title: 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 (LW(Stretch)) and stiffness (LW(Stiff)) 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 LW(Stiff), with mean amplitudes of 34.7 ± 1.6% and 442.4 ± 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 ± 88.1 kPa) compared with those computed on the left anterior descending and left circumflex coronary arteries (416.3 ± 61.5 and 428.7 ± 181.8 kPa, respectively). These findings suggest that local wall stiffness plays a role in the initiation of atherosclerotic lesions.
authors.affiliation: Laboratory of Integrative Cardiovascular Imaging Science, National Institute of Diabetes Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA. jacques.ohayon@imag.fr
authors.forename: Jacques
authors.initials: J
authors.lastname: Ohayon
authors.forename: Ahmed M
authors.initials: AM
authors.lastname: Gharib
authors.forename: Alberto
authors.initials: A
authors.lastname: Garcia
authors.forename: Julie
authors.initials: J
authors.lastname: Heroux
authors.forename: Saami K
authors.initials: SK
authors.lastname: Yazdani
authors.forename: Mauro
authors.initials: M
authors.lastname: Malvè
authors.forename: Philippe
authors.initials: P
authors.lastname: Tracqui
authors.forename: Miguel-Angel
authors.initials: MA
authors.lastname: Martinez
authors.forename: Manuel
authors.initials: M
authors.lastname: Doblare
authors.forename: Gérard
authors.initials: G
authors.lastname: Finet
authors.forename: Roderic I
authors.initials: RI
authors.lastname: Pettigrew
mesh_terms: D000328:Adult; D000368:Aged; D001696:Biomechanical Phenomena; D017023:Coronary Angiography / Q000379:methods*; D003324:Coronary Artery Disease / Q000175:diagnosis* / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology; D003331:Coronary Vessels / Q000473:pathology* / Q000503:physiopathology; D004548:Elasticity; D005260:Female; D020342:Finite Element Analysis; D006439:Hemodynamics; D006801:Humans; D007090:Image Interpretation, Computer-Assisted; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D008955:Models, Cardiovascular; D009200:Myocardial Contraction; D017711:Nonlinear Dynamics; D058226:Plaque, Atherosclerotic / Q000175:diagnosis* / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology; D011237:Predictive Value of Tests; D013314:Stress, Mechanical; D013997:Time Factors; D014057:Tomography, X-Ray Computed