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

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

Study of reproducibility of human arterial plaque reconstruction and its effects on stress analysis based on multispectral in vivo magnetic resonance imaging

“…It is believed that the local stress concentration on the fibrous cap could be the trigger of plaque rupture. Numerous studies have been carried out in this area based on histology data (34) or ex vivo MR images. Recently, in vivo medical imaging technology has enabled determination of more detailed plaque geometries, which allows the FEM simulation to be more realistic and patientspecific.…”

Intravascular Palpography for High-Risk Vulnerable Plaque Assessment

“…An even more promising feature of palpography is the detection of high-stress regions. Using computer simulations, concentrations of circumferential tensile stress were more frequently found in unstable plaques than in stable ones [5,14]. A local increase in circumferential stress in tissue is directly related with an increase of radial strain.…”

The Relationship between CD40 Gene Polymorphism and Unstable Coronary Atherosclerotic Plaques

“…1,2 The composition and morphometry of the vulnerable plaque are thought to be more crucial determinants of ACS likelihood than the extent of stenosis. 3,4 Angiographically visible complex lesions are associated with plaque vulnerability and have been shown to correlate strongly with the clinical severity of UA. Complex lesions are associated with rapid disease progression and a higher restenosis rate after percutaneous transluminal coronary angioplasty as compared with smooth lesions, probably reflecting a tendency toward thrombogenesis, further plaque disruption, or both.…”