Mitral Regurgitation Clinical Presentation

Updated: Nov 28, 2018
  • Author: Ivan Hanson, MD; Chief Editor: Terrence X O'Brien, MD, MS, FACC  more...
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Presentation

History

Symptoms of mitral regurgitation (MR) may be subtle as its progression may be insidious and patients may self-limit their physical activity. [11, 12]  

Acute mitral regurgitation

When associated with coronary artery disease and acute myocardial infarction (typically, inferior myocardial infarction, which may lead to papillary muscle dysfunction), significant acute MR is accompanied by symptoms of impaired LV function, such as dyspnea, fatigue, and orthopnea. In these cases, pulmonary edema is often the initial manifestation because of rapid volume overload on the left atrium and the pulmonary venous system.

Chronic mitral regurgitation

Chronic MR often results from a primary defect of the mitral valve apparatus with subsequent progressive enlargement of the left atrium and ventricle. In this state, patients may remain asymptomatic for years. Patients may have normal exercise tolerance until systolic dysfunction of the LV develops, at which point they may experience symptoms of a reduced forward cardiac output (ie, fatigue, dyspnea on exertion, or shortness of breath). With time, patients may feel chest palpitations if atrial fibrillation develops as a result of chronic atrial dilatation.

Patients with LV enlargement and more severe disease eventually progress to symptomatic congestive heart failure with pulmonary congestion and edema. At this stage of LV dilatation, the myocardial dysfunction often becomes irreversible.

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Physical Examination

On palpation, a brisk carotid upstroke and hyperdynamic cardiac impulse may be noted, and a prominent left ventricular (LV) filling wave may be present.

On auscultation, S1 may be diminished in acute mitral regurgitation (MR) and chronic severe MR with defective valve leaflets, and wide splitting of S2 may occur due to early closure of the aortic valve. S3 may be present due to LV dysfunction or as a result of increased blood flow across the mitral valve. P2 may be accentuated if pulmonary hypertension is present.

If murmurs are present, note and characterize the following features:

  • Quality: Usually high-pitched, blowing

  • Location: Usually best heard over the apex; usually radiates to the left axilla or subscapular region: posterior leaflet dysfunction causes murmur to radiate to the sternum or aortic area, and anterior leaflet dysfunction causes murmur to radiate to the back or top of the head

  • Duration: Usually holosystolic, may be confined to early systole in acute MR, may be confined to late systole in MVP or papillary muscle dysfunction (S1 will probably be normal in these cases since initial closure of mitral valve cusps is unimpeded, and a midsystolic click preceding murmur is suggestive of MVP)

  • Intensity: Little correlation exists between intensity of murmur and severity of MR; intensity may be diminished in severe MR caused by LV dysfunction, acute myocardial infarction, or periprosthetic valve regurgitation

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