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.

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.

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.

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.