Effect of remote aortic injury and thrombosis on cholesterol atherosclerosis

Abstract

Recent tissue culture studies indicate that platelet factors enhance lipoproteins to stimulate proliferation of smooth muscle cells, a key event in atherogenesis. It was of interest to determine if continued remote aortic injury and thrombosis can increase the severity of hypercholesterolemia induced atherosclerosis. Four groups of rabbits were studied, two groups fed 0.5 g cholesterol per day, one group with and one group without massive abdominal aortic white mural non-occlusive thrombosis and injury induced with a permanent indwelling catheter, and two groups fed 1 g cholesterol per day, one group with and one group without similar thrombosis and injury. Serum lipids in the four groups were qualitatively and quantitatively not significantly different from each other at 4, 8, and 12 weeks. When they were sacrificed at 12 weeks the percent intimal surface area in the thoracic aorta (48 ± 22) and arch (75 ± 28) of the rabbits with thrombosis and fed 0.5 g cholesterol per day was significantly ( p < 0.01) greater than the percent intimal area (20 ± 14) and (24 ± 18) of the rabbits without thrombosis. The percent intimal area with lesions in the rabbits fed 1 g cholesterol per day with thrombosis (59 ± 25) and (84 ± 30) was significantly greater ( p < 0.01) than the percent area (24 ± 29) and (32 ± 32) of the rabbits without thrombosis. Since the effects could not be attributed to differing serum lipid levels it is possible that the increased severity of atherosclerosis in the remote arch and thoracic aorta was related to increased permeability, cell proliferation or collagen synthesis possibly stimulated by circulating factors released from the remote massive non-occlusive thrombus or from circulating platelets activated by contact with the injured abdominal aortic wall.