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Influence of residual stress/strain on the biomechanical stability of vulnerable coronary plaques: potential impact for evaluating the risk of plaque rupture

¹National Institutes of Health, National Heart, Lung, and Blood Institute, Pettigrew's Laboratory, Bethesda, Maryland; ²Laboratory Techniques de l’Imagerie de la Modélisation et de la Cognition-Institut de Mathématiques de Grenoble, DynaCell, Centre National de la Recherche Scientifique Unité Mixte de Recherche 5525, Institut de l'Ingénierie et de l'Information de Santé (In³S), Grenoble; and ³Department of Hemodynamics and Interventional Cardiology, Hospices Civils de Lyon and Claude Bernard University, Lyon1; Institut National de la Santé et de la Recherche Médicale E0226 Unit, Lyon, France

Submitted 5 January 2007 ; accepted in final form 20 June 2007

In a vulnerable plaque (VP), rupture often occurs at a site of high stress within the cap. It is also known that vessels do not become free of stress when all external loads are removed. Previous studies have shown that such residual stress/strain (RS/S) tends to make the stress distribution more uniform throughout the media of a normal artery. However, the influence of RS/S on the wall stress distribution in pathological coronaries remains unclear. The aim of this study was to investigate the effects of RS/S on the biomechanical stability of VPs. RS/S patterns were studied ex vivo in six human vulnerable coronary plaque samples. Because the existence of RS/S can only be assessed by releasing it, the opening angle technique was the experimental approach used to study the geometrical opening configurations of the diseased arteries, producing an arterial wall in a near-zero stress state. Reciprocally, these opening geometries were used in finite element simulations to reconstruct the RS/S distributions in closed arteries. It was found that the RS/S 1) is not negligible, 2) dramatically affects the physiological peak stress amplitude in the thin fibrous cap, 3) spotlights some new high stress areas, and 4) could be a landmark of the lipid core's developmental process within a VP. This study demonstrates that plaque rupture is not to be viewed as a consequence of intravascular pressure alone, but rather of a subtle combination of external loading and intraplaque RS/S.

atherosclerosis; zero-stress state; lipid core; plaque growth; finite element analysis

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