Ischemia-induced mitral insufficiency (IMI) can occur when a papillary muscle ruptures in the acute phase of myocardial infarction (MI) or, more commonly, when ischemic heart disease reaches the chronic stage, with or without infarction. In the latter case it can be distinguished from organic mitral regurgitation because the structure of the valve and the subvalvular apparatus are not affected. Many factors contribute to the complex mechanism of IMI: incomplete closure of the valve is mainly a result of changes in the geometry of the left ventricle, the mitral annulus, papillary muscles and to hemodynamic conditions rather than to muscular dysfunction of the papillary muscles. IMI is assessed mainly by Doppler echocardiography. The adverse prognostic value of chronic IMI following an infarction has recently been described. Regurgitant orifice area (ROA) > 20 mm2 and a resting regurgitated volume > 30 ml or an increase in ROA > 13 mm2 on the treadmill-exercise echocardiogram were identified as relevant predictors of death. The therapeutic implications, both surgical and interventional, are currently under development using annuloplasty coupled, perhaps, to new strategies.