title: Necrotic core thickness and positive arterial remodeling index: emergent biomechanical factors for evaluating the risk of plaque rupture.
abstract: 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.
authors.affiliation: National Heart, Lung and Blood Institute, NIH, Bldg. 10, 10 Center Dr., Bethesda, MD 20892, USA. ohayonj2@mail.nih.gov
authors.forename: Jacques
authors.initials: J
authors.lastname: Ohayon
authors.forename: Gérard
authors.initials: G
authors.lastname: Finet
authors.forename: Ahmed M
authors.initials: AM
authors.lastname: Gharib
authors.forename: Daniel A
authors.initials: DA
authors.lastname: Herzka
authors.forename: Philippe
authors.initials: P
authors.lastname: Tracqui
authors.forename: Julie
authors.initials: J
authors.lastname: Heroux
authors.forename: Gilles
authors.initials: G
authors.lastname: Rioufol
authors.forename: Melanie S
authors.initials: MS
authors.lastname: Kotys
authors.forename: Abdalla
authors.initials: A
authors.lastname: Elagha
authors.forename: Roderic I
authors.initials: RI
authors.lastname: Pettigrew
mesh_terms: D003198:Computer Simulation; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000473:pathology*; D003331:Coronary Vessels / Q000000981:diagnostic imaging / Q000473:pathology*; D018450:Disease Progression; D005355:Fibrosis; D006801:Humans; D008955:Models, Cardiovascular; D009336:Necrosis; D011237:Predictive Value of Tests; D015203:Reproducibility of Results; D018570:Risk Assessment; D012421:Rupture; D013314:Stress, Mechanical; D018084:Ultrasonography, Interventional