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Published on: December 2, 2016
Reduction of aortic wall motion inhibits hypertension-mediated experimental atherosclerosis
B I Tropea1, S P Schwarzacher, A Chang
1Division of Vascular Surgery, Stanford University School of Medicine, Stanford, CA, USA.
Insights
Reducing aortic wall motion in hypertensive rabbits significantly decreased plaque formation. This suggests that arterial wall movement may contribute to atherosclerosis development, offering a potential new target for treatment.
Area of Science:
- Cardiovascular Science
- Vascular Biology
- Experimental Atherosclerosis
Background:
- Hypertension is a major risk factor for cardiovascular diseases, including coronary artery disease and peripheral occlusive disease.
- Increased aortic wall motion and plaque formation are observed in hypercholesterolemic animals with experimentally induced hypertension.
Purpose of the Study:
- To test the hypothesis that reducing aortic wall motion, even with continued hypertension, can decrease plaque formation.
- To investigate the role of cyclic arterial wall motion in the development of experimental atherosclerosis.
Main Methods:
- New Zealand White rabbits underwent thoracic aortic banding to induce hypertension and were fed an atherogenic diet.
- An external wrap was applied to a segment of the aorta in some rabbits to reduce wall motion.
- Blood pressure, pulse pressure, and aortic wall motion were measured using intravascular ultrasound; intimal plaque was quantified via morphometry.
Main Results:
- Hypertension and increased aortic wall motion were successfully induced and comparable across coarcted groups.
- The external wrap significantly reduced aortic wall motion in the wrapped segments.
- Intimal thickening was significantly reduced in rabbits with reduced aortic wall motion compared to controls.
Conclusions:
- Localized inhibition of aortic wall motion effectively reduced intimal plaque formation in a hypertensive rabbit model.
- These findings suggest that cyclic arterial wall motion may promote cellular proliferation and lipid uptake, contributing to experimental atherosclerosis.
- Arterial wall motion is a potential therapeutic target for reducing atherosclerosis in hypertensive individuals.
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.
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