HYPERTENSION SUSTAINS PLAQUE PROGRESSION DESPITE REDUCTION OF HYPERCHOLESTEROLEMIA

To assess the effect of hypertension on diet-induced coronary artery plaques after a return to a nonatherogenic diet, 10 cynomolgus monkeys were fed an induction regimen containing 2% cholesterol and 25% peanut oil for 6 months and then were subjected to midthoracic aortic coarctation to induce hypertension. The animals were then fed a nonatherogenic "prudent" ration for 6 additional months (hypertension-regression group). Twelve additional monkeys were fed the atherogenic diet for 6 months; six were killed (lesion-induction control group) and six were changed to the prudent diet for 6 additional months without coarctation (normotension-regression control group). At the end of the induction period, cholesterol levels averaged 744 +/- 178 mg/dl for the 22 animals and were similar for the three groups throughout the induction period. For the animals restored to the nonatherogenic diet (hypertension-regression and normotension-regression groups), serum cholesterol levels fell to 486 +/- 252 mg/dl at 1 month, to 341 +/- 162 mg/dl at 2 months, and to 234 +/- 78 mg/dl at 6 months. There was no significant difference between the hypertensive and normotensive animals. Six months after coarctation, blood pressure proximal to the coarctations for the hypertension-regression group ranged from 100/60 to 220/145 mm Hg with a mean of 166/103 +/- 36/28 mm Hg. Cross-sectional area of coronary plaques was somewhat lower for the normotension-regression control group compared with the lesion-induction control group, but the difference was not significant. Plaque area was, however, markedly greater in the hypertension-regression group than in either the lesion-induction or the normotension-regression groups (p < 0.05 for each) despite progressive reduction in hyperlipidemia. Furthermore, individual mean lesion area for the hypertension-regression group correlated positively, linearly, and significantly with individual levels of mean, systolic, or diastolic pressure (p < 0.001 for each). Regardless of blood pressure level or lesion area, lumen area remained normal because artery size increased with the increase in plaque area (r = 0.73, p < 0.02). Although hypertension sustained lesion progression under these experimental conditions, our findings do not indicate that cholesterol lowering in the presence of hypertension is necessarily without effect on coronary atherosclerosis.