Abstract
Mitral regurgitation (MR) may start during the acute phase of myocardial infarction and it may increase, decrease, or remain unchanged as the necrotic muscle is replaced by fibrous tissue and remodeling of the ventricle takes place. Acute infarction can cause MR because of rupture of papillary muscle (PM) head or dysfunction of the PM and underlying ventricular wall. When MR is due to rupture of a single PM head and the surrounding muscle is not extensively infarcted, it is possible to suture the PM head in place with pledget sutures or to use other techniques of repair of flair leaflets such as chordal transfer or chordal replacement. When MR is due to extensive necrosis of the PM and the ventricular wall, it is safer to replace the mitral valve with preservation of the chordae tendineae. Correction of MR by means of valve repair in patients with healed myocardial infarction is frequently possible when the cause of MR is determined by Doppler echocardiography. The most common cause of MR is incomplete closure of the mitral valve due to apical displacement of the PM. Prolapse of the leaflets is rare in patients with healed myocardial infarction. Mitral annuloplasty decreases or abolishes MR in most cases when lack of coaptation of the leaflets is the problem. Transient ischemia can also cause MR. Successful myocardial revascularization either by angioplasty or coronary artery bypass often cures episodic ischemic MR.
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