Acute myocardial infarction and vascular remodeling

Recent evidence has suggested that plaque rupture and outward remodeling may be associated. A postmortem study, comparing vessel sections from the same nonbranching femoral arterial segment, found that those with the largest vessel area (the greatest amount of outward remodeling) had significantly more markers of plaque vulnerability (more matrix metalloproteinase-secreting macrophages and T-lymphocytes and less collagen-producing smooth muscle cells) compared with those with the least remodeling.(1) These differences were most marked at the shoulders of the plaques where plaque rupture is most prevalent. Thinning of the fibrous cap has been attributed to collagen breakdown (due to macrophages and T-lymphocytes) along with a reduction in smooth muscle cells. To examine the strength of this association, other investigators have compared remodeling patterns in patients with unstable and stable angina.(2-4) However, the heterogenous nature of unstable angina(5) coupled with some uncertainty in the location of plague rupture means that observer bias may be difficult to avoid in these studies. Such methodologic issues can be overcome by examining remodeling in the setting of acute transmural myocardial infarction, for which there are firm diagnostic criteria and a more definite site of plaque rupture. Therefore, we explored this association, using a retrospective care-control design, by comparing the intravascular ultrasound (IVUS) findings of patients with acute myocardial infarction to those with stable angina.