Key result
Low shear stress and increased mural tensile stress may be major determinants underlying atheroma formation and plaque rupture.
Computational modeling of hemodynamics and wall mechanics using imaging data may improve the understanding and treatment of atherosclerosis.
May refine plaque risk assessment via imaging; leaves open whether targeting these stresses alters outcomes.
Atherosclerosis, leading to myocardial infarction and stroke, is the major cause of death and morbidity in Western societies. Atheromatous lesions characteristically occur in regions of branching and marked curvature. Low shear stress and increased mural tensile stress may be major determinants underlying atheroma formation at these sites. Furthermore, the distribution of circumferential tensile stresses may play a critical role in where, why and when advanced atheromatous plaques rupture, leading to catastrophic ischaemic events. Recent advances in the application of computational modelling to in vivo vascular ultrasound and magnetic resonance imaging data should further elucidate the roles of haemodynamic factors and vessel wall mechanics in atherosclerosis. In future this is likely to lead to better use of currently available anti-atherosclerosis strategies. It may also facilitate the discovery, evaluation and development of novel treatments.
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Alice Stanton (1999) conducted a review in Atherosclerosis. Low shear stress and increased mural tensile stress may be major determinants underlying atheroma formation and plaque rupture.
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