Abstract
Ischemic mitral regurgitation (IMR) is present in 20% to 30% of patients after an acute myocardial infarction (AMI). As the population ages and the survival rate following AMI increases, so will the number of people with IMR (1). Left ventricular (LV) remodeling with LV dilatation and dysfunction lead to annular enlargement, reduction of the force available to close the leaflets, leaflet tethering and restriction of leaflet motion resulting in malcoaptation of absolutely normal leaflets and therefore IMR (2). Laplace’s law (pressure is proportional to wall stress divided by radius of curvature) implies that once IMR is initiated, end-diastolic LV volume and wall stress increase in parallel with preload. The increase in wall stress leads to further LV remodeling, which culminates in a spiraling, self-perpetuating cycle of leaflet tethering (3). Pathophysiological causes of IMR are summarized in Figure 1 .
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