Distribution of circumferential stress in ruptured and stable atherosclerotic lesions. A structural analysis with histopathological correlation.

TLDR

Plaque rupture is a leading cause of acute coronary syndromes, yet its underlying mechanism remains controversial. The study tested whether plaque rupture occurs at sites of high circumferential stress by analyzing stress distribution in 24 coronary artery lesions. Histological specimens from 12 lethal myocardial infarction lesions and 12 stable controls were examined with a finite element model at 110 mm Hg to compute circumferential stress distributions. Ruptured plaques showed significantly higher maximum circumferential stress (≈4,100 mm Hg vs 1,440 mm Hg) and many high‑stress regions, with 83 % of ruptures occurring in areas >2,250 mm Hg, suggesting stress concentrations contribute to rupture but are not the sole determinant.

Abstract

BACKGROUND Although rupture of an atherosclerotic plaque is considered to be the cause of most acute coronary syndromes, the mechanism of plaque rupture is controversial. METHODS AND RESULTS To test the hypothesis that plaque rupture occurs at sites of high circumferential stress in the diseased vessel, the distribution of stress was analyzed in 24 coronary artery lesions. Histological specimens from 12 coronary artery lesions that caused lethal myocardial infarction were compared with those from 12 stable control lesions. A finite element model was used to calculate the stress distributions at a mean intraluminal pressure of 110 mm Hg. The maximum circumferential stress in plaques that ruptured was significantly higher than maximum stress in stable specimens (4,091 +/- 1,199 versus 1,444 +/- 485 mm Hg, p < 0.0001). Twelve of 12 ruptured lesions had a total of 31 regions of stress concentration of more than 2,250 mm Hg (mean, 2.6 +/- 1.4 high stress regions per lesion); only one of 12 control lesions had a single stress concentration region of more than 2,250 mm Hg. In seven of 12 lethal lesions (58%), rupture occurred in the region of maximum circumferential stress; in 10 of the 12 lethal lesions (83%), rupture occurred in a region where computed stress was more than 2,250 mm Hg. CONCLUSIONS These data suggest that concentrations of circumferential tensile stress in the atherosclerotic plaque may play an important role in plaque rupture and myocardial infarction. However, plaque rupture may not always occur at the region of highest stress, suggesting that local variations in plaque material properties contribute to plaque rupture.