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Does Relief of Critical Arterial Stenosis Accelerate Distal Atherosclerosis?

Department of Surgery, The Albert Einstein College of Medicine, Montefiore Medical Center,Bronx, New York

Harry R. Davis, Ph.D.t

Schering-Plough Research Division, Kenilworth, New Jersey

Art Runyon-Hass, M.D., Ph.D.

Department of Anesthesiology, Centennial Medical Center, Nashville, Tennessee

Seymour Glagov, M.D.

Department of Pathology, Pritzker School of Medicine, University of Chicago, Illinois

Christopher K. Zarins, M.D.

Division of Vascular Surgery, Stanford University Medical School, Palo Alto, California

Progression of atherosclerosis following balloon angioplasty, arterial bypass, or endarterectomy often limits long-term success of revascularization procedures. Therefore, the authors studied the effect of stenosis and relief of stenosis on the development of distal atherosclerosis in a primate model of diet-induced atherosclerosis. Severe stenosis (78 ± 2% diameter reduction) was produced in the midthoracic aorta in 14 cynomolgus monkeys by a constricting band. In 8 monkeys, the stenosis was left in place for three months, after which the distal aorta was revascularized by removal of the constricting band and by balloon angioplasty of the residual stenosis. The results in this group were compared with those in 6 animals whose stenoses were not reversed and with those in 10 animals with no preexisting stenosis. All three groups received an atherogenic diet for three months with no difference in serum cholesterol (836 to 1059 mg/o) during the three-month diet period. Animals with a stenosis had a significant decrease in surface atherosclerosis in the distal aorta (7 ± 6%) compared with control animals (51 + 8%, P < 0.05). This was accompanied by marked reduction in mural cholesterol content (1.5 ± 0.4 mcg/mm² vs 6.3 ± 1.8 mcg/mm² in controls, P < 0.05) and a decrease in intimal thickness (0.04 ± 0.02 mm vs 0.07 ± 0.01 mm in controls, P < 0.05). After relief of the stenosis, the percent surface atherosclerosis (58 ± 8%), mural cholesterol (5.4 ± 1.0 mcg/mm²), and intimal thickness (0.09 ± 0.01 mm) were no different from controls. Thus, severe stenosis protects the distal vascular tree from intimal plaque formation, despite marked hypercholesterolemia. Following reversal of a stenosis, distal plaque progression does not occur at an accelerated rate but instead occurs at the same rate as without a preexisting stenosis.

Vascular and Endovascular Surgery, Vol. 30, No. 3, 191-200 (1996)
DOI: 10.1177/153857449603000303


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