Age-related development of atherosclerotic plaque stress: a population-based finite-element analysis.
BACKGROUND
In order to identify those age-related factors in the development of coronary atherosclerosis that would affect the stability of the plaque system, we have developed idealized, finite-element, cross-sectional models of the arterial wall and associated lesions, derived from population-based data.


METHODS
The physical development and morphology of coronary plaques was documented in the Pathobiological Determinants of Atherosclerosis in Youth histological study. Using this database, finite-element analysis models were created for five age groups (15-19, 20-24, 25-29 and 30-34 years) and for the 25 largest lesions. Cosmos (Structural Research, Inc., Los Angeles, California, USA) was used to create and analyze the models.


RESULTS
The area of greatest stress shifted from the intima opposite the lesion in the 15-19 years age group to the edge of the cap and adjacent healthy tissue in the later age groups. Increasing age had a strong positive correlation with the shoulder stress level (r = 0.95) and the per cent stenosis correlated well with shoulder stress (r = 0.99, P < 0.002). Increasing the cap stiffness from a soft cap to a fibrous cap in the 30-34 year age group model resulted in a localized increase in shoulder surface stress by 10%. A calcified cap increased this shoulder surface stress by 30%.


CONCLUSIONS
This finite-element analysis of the population-based data shows that the increase in stress appears to be closely related to the impaired load-bearing capability of the lipid pool that develops with age. The shoulder area of the lesion has been shown to be the location of most of the plaque fractures.
Veress
A I
AI
Biomedical Engineering Center, Ohio State University, Cleveland, USA. veress.1@osu.edu
Cornhill
J F
JF
Herderick
E E
EE
Thomas
J D
JD
D000293:Adolescent; D000328:Adult; D000375:Aging / Q000473:pathology* / Q000502:physiology; D003198:Computer Simulation; D003324:Coronary Artery Disease / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D003331:Coronary Vessels / Q000473:pathology* / Q000503:physiopathology; D006801:Humans; D008955:Models, Cardiovascular; D013314:Stress, Mechanical