Biomechanics and Myocardial Damage in Chronic Mitral Regurgitation

Abstract

The 2014 ACC/AHA guidelines for surgery for asymptomatic chronic mitral regurgitation states as a class IIa recommendation that mitral valve (MV) repair could be considered if the left ventricular ejection fraction (LVEF) is greater than 0.60 and the LVESD less than 40 mm if there is a 95% probability of a durable repair with an expected mortality of less than 1%. However, adhering to these guideline surgical triggers uncovers a subset of patients (20% incidence) where the LVEF decreases post repair. Is this due to changing loading conditions or impaired myocyte contractility? In a study at University of Alabama at Birmingham of patients undergoing (MV) repair for chronic mitral regurgitation MRI derived left ventricular (LV) volumes demonstrated reverse diastolic remodelling while left ventricular end systolic remodelling was essentially unchanged following surgery. Myocardial strain rates were normal prior to mitral valve repair. However, in the face of unchanging left ventricular end systolic wall stress, strain rates decreased below normal following MV repair suggesting a decrease in left ventricular contractile performance. LV biopsies of these patients taken at the time of MV repair demonstrated deposition of lipofuscin which is composed of protein and lipid degradation residues. Lipofuscin accumulation may have a deleterious effect on myocyte function. These biopsies also demonstrated extensive myofibrillar degeneration. The desmin cytoskeleton in the myocardium forms a continuous network maintaining a spatial relationship between the contractile apparatus and mitochondria. The LV biopsies demonstrated desmin loss indicating substantial underlying cellular and molecular damage. Implications: At the time of correction of mitral regurgitation substantial LV damage has occurred. This suggests that an even earlier repair of mitral regurgitation should be considered.