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Am J Physiol Heart Circ Physiol (June 27, 2008). doi:10.1152/ajpheart.00005.2008
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Submitted on January 2, 2008
Revised on May 23, 2008
Accepted on June 11, 2008

Necrotic Core Thickness and Positive Arterial Remodeling Index: Emergent Biomechanical Factors for Evaluating the Risk of Plaque Rupture

Jacques Ohayon1*, Gerard Finet, Ahmed M Gharib1, Daniel Herzka2, Philippe Tracqui3, Julie Heroux1, Gilles Rioufol4, Melanie Kotys2, Abdalla Elagha1, and Roderic I. Pettigrew1

1 NIH
2 Philips Research North America
3 University Joseph Fourier, Institut de l?Ingnierie et de l?Information de Sant (In3S), CNRS UMR 5525
4 Hospices Civils de Lyon and Claude Bernard University, Lyon1, INSERM E0226

* To whom correspondence should be addressed. E-mail: jacques.ohayon{at}imag.fr.

Fibrous cap thickness (Capthick) is often considered as diagnostic of the degree of plaque instability. Necrotic core area (Corearea) and the arterial remodeling index (Remodindex), on the other hand, are difficult to use as clinical morphological indices: literature data show a wide dispersion of Corearea thresholds above which plaque becomes unstable. Although histopathology shows a strong correlation between Corearea and Remodindex, it remains unclear how these interact and affect peak cap stress (Capstress) - 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. Capstress value was calculated on 5,500 idealized atherosclerotic vessel models, which had the original feature of mimicking the positive arterial remodeling process described by Glagov. Twenty four non-ruptured plaques acquired by IVUS 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 Capstress. It was found that: (i) 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 (ii) 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.




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