Owing to the pathophysiologic changes described earlier, chronic MR results in LA and LV dilatation, pulmonary venous hypertension, heart failure, and arrhythmias. Patients commonly complain of typical heart failure symptoms: fatigue, dyspnea on exertion, orthopnea, chest discomfort, shortness of breath, and peripheral edema. Arrhythmias can provoke palpitations.
The characteristic blowing, holosystolic murmur is best heard at the LV apex (which may be displaced to the axilla), and may radiate to the axilla or left infrascapular area overlying the LA. Radiation of the murmur to the parasternal region can occur if valve pathology creates an anteriorly directed regurgitant jet. The murmur increases in intensity with maneuvers that increase afterload (eg, handgrip or arterial compression with blood pressure cuff) or preload (such as squatting). Murmur intensity does not correspond well to MR severity. The timing of the murmur in systole can vary depending on the MV pathology; with MV prolapse, the murmur is mid-late systolic, whereas an early systolic murmur is observed with functional MR. The mitral component of S1 is soft or absent. An S3 and low-pitch, soft diastolic flow murmur can be present from LA volume overload. Other physical examination findings consistent with heart failure may be present, including rales, jugular venous distension, pitting-dependent edema, and laterally displaced cardiac point of maximal impulse. A parasternal heave may be palpated if pulmonary hypertension is present. As with more advanced heart failure, ascites, hepatosplenomegaly, or cardiac wasting can occur.
Acute MR manifests as pulmonary edema and acute decompensation, and is usually due to valve destruction from endocarditis, ruptured or flail chordae from myxomatous MV prolapse, or papillary muscle dysfunction with active ischemia, or papillary muscle rupture following acute myocardial infarction. Acute MR generates a soft, short, early, systolic murmur as the systolic pressures in the noncompliant LA and LV equalize rapidly, halting regurgitant flow early and making auscultatory diagnosis difficult. Isolated right middle or upper lobe rales and lobar consolidation can be present when the regurgitant jet is directed at the right upper pulmonary vein with acute MR, although bilateral pulmonary edema is more common.15
Owing to the insidious progression of symptoms, patients often do not appreciate their slow decline in functional capacity. Patients may experience symptoms of dyspnea, orthopnea, pulmonary edema, and hemoptysis. With less blood flow across the stenotic valve, the LV is often small and underfilled, and can manifest as symptoms of hypotension or dizziness with exertion or standing up. Atrial arrhythmias, such as atrial fibrillation, from the dilated LA are common and are noted as palpitations or tachycardia. Lastly, thromboembolic phenomenon, including stroke or embolism to the coronary arteries or visceral organs, can be the sentinel event.
In developed countries, MS usually manifests two to three decades after an episode of acute rheumatic fever; hence, pregnancies are generally unaffected. However, in developing countries where rheumatic fever is endemic, individuals may experience multiple episodes of rheumatic fever, which accelerates the development of MS. In this situation, MS can be seen in the second and third decades of life, and often complicates pregnancy with resultant miscarriages, pulmonary edema, or death.
Auscultation for MS is best performed with the patient in the left lateral decubitus position to reveal the “opening snap” of the mitral leaflets, followed by a soft diastolic rumbling murmur and prominent S1 in the apical region. Irregular rhythms are common. Patients with pulmonary hypertension can have a prominent pulmonic component of the second heart sound, a right ventricular heave, and signs of right heart failure such as peripheral edema, hepatosplenomegaly, and ascites frequently in the absence of rales (unless acute decompensation).
Chest radiographs can show prominent pulmonary vasculature and LA enlargement, but pulmonary edema is less common because the pulmonary vessels have remodeled and are “protected” from any elevations in LA pressure unless in the setting of acute hemodynamic decompensation such as paroxysmal rapid atrial fibrillation. Electrocardiogram can reveal LA enlargement and atrial arrhythmias with an absence of LV hypertrophy.