title: Reduction of aortic wall motion inhibits hypertension-mediated experimental atherosclerosis.
abstract: Hypertension is a well-known risk factor for coronary artery disease and carotid and lower extremity occlusive disease. Surgically induced hypertension in hypercholesterolemic animals results in increased aortic wall motion and increased plaque formation. We tested the hypothesis that reduction in aortic wall motion, despite continued hypertension, could reduce plaque formation. New Zealand White rabbits (n=26) underwent thoracic aortic banding to induce hypertension and were fed an atherogenic diet for 3 weeks. In 13 rabbits, a segment of aorta proximal to an aortic band was externally wrapped to reduce wall motion. All animals were fed an atherogenic diet for 3 weeks. Four groups were studied: 1, coarctation control (no wrap, n=7); 2, coarctation with loose wrap (n=6); 3, coarctation with firm wrap (n=7); and 4, control (noncoarcted, n=6). Wall motion, blood pressure, and pulse pressure were measured at standard reference sites proximal and distal to the coarctation by use of intravascular ultrasound. Quantitative morphometry was used to measure intimal plaque. Mean arterial pressure and cyclic aortic wall motion were equally increased proximal to the aortic coarctation in all 3 coarcted rabbit groups compared with the control group (P:<0.001). Wall motion in the segment of aorta under the loose and firm wraps was no different from the control value. The external wrap significantly reduced intimal thickening in the 4 groups by the following amounts: group 1, 0.30+/-0.03 mm(2); group 2, 0.06+/-0.02 mm(2); group 3, 0. 04+/-0.02 mm(2); and group 4, 0.01+/-0.01 mm(2) (P:<0.001). Localized inhibition of aortic wall motion in the lesion-prone hypertensive aorta resulted in significant reduction in intimal plaque formation. These data suggest that arterial wall cyclic motion may stimulate cellular proliferation and lipid uptake in experimental atherosclerosis.
authors.affiliation: Division of Vascular Surgery, Stanford University School of Medicine, Stanford, CA, USA.
authors.forename: B I
authors.initials: BI
authors.lastname: Tropea
authors.forename: S P
authors.initials: SP
authors.lastname: Schwarzacher
authors.forename: A
authors.initials: A
authors.lastname: Chang
authors.forename: C
authors.initials: C
authors.lastname: Asvar
authors.forename: P
authors.initials: P
authors.lastname: Huie
authors.forename: R K
authors.initials: RK
authors.lastname: Sibley
authors.forename: C K
authors.initials: CK
authors.lastname: Zarins
mesh_terms: D000818:Animals; D001013:Aorta, Thoracic / Q000473:pathology / Q000503:physiopathology*; D001161:Arteriosclerosis / Q000209:etiology* / Q000473:pathology; D001696:Biomechanical Phenomena; D004032:Diet; D004195:Disease Models, Animal; D006439:Hemodynamics; D006973:Hypertension / Q000150:complications*; D008297:Male; D011817:Rabbits; D017539:Tunica Intima / Q000473:pathology; D017540:Tunica Media / Q000473:pathology