Effects of fibrous cap thickness on peak circumferential stress in model atherosclerotic vessels.
It is likely that factors other than stenosis severity predispose some atherosclerotic plaques to rupture. Because focal increases in circumferential stress may be an important mechanism of plaque rupture, we examined peak circumferential stress of atherosclerotic lesions by using finite element analysis based on idealized two-dimensional cross sections of diseased vessels similar to intravascular ultrasound images. The study was designed to test the hypothesis that subintimal plaque structural features such as thickness of the fibrous cap are more important factors in the distribution of stress in the plaque than stenosis severity. The analysis incorporated equilibrium biomechanical parameters from normal and diseased vessels and determined the stress distribution within the plaque at a mean luminal internal pressure of 110 mm Hg. With a constant luminal area reduction of 70%, maximum circumferential stress (sigma max) normalized to luminal pressure (sigma max/P) increased from 6.0 to 24.8 as the thickness of the lipid pool was increased from 38% to 54% of the plaque thickness because of the thinner fibrous cap over the lipid pool. When the lipid pool thickness was constant, increasing the stenosis severity from 70% to 91% by increasing the fibrous cap thickness decreased sigma max/P from 24.8 to 4.7. When no lipid pool was present and the stenosis severity was increased from 70% to 99%, sigma max/P decreased from 5.3 to 4.7. Thus, reducing the fibrous cap thickness dramatically increases peak circumferential stress in the plaque, whereas increasing the stenosis severity actually decreases peak stress in the plaque.(ABSTRACT TRUNCATED AT 250 WORDS)
Loree
H M
HM
Department of Mechanical Engineering, Massachusetts Institute of Technology, Cambridge.
Kamm
R D
RD
Stringfellow
R G
RG
Lee
R T
RT
D001161:Arteriosclerosis / Q000503:physiopathology*; D001696:Biomechanical Phenomena; D003251:Constriction, Pathologic; D003327:Coronary Disease / Q000503:physiopathology; D008055:Lipids / Q000032:analysis; D008955:Models, Cardiovascular; D009203:Myocardial Infarction / Q000503:physiopathology; D013314:Stress, Mechanical
D008055:Lipids