Percutaneous mitral valve repair: a fertile field of innovative treatment strategies.

The mitral valve is a complex structure composed of the leaflets, annulus, chordae tendineae, and papillary muscles. Competency of the mitral valve is dependent on the proper function of each of these component structures. The pathophysiological triad of mitral regurgitation (MR) was originally described by Carpentier in 1983.1 It included the etiology of the valve lesion, the valve lesion itself, and the resultant valve dysfunction. He subsequently described a classification of leaflet dysfunction in MR that is commonly used and relevant for patient selection and evaluation of percutaneous mitral valve repair (PMVR). In type I dysfunction, there is normal leaflet motion, and valvular incompetence is due to either annular dilatation or leaflet perforation. Type II mitral dysfunction includes patients with increased leaflet motion (prolapse) of one or both leaflets so that there is failure of coaptation during systole resulting in mitral regurgitation. Patients in this category are those with degenerative myxomatous disease of the valve with chordal and/or papillary muscle elongation or rupture. Patients with type IIIa dysfunction have restriction of leaflet motion during both systole and diastole caused by leaflet and subvalvular apparatus thickening and fusion (rheumatic heart disease). The cause of valvular incompetence in patients with type IIIb dysfunction is restricted leaflet motion during systole caused by apical displacement of the papillary muscle from ventricular enlargement in dilated cardiomyopathy (functional MR) and lateral displacement of a posterior papillary muscle in ischemic MR. Patients may have a combination of causes of dysfunction (annular dilation, apical papillary muscle displacement), especially in advanced disease. Patients with MR for purposes of surgical and percutaneous intervention can broadly be categorized as having intrinsic disease (type II) and functional or ischemic (type I or type IIIb).