title: Strain distribution over plaques in human coronary arteries relates to shear stress.
abstract: Once plaques intrude into the lumen, the shear stress they are exposed to alters with hitherto unknown consequences for plaque composition. We investigated the relationship between shear stress and strain, a marker for plaque composition, in human coronary arteries. We imaged 31 plaques in coronary arteries with angiography and intravascular ultrasound. Computational fluid dynamics was used to obtain shear stress. Palpography was applied to measure strain. Each plaque was divided into four regions: upstream, throat, shoulder, and downstream. Average shear stress and strain were determined in each region. Shear stress in the upstream, shoulder, throat, and downstream region was 2.55+/-0.89, 2.07+/-0.98, 2.32+/-1.11, and 0.67+/-0.35 Pa, respectively. Shear stress in the downstream region was significantly lower. Strain in the downstream region was also significantly lower than the values in the other regions (0.23+/-0.08% vs. 0.48+/-0.15%, 0.43+/-0.17%, and 0.47+/-0.12%, for the upstream, shoulder, and throat regions, respectively). Pooling all regions, dividing shear stress per plaque into tertiles, and computing average strain showed a positive correlation; for low, medium, and high shear stress, strain was 0.23+/-0.10%, 0.40+/-0.15%, and 0.60+/-0.18%, respectively. Low strain colocalizes with low shear stress downstream of plaques. Higher strain can be found in all other plaque regions, with the highest strain found in regions exposed to the highest shear stresses. This indicates that high shear stress might destabilize plaques, which could lead to plaque rupture.
authors.affiliation: Department of Biomedical Engineering, Thoraxcenter, Erasmus Medical Center, Rotterdam, The Netherlands. f.gijsen@erasmusmc.nl
authors.forename: Frank J H
authors.initials: FJ
authors.lastname: Gijsen
authors.forename: Jolanda J
authors.initials: JJ
authors.lastname: Wentzel
authors.forename: Attila
authors.initials: A
authors.lastname: Thury
authors.forename: Frits
authors.initials: F
authors.lastname: Mastik
authors.forename: Johannes A
authors.initials: JA
authors.lastname: Schaar
authors.forename: Johan C H
authors.initials: JC
authors.lastname: Schuurbiers
authors.forename: Cornelis J
authors.initials: CJ
authors.lastname: Slager
authors.forename: Wim J
authors.initials: WJ
authors.lastname: van der Giessen
authors.forename: Pim J
authors.initials: PJ
authors.lastname: de Feyter
authors.forename: Anton F W
authors.initials: AF
authors.lastname: van der Steen
authors.forename: Patrick W
authors.initials: PW
authors.lastname: Serruys
mesh_terms: D000368:Aged; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000503:physiopathology*; D003326:Coronary Circulation; D003331:Coronary Vessels / Q000000981:diagnostic imaging / Q000503:physiopathology*; D018450:Disease Progression; D005260:Female; D006801:Humans; D007090:Image Interpretation, Computer-Assisted; D008297:Male; D008875:Middle Aged; D008955:Models, Cardiovascular; D012422:Rupture, Spontaneous; D013314:Stress, Mechanical; D018084:Ultrasonography, Interventional