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Question:

A 35-year-old man comes to the office with progressive fatigue, dyspnea on exertion, and lower extremity edema over the last 2 weeks.  Preceding these symptoms, he had an episode of fever, runny nose, and myalgias that resolved after several days.  The patient has no other medical history, takes no medications, and has no significant family history.  He occasionally drinks alcohol and does not use tobacco.  Blood pressure is 112/74 mm Hg, and pulse is 98/min and regular.  Physical examination reveals jugular venous distension, bibasilar crackles on lung auscultation, and 2+ pitting edema involving the lower extremities.  Which of the following echocardiographic findings is most likely to be seen in this patient?

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Explanation:

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This patient's presentation with dyspnea, lower extremity edema, jugular venous distension, and pulmonary crackles is consistent with decompensated heart failure.  In a young patient who develops heart failure following a symptomatic viral prodrome (eg, fever, sinus congestion, myalgias), dilated cardiomyopathy (DCM) due to viral myocarditis should be suspected.  A number of viruses have been implicated in causing DCM including coxsackievirus, adenovirus, and influenza virus.  It is believed that an inadequate immune response to the viral infection allows virus to infect and persist inside cardiomyocytes, resulting in damage due to a direct cytotoxic effect or a destructive autoimmune reaction.

Depletion of cardiomyocytes with subsequent fibrosis causes weakened myocardial contractility (systolic dysfunction), volume overload, and ventricular dilation (eccentric hypertrophy) as surviving myocytes respond to increased wall stress.  Other causes of DCM include genetic disease, pregnancy, infiltrative disease (eg, late manifestation of amyloidosis or hemochromatosis), and drugs/toxins (eg, anthracyclines, chronic alcohol abuse).

(Choice A)  Concentric left ventricular (LV) hypertrophy with thickened walls and abnormal diastolic relaxation is characteristic of hypertensive heart disease due to long-standing uncontrolled hypertension.  Initially, the LV cavity is reduced in size and there is normal systolic function; however, over time, high afterload pressures can cause progressive systolic dysfunction, LV cavity enlargement, and heart failure.

(Choice C)  High systolic pressure gradient across the aortic valve is present in aortic stenosis; concentric LV hypertrophy can occur due to LV pressure overload.  Aortic stenosis can develop in relatively young patients due to calcification of a bicuspid aortic valve; however, a crescendo-decrescendo systolic murmur is expected on examination.

(Choice D)  Regional wall motion abnormality is suggestive of ischemic heart disease (eg, myocardial infarction).  Contractile function is impaired in the damaged portion of myocardium, resulting in systolic dysfunction with LV volume overload, eccentric hypertrophy, and LV cavity enlargement.  Ischemic heart disease is unlikely in this young patient without significant risk factors for cardiovascular disease.

(Choice E)  In patients with hypertrophic cardiomyopathy, systolic anterior motion of the mitral valve may worsen LV outflow tract obstruction.  Clinical features of hypertrophic cardiomyopathy include exercise-induced syncope (due to outflow obstruction) and sudden cardiac death (due to ventricular arrhythmia) in young athletes.

Educational objective:
Dilated cardiomyopathy results from direct damage to cardiomyocytes leading to myocardial contractile dysfunction (systolic dysfunction), volume overload, and ventricular dilation.  Viral myocarditis is a common cause of dilated cardiomyopathy and should be suspected in young patients who develop heart failure following a symptomatic viral prodrome.