A 63-year-old man comes to the emergency department due to progressive dyspnea and fatigue. Over the last week, he has not been able to lie flat due to difficulty breathing and has had to sleep in a sitting position. He had an anterior myocardial infarction 6 months ago and has not been compliant with his medication regimen since that time. Medical history is also significant for hypertension. The patient is an ex-smoker with a 30-pack-year history. He does not drink alcohol. His father died of a heart attack at age 60. Blood pressure is 170/100 mm Hg, and pulse is 100/min and regular. Oxygen saturation is 90% on room air. He is afebrile. Auscultation reveals crackles at the lung bases, an S3 gallop, and a II/VI holosystolic murmur over the apex. The patient is admitted to the hospital, and after treatment with diuretics and vasodilators his condition improves significantly. Three days later there are no appreciable gallops or murmurs on cardiac examination. Which of the following best explains the murmur heard at the time of the initial examination?
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This patient's presentation with fatigue, progressive dyspnea, orthopnea, pulmonary crackles, and an S3 heart sound is consistent with decompensated heart failure. Appropriate treatment with diuretics and vasodilators resulted in symptomatic improvement and disappearance of the apical holosystolic murmur, which was most likely due to secondary (functional) mitral valve regurgitation (MR).
Whereas primary MR is caused by an intrinsic defect of the mitral valve apparatus (eg, cleft in a valve cusp, myxomatous degeneration of the chordae tendineae), secondary MR occurs due to other factors. Decompensated heart failure is a common cause of secondary MR because it leads to an increase in left ventricular end-diastolic volume (LVEDV), or preload, with dilation of the mitral valve annulus (the tissue on which the mitral valve cusps are mounted) and taut stretching of the chordae tendineae. The dilated annulus and restricted movement of the chordae tendineae can cause insufficient closure of an intrinsically normal mitral valve, resulting in MR. Systemic hypertension can also contribute to secondary MR by favoring relatively lower-resistance regurgitant flow.
Treatment with diuretics to reduce LVEDV and vasodilators to reduce blood pressure can lead to resolution of heart failure-induced MR.
(Choice A) Calcification of the mitral valve annulus may occur with aging, and can be accelerated by hypertension or advanced kidney disease. It is usually an incidental finding that does not affect mitral valve function.
(Choice B) Increased flow velocity through the aortic valve occurs with aortic valve stenosis. The resulting murmur is crescendo-decrescendo and best heard at the right second intercostal space (rather than holosystolic and best heard at the apex).
(Choice C) Chordae tendineae rupture is a potential cause of primary MR that can occur in the setting of bacterial endocarditis, connective tissue disease (eg, Marfan syndrome), or acute myocardial infarction. The resulting murmur does not resolve with diuretics and vasodilators; surgical repair is typically required.
(Choice E) Thickened and deformed mitral valve cusps can occur in rheumatic heart disease and are a potential cause of primary MR. Such a murmur does not resolve with treatment of decompensated heart failure. In addition, mitral stenosis (evidenced by an opening snap and mid-diastolic rumble) is more likely than MR to occur with rheumatic heart disease.
Educational objective:
Decompensated heart failure is a common cause of secondary (functional) mitral valve regurgitation. Increased left ventricular end-diastolic volume causes dilation of the mitral valve annulus and restricted movement of the chordae tendineae with subsequent regurgitation. Treatment with diuretics and vasodilators can improve heart failure-induced MR.