A physician-validated, board-style question from the Active Transport QBank. Try it, then check the reasoning for every option.
A 45-year-old African American man with a history of alcohol use disorder presents to the clinic with increasing fatigue and shortness of breath over the past 3 months. He reports orthopnea and occasional paroxysmal nocturnal dyspnea. On examination, his blood pressure is 130/85 mmHg, pulse is 90/min, and respiratory rate is 18/min. Cardiac auscultation reveals a displaced apex beat and an S3 gallop. An echocardiogram shows dilated cardiac chambers with reduced ejection fraction. Which of the following is the most likely underlying mechanism for this patient's cardiac condition?
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A
Congenital heart disease causing structural defectsIncorrect. Congenital heart disease would have been diagnosed earlier and doesn't fit the late-onset DCM picture.
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B
Valvular stenosis leading to pressure overloadIncorrect. Valvular stenosis would produce a characteristic murmur and concentric hypertrophy, not dilation.
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C
Chronic alcohol toxicity leading to direct myocardial damageCorrect. Chronic alcohol toxicity directly damages cardiac myocytes, causing dilated cardiomyopathy as described.
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D
Coronary artery disease causing ischemic changesIncorrect. Coronary artery disease causes ischemic cardiomyopathy with regional wall motion abnormalities, not described.
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E
Chronic hypertension causing left ventricular hypertrophyIncorrect. Hypertensive cardiomyopathy causes concentric hypertrophy first, not the global dilation seen here with only mildly elevated BP.
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Answer: C. The vignette describes a patient with typical features of dilated cardiomyopathy (DCM), including a history of alcohol use, symptoms of heart failure, and echocardiographic findings of dilated chambers. Chronic alcohol use can lead to direct myocardial damage, contributing to DCM. This eliminates the option of hypertension, as the blood pressure is normal and there is no mention of left ventricular hypertrophy. Coronary artery disease is ruled out by the absence of specific ischemic symptoms and risk factors.