Multiaxial Mechanical Characteristics of Carotid Plaque Analysis by Multiarray Echotracking System Anna Paini, MD; Pierre Boutouyrie, MD, PhD; David Calvet, MD; Mustapha Zidi, PhD; Enrico Agabiti-Rosei, MD; Ste ´phane Laurent, MD, PhD Background and Purpose—Carotid plaque rupture depends on the various types of mechanical stresses. Our objective was to determine the multiaxial mechanical characteristics of atherosclerotic plaque and adjacent segment of the common carotid artery. Methods—A novel noninvasive echotracking system was used to measure intima-media thickness, diameter, pulsatile strain, and distensibility at 128 sites on a 4-cm long common carotid artery segment. The study included 62 patients with recent cerebrovascular ischemic event and either a plaque on the far wall of common carotid artery (n=25) or no plaque (n=37). Results—The mechanical characteristics of the carotid segment devoid of plaque did not differ between the two groups. Among patients with plaque, 16 had a larger radial strain at the level of plaque than at the level of adjacent common carotid artery (pattern A: outward-bending strain). The eight patients who had an opposite pattern (inward-bending strain) were more often dyslipidemic (100% versus 56% P=0.03) and type 2 diabetic (63% versus 12%, P=0.04) than pattern A patients. Strain gradient significantly decreased in parallel with the presence of dyslipidemia and/or type 2 diabetes. Longitudinal gradients of distensibility and Young’s elastic modulus were consistent with strain gradients. Conclusions—Type 2 diabetes and dyslipidemia were associated with a stiffer carotid at the level of the plaque than in the adjacent common carotid artery leading to an inward-bending stress. The analysis of plaque mechanics along the longitudinal axis may afford useful information, because repetitive bending strain of an atherosclerotic plaque may fatigue the wall material and result in plaque rupture. (Stroke. 2007;38:117-123.) Key Words: atherosclerotic plaque  carotid artery  mechanics  stiffness  ultrasound P laque rupture has become identified as a critical step in the evolution of atherosclerotic plaque. It is of major importance to detect which plaques are vulnerable, 1 although not yet ruptured, and, specifically, to identify which patients will have a stroke. Rupture mechanisms are complex pro- cesses, which are dependent on plaque morphology and com- position and mechanical characteristics. 2–4 Mildly stenotic carotid plaques with a thin fibrous cap and a lipid-rich core are more susceptible to rupture than plaques with a high degree of fibrosis and calcifications. 1 Although various theoretical and animal models 4,5 or postmortem studies 6 have improved our knowledge of the mechanics of plaque rupture, few studies have clearly docu- mented in vivo in humans the mechanical characteristics of large arteries at the site of atherosclerotic plaque and its vicinity. 7,8 Either in vitro or in vivo in animals, most studies have focused on radial strain at the site of the plaque, 5 and few have addressed the issue of local elastic properties of the surrounding arterial wall material in the longitudinal axis either upstream or downstream of the plaque. 9 To our knowledge, no data on the longitudinal axis have been obtained noninvasively in humans. Our working hypothesis was that longitudinal strain gradi- ents, generated by wall heterogeneity between plaque and adjacent wall materials, (1) could be noninvasively detected along the longitudinal axis of the carotid artery under in vivo conditions and (2) could be influenced by classic cardiovas- cular risk factors such as age, smoking, hypertension, diabe- tes, and dyslipidemia. We took advantage of 128 radiofre- quency (RF) lines multiarray echotracking technology to characterize the mechanical properties of adjacent segments along the common carotid artery (CCA): (1) in the radial, circumferential, and longitudinal axes; and (2) both at the site of plaque and in its vicinity. Received May 24, 2006; final revision received July 19, 2006; accepted August 28, 2006. From the Department of Pharmacology (A.P., P.B., S.L.), Universite ´ Paris-Descartes, Faculte ´ de Me ´decine, INSERM 652, Ho ˆpital Europe ´en Georges Pompidou, Paris, France; the Department of Medical and Surgical Sciences (A.P., E.A.-R.), University of Brescia, Brescia, Italy; Service de Neurologie (D.C.), Ho ˆ pital Sainte-Anne, Universite ´ Rene ´ Descartes, Faculte ´ de Me ´decine Paris, Paris, France; and Institut Superieur des Biosciences de Paris (M.Z.), Universite ´ Paris 12 Val de Marne, Cre ´teil cedex, France. Correspondence to Pr. Ste ´phane Laurent, Department of Pharmacology and INSERM U652, Ho ˆpital Europe ´en Georges Pompidou, Assistance Publique–Ho ˆpitaux de Paris, Universite ´ Paris 5, 20, rue Leblanc, 75015 Paris, France. E-mail stephane.laurent@egp.ap-hop-paris.fr © 2006 American Heart Association, Inc. Stroke is available at http://www.strokeaha.org DOI: 10.1161/01.STR.0000251796.38954.b2 117 by guest on September 11, 2015 http://stroke.ahajournals.org/ Downloaded from