heart disease is a common clinical problem and mitral valve regurgitation is the lesion seen most frequently. to structural changes in the leaflets or the subvalvar apparatus. Mitral valve prolapse occurs when Torin 2 part (or all) of one (or both) of the valve Torin 2 leaflets displace retrogradely into the left atrium during systole. In developed countries this is the most common cause of chronic mitral regurgitation. Several causative genetic chromosomal abnormalities have been identified although the disease may also be acquired. A defect in collagen results in the valve leaflets and chordae tendineae becoming baggy and fragile. As a result when the valve closes the leaflets are not pulled taught and prolapse into the left atrium. The chordae are prone to rupture and over time there is annular dilatation. Although many patients remain asymptomatic and have a normal life expectancy between 5% and 10% of patients may progress to severe mitral regurgitation (Barlow and Pocock 1979 Patients who develop symptoms or have signs of significant mitral regurgitation with left ventricular dilatation and/or dysfunction should be considered for surgery. The Torin 2 current surgical options are mitral valve replacement with a mechanical or biological prosthesis or repair of the patient’s native valve. Although there are no randomised trials comparing mitral valve replacement and repair a meta-analysis of the observational studies favoured mitral repair in survival outcomes (Shuhaiber and Anderson 2007 The most common lesion identified is usually Torin 2 prolapse of the middle scallop of the posterior leaflet. Repairs of the anterior leaflet or both leaflets are more complicated. The goals of surgical repair are to ensure an adequate surface of coaptation of both leaflets in systole restore full leaflet motion and prevent progressive annular dilatation by inserting an annuloplasty ring. The operative mortality Rabbit Polyclonal to IkappaB-alpha. is typically up to 3% (Gillinov et al. 1998 and recurrence of the mitral regurgitation may occur in up to 30% of patients (Filsoufi and Carpentier 2007 Mitral regurgitation may Torin 2 result from rheumatic heart disease although mitral stenosis or mixed mitral valve disease occur more commonly. Ischaemic mitral regurgitation results from the sequelae of underlying coronary artery disease. Acute myocardial ischaemia may Torin 2 result in transient dysfunction of the subvalvar apparatus and myocardial infarction may cause permanent dysfunction of the subvalvar apparatus. Generally the outcome of patients with ischaemic mitral regurgitation is usually worse than those patients with similarly severe regurgitation from another cause due to the superimposed left ventricular dysfunction. In patients with acute papillary muscle rupture urgent mitral valve surgery with revascularisation should be considered. The case for surgery with chronic ischaemic mitral regurgitation is usually less clear cut. Mitral valve replacement and/or mitral valve annuloplasty with concomitant coronary artery grafting needs to be considered. With functional mitral regurgitation there is incomplete mitral valve closure in the setting of a structurally normal valve. This may occur due to global left ventricular dysfunction reducing the ventricular force acting to close the leaflets dilatation of the mitral annulus and alterations in left ventricular geometry at the site from which the papillary muscles arise. Although all three factors may contribute to the mitral regurgitation it appears that the predominant mechanism is usually apical displacement of the papillary muscles with tenting of the leaflets away from the annulus and subsequent incomplete leaflet coaptation (Levine and Schwammenthal 2005 Functional mitral regurgitation is found frequently in patients with impaired left ventricular systolic function and is associated with a worse prognosis in this group of patients. Furthermore there is an incremental risk of mortality with increasing grades of mitral regurgitation. In a 10 year cohort study the prevalence and prognostic implication of mitral regurgitation was evaluated in patients undergoing echocardiography within 30 days of myocardial infarction. Mitral regurgitation was found in 50%.