Last updated on:July 14th, 2021
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Acute heart failure
Acute mitral insufficiency results in acute heart failure. Potential symptoms include cough, ankle swelling, exertional dyspnea, paroxysmal nocturnal dyspnea, orthopnea, and dyspnea at rest. These symptoms are due to the rapid change in the valvular architecture. Blood is forced back into the left atrium, which dilates to accommodate the increased volume. The elevated left atrial pressure causes pulmonary vascular congestion. Cardiac output is also reduced, as a portion of the blood pumped is redirected back into the left atrium. Furthermore, the left ventricle has to rapidly adjust to a large increase in preload from the dilated left atrium, while the right side of the heart has to work against a greater afterload. This causes fluid to accumulate in the peripheral tissues.
Acute mitral insufficiency can be caused by infective endocarditis, typically due to rupture of affected chordae tendineae. Note that infective endocarditis is more common in valves that are already abnormal. Therefore, it is not always clear if the valvular dysfunction preceded the infection or was caused by it. Patients with infective endocarditis can be asymptomatic, or manifest only subtle symptoms such as fever, lethargy and weight loss. Less often, symptoms may occur secondary to distal embolic complications or septic embolism.
While rheumatic fever typically gives rise to chronic mitral regurgitation over a period of months to years, acute mitral regurgitation can also occur following rupture of the chordae. Symptoms of acute rheumatic fever include fever, arthritis, chorea, and a rash.
Transient mitral regurgitation and a functional systolic murmur may occur during episodes of acute ischemia; this is due to regional compromise of the papillary muscles. The valve leaflets are tethered to these muscles, resulting in mitral regurgitation. Persistent mitral regurgitation may develop if papillary muscle rupture occurs; this tends to occur within the first week post-infarction; and is rare after two weeks post-infarction.
Mitral valve prolapse
Mitral valve prolapse (MVP) occurs when one or more of the mitral leaflets move into the atrium during systole. This is a risk factor for chordal rupture and thus, acute mitral regurgitation. The most common cause of MVP is myxomatous degeneration, a non-inflammatory loss of leaflet structure due to changes in the collagen within the valve. It is unclear why this occurs, but there is a degree of inheritability. MVP is also more common in connective tissue disorders such as Marfan syndrome and Ehlers-Danlos syndrome.
Connective tissue disease
Systemic lupus erythematosus (SLE) can affect the valves of the heart; this is termed Libman-Sacks endocarditis. Thrombi form on the valve, leading to progressive thickening, edema and scarring. Similar changes can occur antiphospholipid syndrome. These degenerative changes can lead to rupture of the chordae tendineae, leading to acute mitral insufficiency.
Blunt chest trauma
Blunt chest trauma can give rise to mitral regurgitation. Unfortunately, these patients often have multiple injuries, complicating the clinical picture. The atrioventricular valves appear to be particularly susceptible to blunt injury, with papillary muscle avulsion, tearing of the chordae tendineae, and perforation of leaflets being potential sequalae.