Acute myocardial infarction and vascular remodeling

Recent evidence has suggested that plaque rupture and outward remodeling ma y be associated. A postmortem study, comparing vessel sections from the sam e nonbranching femoral arterial segment, found that those with the largest vessel area (the greatest amount of outward remodeling) had significantly m ore markers of plaque vulnerability (more matrix metalloproteinase-secretin g macrophages and T-lymphocytes and less collagen-producing smooth muscle c ells) compared with those with the least remodeling.(1) These differences w ere most marked at the shoulders of the plaques where plaque rupture is mos t prevalent. Thinning of the fibrous cap has been attributed to collagen br eakdown (due to macrophages and T-lymphocytes) along with a reduction in sm ooth muscle cells. To examine the strength of this association, other inves tigators have compared remodeling patterns in patients with unstable and st able angina.(2-4) However, the heterogenous nature of unstable angina(5) co upled with some uncertainty in the location of plague rupture means that ob server bias may be difficult to avoid in these studies. Such methodologic i ssues can be overcome by examining remodeling in the setting of acute trans mural myocardial infarction, for which there are firm diagnostic criteria a nd a more definite site of plaque rupture. Therefore, we explored this asso ciation, using a retrospective care-control design, by comparing the intrav ascular ultrasound (IVUS) findings of patients with acute myocardial infarc tion to those with stable angina.