Progression of aortic stenosis after an acute myocardial infarction

Background Myocardial infarction (MI) has been shown to induce fibrotic remodelling of the mitral and tricuspid valves. It is unknown whether MI also induces pathological remodelling of the aortic valve and alters aortic stenosis (AS) progression. We thus compared AS progression after an acute MI and in patients with/without history of MI, and assessed post-MI pathobiological changes within the aortic valve leaflets in a sheep model. Methods Serial echocardiograms in human patients with AS were retrospectively analysed and compared between 3 groups: (1) acute MI at baseline (n=68), (2) prior history of MI (n=45) and (3) controls without MI (n=101). Annualised progression rates of AS severity were compared between these 3 groups. In addition, aortic valves were harvested from 15 sheep: (1) induced inferior MI (n=10) and (2) controls without MI (n=5), for biological and histological analyses. Results In humans, the acute MI, previous MI and control groups had comparable baseline AS severity. Indexed aortic valve area (AVA(i)) declined faster in the acute MI group compared with controls (-0.07 +/- 0.06 vs -0.04 +/- 0.04 cm(2)/m(2)/year; p=0.004). After adjustment, acute MI status was significantly associated with faster AVA(i) progression (mean difference: -0.013 (95% CI -0.023 to -0.003) cm(2)/m(2)/year, p=0.008). In the post-MI experimental animal model, aortic valve thickness and qualitative/quantitative expression of collagen were significantly increased compared with controls. Conclusions The results of this study suggest that AS progression is accelerated following acute MI, which could be caused by increased collagen production and thickening of the aortic valve after the ischaemic event.

Automated summary

The progression of aortic stenosis is found to be accelerated following acute myocardial infarction, possibly due to increased collagen production and thickening of the aortic valve after the ischemic event.