Key result
While there was no difference in left ventricular reverse remodeling at 2 years, mitral-valve repair was associated with a significantly higher rate of recurrent moderate or severe mitral regurgitation compared to replacement (58.8% vs. 3.8%).
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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Hernández‐Vaquero et al. (2016) conducted an editorial in Chronic ischemic mitral regurgitation (n=251). Chordal sparing mitral valve replacement vs. Mitral-valve repair was evaluated on Degree of left ventricular reverse remodeling (left ventricular end-systolic volume index). While there was no difference in left ventricular reverse remodeling at 2 years, mitral-valve repair was associated with a significantly higher rate of recurrent moderate or severe mitral regurgitation compared to replacement (58.8% vs. 3.8%).
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