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.
CITATION STYLE
Xu, C., Glagov, S., Zatina, M. A., & Zarins, C. K. (1991). Hypertension sustains plaque progression despite reduction of hypercholesterolemia. Hypertension, 18(2), 123–129. https://doi.org/10.1161/01.hyp.18.2.123
Mendeley helps you to discover research relevant for your work.