Mitral Valve Adaptation
Can We Win the Race?
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- echocardiography, three-dimensional
- mitral valve
- mitral valve insufficiency
- myocardial infarction
See Article by Nishino et al
Ischemic mitral regurgitation (IMR) is a common complication of ischemic heart disease that doubles mortality after myocardial infarction (MI) and is a major driving factor increasing heart failure.1,2 IMR is caused by post-MI left ventricle (LV) remodeling: inferior wall bulging displaces the papillary muscle, tethering the leaflets into the LV cavity, and restricting their closure.3 The mitral valve (MV) has been thought of as an unchanging structure. However, its ability to adapt to expansion of the remodeling LV is increasingly recognized.4–7 Although mechanically displacing the papillary muscles without MI causes compensatory MV growth,8 this adaptive process is altered in the infarcted ventricle by excessive profibrotic processes, impairing closure, and augmenting MR.9–11 There is a need to understand the timing of compensatory valve growth versus counterproductive fibrosis and the potential effects of therapy on these competing processes.12 IMR can vary from early post-MI to the chronic stage, but previous studies have mainly focused on IMR in the subacute or chronic setting, and little is known about the mechanism of acute IMR.
The study by Nishino et al13 in this issue of Circulation: Cardiovascular Imaging provides new insights into the mechanism of acute IMR. This sophisticated 3-dimensional echocardiographic study included 80 patients with significant IMR (44 patients with acute IMR; 36 with chronic IMR) compared with 3 …