A 34-year-old woman with a history of idiopathic dilated cardiomyopathy comes to the emergency department due to progressive weight gain and dyspnea on exertion. She did not take her medications over the recent holiday period. Blood pressure is 110/70 mm Hg and pulse is 90/min and regular. Oxygen saturation is 92% on room air. On physical examination, jugular venous distension is observed with significant pedal edema. There are bibasilar crackles. Cardiac auscultation reveals a grade 3/6 holosystolic murmur best heard at the apex. The patient is admitted to the hospital and started on appropriate therapy with intravenous diuretics. Four days later, her symptoms have improved and she is ready for discharge. Weight has decreased by 5 kg (11 lb) since admission. On examination, the lungs are clear on auscultation and no heart murmurs are heard. Which of the following best explains the heart murmur heard in this patient on admission?
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This patient with a history of dilated cardiomyopathy exhibits signs and symptoms of decompensated heart failure (eg, dyspnea, weight gain, jugular venous distension, pulmonary crackles). She has an apical holosystolic murmur that disappears following treatment with intravenous diuretics; this transient murmur is most likely due to secondary (functional) mitral regurgitation (MR).
Whereas primary MR is caused by an intrinsic defect of the mitral valve (eg, cleft in a valve cusp, myxomatous degeneration), secondary MR occurs due to other factors. Decompensated heart failure can cause secondary MR due to markedly increased left ventricular end-diastolic volume (LVEDV), or preload. The increased preload results in dilation of the mitral valve annulus (the tissue on which the mitral valve cusps are mounted). In addition, lateral displacement of the papillary muscles results in taut stretching of the mitral valve chordae tendineae. The dilated annulus and restricted movement of the chordae tendineae cause insufficient closure of an intrinsically normal mitral valve, resulting in MR.
Treatment of decompensated heart failure reduces LVEDV, restores previous mitral valve annulus size and papillary muscle position, and leads to resolution of the secondary MR.
(Choice A) Dynamic LV outflow tract obstruction occurs in hypertrophic cardiomyopathy. There is an associated crescendo-decrescendo systolic murmur that is most prominent with maneuvers or conditions that decrease LV preload.
(Choices B and C) With a patent foramen ovale or other type of atrial septal defect (ASD), blood flow through the defect itself does not generate a murmur. An ASD murmur is caused by increased blood volume in the right side of the heart and increased flow across the right ventricular outflow tract (pulmonic valve flow murmur). Such a murmur is unlikely to vary significantly with treatment of decompensated heart failure.
(Choice E) Mitral valve prolapse involves excessive displacement of one or both mitral valve cusps into the left atrium during systole. The prolapse results in a mid-systolic click that may be followed by an MR murmur. Decreased preload causes the click (and murmur) to occur earlier in systole, whereas increased preload causes the click to occur later in systole or disappear altogether.
Educational objective:
Decompensated heart failure is a common cause of secondary (functional) mitral regurgitation. Increased left ventricular end-diastolic volume (LVEDV) causes impaired valve closure due to dilation of the mitral valve annulus and lateral papillary muscle displacement with restricted movement of the chordae tendineae. The mitral regurgitation resolves with reduction in LVEDV, resulting in disappearance of the associated murmur.