data from clinical and histopathologic studies suggest that inflammation plays a key role in instability of atherosclerotic plaque as patients with acute coronary syndromes present diffuse inflammatory infiltrates in the coronary arteries.Objectives
to assess and locate the distribution of vulnerable plaques and inflammatory infiltrates in patients who died of acute myocardial infarction.Material and Methods
we examined the coronary arteries from 64 patients who died of myocardial infarction using light microscopy.Infarction was defined according to the classic criteria. The time from symptom onset to death was < 5 days for all cases and the autopsies were performed within 6 hours after death. Patients with neoplasms, autoimmune diseases and those with a history of an infectious condition 90 days before dying were excluded from the study.Coronary arteries were carefully dissected and decalcified if necessary. Then they were embedded in paraffin. The vessels were cut transversely at 2-mm intervals along the coronary tree and arterial sections were stained with hematoxylin and eosin for further evaluation with light microscopy. The following variables were evaluated in culprit and non-culprit coronary arteries: presence of thrombus, plaque rupture, intraplaque hemorrhage and inflammatory infiltrate. A p value < 0.05 was considered statistically significant.Results
The presence of thrombus and intraplaque hemorrhage was significantly greater in culprit coronary arteries compared to non-culprit vessels (70,3% versus 37,5%; p < 0.001, and 68,7% versus 51,5%; p=0.04, respectively). There were no significant differences in the presence of inflammatory infiltrates in atherosclerotic plaques from culprit and non-culprit coronary arteries (78,1% versus 70,3%; p=0,3).Conclusion
Inflammatory activity was demonstrated in acute myocardial infarction affecting not only the infarct-related artery but also other coronary vessels. Plaque accident was also present in more than one coronary artery.