Progression of aortic stenosis after an acute myocardial infarction

Abstract

BackgroundMyocardial 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.MethodsSerial 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.ResultsIn humans, the acute MI, previous MI and control groups had comparable baseline AS severity. Indexed aortic valve area (AVAi) declined faster in the acute MI group compared with controls (−0.07±0.06 vs −0.04±0.04 cm2/m2/year; p=0.004). After adjustment, acute MI status was significantly associated with faster AVAi progression (mean difference: −0.013 (95% CI −0.023 to −0.003) cm2/m2/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.ConclusionsThe 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.

The impact of moderate aortic stenosis in acute myocardial infarction: A multicenter retrospective study

“…Secondly, patients with moderate AS may potentially be at the upper limit of AS disease progression (moderate to severe AS), therefore resulting in a similarly poor prognosis to those with severe AS. In addition, a rapid progression in the severity of AS may occur, especially after an ACS; supporting this are some studies demonstrating accelerated progression of AS following acute MI, which was related to increased collagen expression and aortic valve thickening noted in animal models 12 . Lastly, moderate AS in the setting of ACS can additionally worsen myocardial ischemia and complicate the short‐term outcomes through the following mechanisms: Elevated LV pressure caused by AS has a linear correlation with increased coronary resistance 13 …”

“…In addition, a rapid progression in the severity of AS may occur, especially after an ACS; supporting this are some studies demonstrating accelerated progression of AS following acute MI, which was related to increased collagen expression and aortic valve thickening noted in animal models. 12 Lastly, moderate AS in the setting of ACS can additionally worsen myocardial ischemia and complicate the short-term outcomes through the following mechanisms:…”

Moderate aortic stenosis in patients with myocardial infarction: A guilty bystander?

“…Moreover, AS progression has been shown to accelerate after an acute MI due to increased collagen production and thickening of the aortic valve following the ischemic event. 3 These findings support the need for close monitoring of patients with moderate AS after myocardial infarction and raise the hypothesis that they could benefit from earlier treatment of valvular disease.…”

“…Indeed, the increased afterload due to the presence of moderate AS could exacerbate the myocardial ischemia in the acute phase of MI and contribute to the adverse left ventricular remodeling in the following months. Moreover, AS progression has been shown to accelerate after an acute MI due to increased collagen production and thickening of the aortic valve following the ischemic event 3 . These findings support the need for close monitoring of patients with moderate AS after myocardial infarction and raise the hypothesis that they could benefit from earlier treatment of valvular disease.…”