title: Evaluation of endothelial shear stress and 3D geometry as factors determining the development of atherosclerosis and remodeling in human coronary arteries in vivo. Combining 3D reconstruction from angiography and IVUS (ANGUS) with computational fluid dynamics.
abstract: The predilection sites of atherosclerotic plaques implicate rheologic factors like shear stress underlying the genesis of atherosclerosis. Presently no technique is available that enables one to provide 3D shear stress data in human coronary arteries in vivo. In this study, we describe a novel technique that uses a recently developed 3D reconstruction technique to calculate shear stress on the endothelium with computational fluid dynamics. In addition, we calculated local wall thickness, the principal plane of curvature, and the location of plaque with reference to this plane, relating these results to shear stress in a human right coronary artery in vivo. Wall thickness and shear stress values for the entire vessel for three inflow-velocity values (10 cm/second, 20 cm/second, and 30 cm/second equivalents with the Reynolds numbers 114,229, and 457) were as follows: 0.65 +/- 0.37 mm (n = 1600) and 19.6 +/- 1.7 dyne/cm2; 46.1 +/- 8.1 dyne/cm2 and 80.1 +/- 16.8 dyne/cm2 (n = 1600). Curvature was 25 +/- 9 (m-1), resulting in Dean numbers 20 +/- 8; 46 +/- 16, and 93 +/- 33. Selection of data at the inner curvature of the right coronary artery provided wall thickness values of 0.90 +/- 0.41 mm (n = 100), and shear stress was 17 +/- 17, 38 +/- 44, and 77 +/- 54 dyne/cm2 (n = 100), whereas wall thickness values at the outer curve were 0.37 +/- 0.17 mm (n = 100) and shear stress values were 22 +/- 17, 60 +/- 44, and 107 +/- 79 dyne/cm2 (n = 100). These findings could be reconciled by an inverse relationship between wall thickness and shear stress for each velocity level under study. For the first time for human vessels in vivo, evidence is presented that low shear stress promotes atherosclerosis. As the method is nondestructive, it allows repeated measurements in the same patient and will provide new insights in the progress of atherosclerosis.
authors.affiliation: Thoraxcenter, University Hospital Dijkzigt, Rotterdam, The Netherlands.
authors.forename: R
authors.initials: R
authors.lastname: Krams
authors.forename: J J
authors.initials: JJ
authors.lastname: Wentzel
authors.forename: J A
authors.initials: JA
authors.lastname: Oomen
authors.forename: R
authors.initials: R
authors.lastname: Vinke
authors.forename: J C
authors.initials: JC
authors.lastname: Schuurbiers
authors.forename: P J
authors.initials: PJ
authors.lastname: de Feyter
authors.forename: P W
authors.initials: PW
authors.lastname: Serruys
authors.forename: C J
authors.initials: CJ
authors.lastname: Slager
mesh_terms: D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000209:etiology*; D003331:Coronary Vessels / Q000033:anatomy & histology*; D004452:Echocardiography; D004730:Endothelium, Vascular / Q000502:physiology*; D006801:Humans; D007091:Image Processing, Computer-Assisted; D013314:Stress, Mechanical