Mitral Valve Leaflet Remodeling After Myocardial Infarction: Good or Evil?

Abstract

> When you are feeling fit and the sun is shining and you do not want to believe that the whole universe is a mere mechanical dance of atoms, it is nice to be able to think of this great mysterious Force rolling on through the centuries and carrying you on its crest. > > —C.S. Lewis It is a matter of force. It is a balance of valve closing force and tethering force that affects mitral valve coaptation. Ischemic mitral regurgitation develops secondary to left ventricular dysfunction generally with structurally normal leaflets. However, it seems it is not simply a matter of force when we see the fact that valve leaflets histologically change after myocardial infarction. The leaflets can stretch, can grow in area, and can increase in thickness. Recent studies have shown evidence of leaflet remodeling and have proposed new insights from the biological reaction of the leaflet.1–3 Some specific biological markers are activated in the ischemic environment and cause histopathologic changes in the leaflet. Thus, it is not just about the force, and we cannot ignore the leaflet pathology and function when we consider the mechanism of ischemic mitral regurgitation. Mitral valve complex is becoming more complex. See Article by Beaudoin et al Ischemic mitral regurgitation had been traditionally explained as papillary muscle ischemic dysfunction that causes the loss of support of both anterior and posterior leaflets, before the concept of leaflet tethering caused by ischemic left ventricular remodeling was proposed as a main mechanism of loss of coaptation in the 1990s.4 Since then, the role …