Peripheral neuropathy CS Spinal stenosis D Osteoarthritis E Right popliteal vein thrombosis

30 ABI is measured as the ratio of the highest right/left dorsalis pedis/posterior tibial artery systolic pressure divided by the highest right/left brachial artery systolic pressure. A normal ABI is 1.0 to 1.3. Most patients with peripheral vascular disease have an ABI <0.9. Severe disease (rest ischemia), i an ABI of <0.4. An ABI >1.3 suggests a calcified, non- compressible vessel.

31 Peripheral neuropathy would be unlikely to present as pain with exercise. Spinal stenosis commonly presents as pain with standing and after a variable walking distance, most prominently with spinal extension, and is usually relieved by flexing forward, sitting, or lying. Like spinal stenosis, osteoarthritis may cause pain on walking but is usually independent of grade; neither condition can account for the patient's other findings including bruit, diminished pulses, and dependent rubor. Popliteal vein thrombosis may present with localized pain and Popliteal vein thrombosis may present with localized pain and erythema, but the pain would not be exertional, cannot account for bilateral pain, and ABI is unaffected.

32 Question 7 A 55-year-old man with coronary artery disease is evaluated 2 weeks after having had a myocardial infarction. On discharge, his medications included aspirin, sustained-release metoprolol, isosorbide mononitrate, lisinopril, and atorvastatin. Echocardiogram at that time showed inferior and posterior wall akinesis and a left ventricular ejection fraction of 40%. On examination, his heart rate is 60/min and his blood pressure is 130/70 mm Hg. Jugular venous pressure is normal and the chest is clear. Cardiac rhythm is regular, with normal S1 and S2 and no murmurs or extra heart sounds. Laboratory results from yesterday are potassium 5.7 meq/l (5.7 mmol/l), creatinine 1.0 mg/dl (88.42 µmol/l), and LDL cholesterol 65 mg/dl (1.68 mmol/l). Lisinopril therapy is stopped.

33 Which of the following medications should be started in this patient? A Valsartan B Spironolactone C Amlodipine i D Eplerenone E Hydralazine

34 This patient developed hyperkalemia as a side effect of angiotensin-converting enzyme (ACE) inhibitor therapy. The incidence of hyperkalemia is similar among patients taking ACE inhibitors, angiotensin-receptor blockers (ARBs), and spironolactone, and therefore, switching to valsartan or spironolactone would not be appropriate. In patients who cannot tolerate an ACE inhibitor or an ARB, the combination of hydralazine and nitrates should be used. This combination improves mortality over placebo (although not as much as with an ACE inhibitor).

35 In general, discontinuation of an ACE inhibitor should be considered if the potassium level el rises above 5.55 meq/l. Another side effect of ACE inhibitor therapy that occurs rarely is renal insufficiency, although renal insufficiency alone should not preclude treatment with ACE inhibitors. Although the risk of worsening renal function with ACE inhibitor therapy rises with the degree of baseline renal dysfunction, patients with the greatest degree of renal insufficiency generally derive the greatest long- term renoprotective effect from ACE inhibitor therapy. Some authors have proposed continuation of ACE inhibitor therapy if creatinine level increases 30% above baseline and stabilizes within 2 to 3 weeks. If the creatinine level remains elevated more than 30% above baseline after 4 weeks of ACE inhibitor therapy, dose reduction and/or further evaluation for other causes of renal insufficiency (such as nonsteroidal antiinflammatory drug use or renal artery stenosis) may be indicated.

36 Spironolactone for treatment of systolic heart failure is indicated only for patients with severe symptoms. Although vasodilator therapy is generally desirable for treatment of systolic heart failure, amlodipine has a neutral effect on morbidity and mortality in heart failure. Eplerenone, an aldosterone receptor selective antagonist, is currently indicated only for treatment of hypertension or for treatment of left ventricular dysfunction complicating myocardial infarction.

37 Question 8 A 23-year-old man is evaluated for palpitations p that occur during exercise. He is otherwise healthy and takes no medications. Both the physical examination and the resting electrocardiogram are normal. A stress test demonstrates sustained monomorphic ventricular tachycardia at 201/min at peak exercise. There were no ischemic changes until the arrhythmia developed. The ventricular tachycardia had a left bundle and inferior axis morphology and terminated spontaneously after 7 minutes of rest. An echocardiogram is normal, and an MRI shows no abnormalities in the right or left ventricles.

38 What is the most likely etiology of ventricular tachycardia in this patient? A Coronary spasm B Idiopathic CA Arrhythmogenic right ventricular ti cardiomyopathy D Infiltrative ti heart disease E Anomalous origin of the coronary arterie

39 Unlike other types of ventricular tachycardia, idiopathic ventricular tachycardia (ventricular tachycardia without structural heart disease) carries a good prognosis. Idiopathic ventricular tachycardia is diagnosed based on the electrocardiogram characteristics of ventricular tachycardia after excluding the presence of structural heart disease. Fewer than 5% of patients presenting with ventricular tachycardia have the idiopathic type. Because the prognosis is good in these patients, therapy is aimed at controlling symptoms. Medical therapy can be tried initially with β- blockers for those with right ventricular outflow tract tachycardia, and verapamil for those with idiopathic left ventricular tachycardia. For refractory symptoms, the cure rate with radiofrequency catheter ablation is excellent.

40 Coronary spasm can result in ventricular arrhythmia, but patients usually present with chest pain and STsegment elevation, which this patient did not report. The normal resting electrocardiogram, MRI, and echocardiogram rule out infiltrative diseases or arrhythmogenic right ventricular cardiomyopathy (fatty infiltration of the right ventricle). Anomalous origin of the coronary arteries can result in ventricular tachycardia or ventricular fibrillation in young people, but an MRI would detect this defect.

41 Question 9 A29-year-old man is evaluated following a syncopal episode. He was seated in his office typing and lost consciousness for approximately 60 seconds. There was no prodrome of dizziness, i palpitations, ti nausea, chest pain, or visual impairment. There was no confusion following the episode. He has no prior known medical illnesses. He has noticed exertional dyspnea and occasional palpitations for the last 5 years. He takes no medications.

42 On physical examination he is in no acute distress. Heart rate is 50/min. Blood pressure is 125/75 mm Hg. There are no orthostatic changes when he goes from a supine to a standing position. Funduscopic examination is normal with no arterial venous nicking or retinopathy. There is no jugular venous distention and carotids are 2+ with normal upstrokes. Lungs are clear. Cardiac examination shows no murmur at rest or during a Valsalva maneuver. A soft S4 gallop is present. Extremities are without edema.

43 Electrocardiography shows sinus bradycardia, first- degree atrioventricular block, left ventricular hypertrophy, and secondary ST- and T-wave changes. An echocardiogram shows normal left and right ventricular systolic function, a left ventricular ejection fraction of 73%, marked asymmetric septal hypertrophy, moderate concentric left ventricular hypertrophy, a small left ventricular cavity, and reduced early and accentuated late ventricular diastolic filling. A tilt-table test is normal.

44 What is the most likely cardiac diagnosis in this patient? A Hypertrophic cardiomyopathy B Dilated cardiomyopathy C Athlete's heart D Restrictive cardiomyopathy E Hypertensive cardiomyopathy

45 This patient's clinical presentation and diagnostic findings are indicative of hypertrophic cardiomyopathy. Although most patients with hypertrophic cardiomyopathy are asymptomatic, symptoms of pulmonary congestion, chest pain, fatigue, palpitations, dizziness, and syncope may develop. In patients with hypertrophic cardiomyopathy, syncope sometimes results from left ventricular outflow tract obstruction; however, absence of a murmur (as in this patient) does not exclude hypertrophic cardiomyopathy. Syncope in patients without left ventricular outflow tract obstruction may be caused by arrhythmias secondary to arrhythmogenic ventricular muscle.

46 Lack of a prodrome preceding the syncopal episode makes a vasovagal etiology unlikely, and vasodepressor syncope is unlikely given the normal tilt-table test. Normal left ventricular systolic function on echocardiography excludes a dilated cardiomyopathy y as a possible cause.

47 The remaining entities listed are associated with normal left ventricular systolic function and variable degrees of left ventricular hypertrophy. The degree and pattern of left ventricular hypertrophy in this patient is atypical for endurance training or athlete's heart, which would more commonly show an increased left ventricular chamber size at the upper limits of normal and a pattern of eccentric as opposed to asymmetric septal hypertrophy p y and/or concentric left ventricular hypertrophy. p y In addition, athlete's heart is not associated with impaired left ventricular diastolic filling. Restrictive cardiomyopathy shows a restrictive filling pattern in which peak early filling is rapid, duration of early filling is abbreviated, and the atrial contribution to filling is reduced. This patient does not exhibit a restrictive filling pattern.

48 Differentiation of hypertrophic cardiomyopathy from hypertensive cardiomyopathy is not always possible on the basis of diagnostic studies. The presence of dynamic left ventricular obstruction or unusual patterns of left ventricular hypertrophy h (such as asymmetric hypertrophy of the left ventricular septum, anterolateral wall, or apex) favors diagnosis of hypertrophic cardiomyopathy. In this patient, asymmetric septal hypertrophy is present. In addition, in hypertensive cardiomyopathy, a longstanding history of hypertension would be expected in order to explain the magnitude of this patient's left ventricular hypertrophy. p y

49 Question 10 A 23-year-old woman from Mexico is evaluated at 23 weeks of pregnancy. She has been experiencing increasing shortness of breath over the past 2 months. On examination, her blood pressure is 100/60 mm Hg, her pulse is regular at 88/min, and her respiratory rate is 26/min. Her jugular venous pressure is 18 cm H2O, carotid upstrokes are brisk, and bibasilar crackles are auscultated on pulmonary examination. On cardiac examination, the apical impulse is faint in the mid left 6th intercostal space, and there is a forceful sternal heave. The S1 is loud and there is a fixed split S2 and a soft systolic apical murmur. It is unclear whether there is a gallop or murmur in diastole.

50 Which is the most likely diagnosis? A Congenital aortic stenosis B Rheumatic mitral stenosis C Peripartum cardiomyopathy D Patent ductus arteriosus E Normal findings of pregnancy

51 This patient is from a region with a high prevalence of rheumatic heart disease and has symptoms of mitral stenosis. Her physical examination shows a loud S1 due to the forceful closing of the stenotic valve. Her S2 has a fixed split due to accompanying pulmonary hypertension and a prolonged right ventricular ejection time. Although the classic findings of mitral stenosis (an opening snap and a low-pitched diastolic rumble) were not appreciated in this case, auscultation of these findings often is difficult, particularly in a pregnant patient

52 Mitral stenosis is more common in women than men, and the age at symptom onset varies worldwide. Patients are often asymptomatic until there is a superimposed hemodynamic stress, such as pregnancy. Congenital aortic stenosis is characterized by a loud systolic murmur at the cardiac base. Peripartum cardiomyopathy typically presents later in pregnancy; although physical examination findings might be similar, the demographics in this case suggest that rheumatic valve disease is more likely. A patent ductus arteriosus results in a continuous cardiac A patent ductus arteriosus results in a continuous cardiac murmur. In pregnancy, a basal systolic ejection murmur is normal, but signs of heart failure are definitely abnormal.