Is arterial wall-strain stiffening an additional process responsible for atherosclerosis in coronary bifurcations?: an in vivo study based on dynamic CT and MRI

Abstract

Coronary bifurcations represent specific regions of the arterial tree that are susceptible to atherosclerotic lesions. While the effects of vessel compliance, curvature, pulsatile blood flow, and cardiac motion on coronary endothelial shear stress have been widely explored, the effects of myocardial contraction on arterial wall stress/strain (WS/S) and vessel stiffness distributions remain unclear. Local increase of vessel stiffness resulting from wall-strain stiffening phenomenon (a local process due to the nonlinear mechanical properties of the arterial wall) may be critical in the development of atherosclerotic lesions. Therefore, the aim of this study was to quantify WS/S and stiffness in coronary bifurcations and to investigate correlations with plaque sites. Anatomic coronary geometry and cardiac motion were generated based on both computed tomography and MRI examinations of eight patients with minimal coronary disease. Computational structural analyses using the finite element method were subsequently performed, and spatial luminal arterial wall stretch (LWStretch) and stiffness (LWStiff) distributions in the left main coronary bifurcations were calculated. Our results show that all plaque sites were concomitantly subject to high LW Stretch and high LWStiff, with mean amplitudes of 34.7 Ϯ 1.6% and 442.4 Ϯ 113.0 kPa, respectively. The mean LW Stiff amplitude was found slightly greater at the plaque sites on the left main coronary artery (mean value: 482.2 Ϯ 88.1 kPa) compared with those computed on the left anterior descending and left circumflex coronary arteries (416.3 Ϯ 61.5 and 428.7 Ϯ 181.8 kPa, respectively). These findings suggest that local wall stiffness plays a role in the initiation of atherosclerotic lesions. atherosclerosis; coronary disease; wall stiffness; wall stress; biomechanics; computed tomography; magnetic resonance imaging ATHEROSCLEROSIS is a chronic inflammatory disease with systemic manifestations (12,30). Although the coronary and peripheral systems in their entirety are exposed to the same atherogenic cells and molecules in the plasma, atherosclerotic lesions form at specific regions of the arterial tree. Such lesions appear in the vicinity of branch points, the outer wall of bifurcations, and the inner wall of curves (8,18,43). In a pathological study of human coronary lesions, Kolodgie et al. (24) found that healed plaque ruptures were predominantly found in the proximal portions of the left anterior descending (LAD), right coronary (RCA), left circumflex (LCx), and left main (LM) arteries.The coronary arterial wall is constantly subjected to both flow-induced shear stress and wall strain/stress (WS/S) by blood pressure and myocardial contraction. Low or oscillatory endothelial shear stress (ESS) is not the only mechanical stimulus that promotes the inflammatory process by inducing an oxidative response in vascular endothelial cells (ECs) (27). Several biological studies (26, 28, 29) performed on cultured ECs have reported that, above an endothelial cyclic stretch threshold o...

Image-based modeling for better understanding and assessment of atherosclerotic plaque progression and vulnerability: Data, modeling, validation, uncertainty and predictions

“…Ohayon et al (2011) also included heart contraction in their multi-patient coronary plaque study using 3D structural models based on in vivo CT (for morphology) and MRI (for ventricle contraction). Data from eight patients were used in their study.…”

“…The mechanisms causing plaque rupture and subsequent clinical events are not fully understood (Fuster, 1998; Fuster et al, 1990; Naghavi et al, 2003a, 2003b). Considerable progress has been made in recent years in medical imaging (Yuan et al, 2001a, 2001b; Underhill, et al, 2010), histopathological analysis (Stary et al, 1992, 1994, 1995; Virmani et al, 2000, 2006), biomechanical plaque material properties (Finet et al, 2004; Le Floc'h et al, 2012; Baldewsing et al, 2008), mechanical stress risk factors (Richardson et al, 1989; Arroyo and Lee, 1999; Ohayon et al, 2011; Loree et al, 1992). and computational models (Tang, 2006; Friedman et al, 2010) for better understanding of plaque progression, rupture and to develop possible better patient screening and plaque assessment schemes.…”

A parametric model for analysing atherosclerotic arteries: On the FSI coupling

“…The results suggested that severe stenosis may inhibit wall motion. Ohayon et al [33] quantified the WSS and the stiffness in coronary bifurcations and investigated the correlations with atheroma plaque sites.…”

Unsteady blood flow and mass transfer of a human left coronary artery bifurcation: FSI vs. CFD

“…Moreover Ding et al [37] used medical imaging technique to study the arterial motion without considering the compliance itself. In a previous study [38] we analyzed the coronary wall stiffness of 8 patients trying to find correlation with the atheromatous plaque locations, neglecting the contribution of the blood flow. The aim of this work is to evaluate how the wall compliance can affect the blood flow pattern and the WSS in a human LCA using comparing FSI and CFD analysis.…”