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Necrotic core thickness and positive arterial remodeling index: emergent biomechanical factors for evaluating the risk of plaque rupture

¹National Heart, Lung and Blood Institute, National Institutes of Health, 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, Grenoble; 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 Unit 886, Lyon, France; and ⁴Philips Research North America, Clinical Sites Research Program, Briarcliff Manor, New York

Submitted 2 January 2008 ; accepted in final form 11 June 2008

Fibrous cap thickness is often considered as diagnostic of the degree of plaque instability. Necrotic core area (Core_area) and the arterial remodeling index (Remod_index), on the other hand, are difficult to use as clinical morphological indexes: literature data show a wide dispersion of Core_area thresholds above which plaque becomes unstable. Although histopathology shows a strong correlation between Core_area and Remod_index, it remains unclear how these interact and affect peak cap stress (Cap_stress), a known predictor of rupture. The aim of this study was to investigate the change in plaque vulnerability as a function of necrotic core size and plaque morphology. Cap_stress value was calculated on 5,500 idealized atherosclerotic vessel models that had the original feature of mimicking the positive arterial remodeling process described by Glagov. Twenty-four nonruptured plaques acquired by intravascular ultrasound on patients were used to test the performance of the associated idealized morphological models. Taking advantage of the extensive simulations, we investigated the effects of anatomical plaque features on Cap_stress. It was found that: 1) at the early stages of positive remodeling, lesions were more prone to rupture, which could explain the progression and growth of clinically silent plaques and 2) in addition to cap thickness, necrotic core thickness, rather than area, was critical in determining plaque stability. This study demonstrates that plaque instability is to be viewed not as a consequence of fibrous cap thickness alone but rather as a combination of cap thickness, necrotic core thickness, and the arterial remodeling index.

atherosclerosis; coronary disease; expansive remodeling; wall stress; biomechanics

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