Acute mitral regurgitation can develop as a result of a myocardial infarction, blunt chest trauma, or detachment of the mitral valve leaflets and rupture of the papillary muscles or chordae tendineae in infective endocarditis. Rupture of the papillary muscles due to myocardial infarction is fatal in 80–90% of cases.
Chronic mitral regurgitation is caused by valve damage in systemic diseases: rheumatic fever, scleroderma, lupus erythematosus and Löffler endocarditis. About 14% of isolated mitral regurgitation cases are associated with rheumatic heart disease.
Mitral regurgitation can result from mitral valve prolapse or rupture, or from shortening or lengthening of the chordae tendineae and papillary muscles.
Relative mitral regurgitation develops when the left ventricular cavity and the fibrous ring widen without damage to the valve apparatus. Such changes are seen in dilated cardiomyopathy, progressive coronary heart disease and arterial hypertension, myocarditis and aortic regurgitation.
Rare causes of mitral regurgitation include calcification of the leaflets, hypertrophic cardiomyopathy and others. Congenital mitral regurgitation is seen with cleft mitral valve leaflets and parachute deformity of the valve.
In severe cases, the valve is replaced through heart surgery. The valves are repaired or replaced with a prosthetic valve. In suitable patients, valve surgery is performed through a small incision without cutting the breastbone.
Information on this site is general and does not replace an examination by a doctor.