Ischemic mitral regurgitation: Changing rationale of reparative surgical strategy

In ischemic mitral regurgitation (IMR) the mitral valve (MV) has been seen as a passive bystander of a ventricular problem based on papillary muscles (PMs) displacement. Then, surgical treatment was on the concept that annular overreduction could restore coaptation. However, isolated restrictive mitral annuloplasty did not result in stable and satisfying long term freedom from recurrent mitral regurgitation (MR). The cause of this failure is intrinsic to the MV, which is a living and plastic structure, that reacts to changes in stretching or in mechanical stress. Bio-humoral mechanisms that have, as purpose, the adaptation of the valve to a new environment, are activated. If valve adaptation is balanced, the leaflets increase both surface and length and the chords lengthen, with no or mild MR. In contrast, if valve adaptation is unbalanced, the leaflets become stiff and fibrotic, and rigid and thick chords tether the MV causing significant MR. These changes are mediated mainly by the transforming growth factor β (TGF-β), at the basis of MV changes. Then, the MV shows different degrees of adaptation and any surgical strategy should take into account not only annular size but also the different anatomical aspect of the valve. Chordal tethering should always be eliminated and the length and surface of the valve, if insufficient, have to be augmented by means of a pericardial patch. MV repair due to IMR is a complex procedure, more challenging than perceived, which has, as prerequisite, the knowledge of the mechanisms that cause IMR and the variable anatomy of the MV.