The most common etiologies for mitral regurgitation (MR) include mitral valve prolapse syndrome, coronary artery disease, infective endocarditis, rheumatic heart disease, collagen vascular disease, and, recently, anoretic drugs have also been reported to cause MR. In chronic severe MR, forward cardiac output is maintained for the development of afterload reduction with increase in compensatory left ventricular (LV) end-diastolic volume and LV ejection fraction. It is well established that some patients with asymptomatic mitral regurgitation develop irreversible contractile dysfunction of the LV, which is often masked by the afterload-reducing effect of the regurgitant flow; cardiologist have to use some variables, like LV chamber elastance, LV End-Systolic dimensions and volumes, left atrial area combined with ejection fraction, in their clinical evaluations tube able to predict surgery mortality. Careful and periodic evaluation of left ventricular function and size is essential to optimize the timing of surgical intervention in these patients. After symptoms occur, outcome is improved with surgical interventions compared to medical therapy, with a reported survival of only 45% at 5 years without surgical intervention. Vasodilators, diuretics, and recently, angiotensin receptor antagonists have been used in MR medical therapy. Long-term carvedilol therapy in patients with chronic heart failure may prevent or partially reverse progressive left ventricular dilatation. Concomitant by, it has been associated with recovery of diastolic reserve and a decrease in mitral regurgitation.