From: Doug Skrecky (oberon@vcn.bc.ca)
Date: Thu Nov 19 1998 - 13:47:51 MST
Authors
MacMahon S. Sharpe N. Gamble G. Hart H. Scott J. Simes J. White H.
Institution
Department of Medicine, University of Auckland, New Zealand.
macmahon:ctru.auckland.ac.nz
Title
Effects of lowering average of
below-average cholesterol levels on the progression of
carotid atherosclerosis: results of the LIPID Atherosclerosis Substudy. LIPID
Trial Research Group [published erratum appears in Circulation 1996 Jun
23;97(24):2479].
Source
Circulation. 97(18):1784-90, 1998 May 12.
Abstract
BACKGROUND: Cholesterol lowering in patients with
above-average cholesterol levels has been shown to reduce
the progression of atherosclerosis and lower the risk of coronary heart
disease events. However, there has been uncertainty about the effects of
cholesterol lowering in patients with
average or below-average cholesterol
levels. METHODS AND RESULTS: In this study, 522 patients with a history of
myocardial infarction or unstable angina and with baseline levels of total
cholesterol between 4 and 7 mmol/L (mean, 5.7 mmol/L) were randomized to
treatment with a low fat diet plus pravastatin (40 mg daily) or to a low fat
diet plus placebo. Treatment with pravastatin reduced the levels of total
cholesterol by 19%, LDL cholesterol by 27%, apolipoprotein B by 19%, and
triglycerides by 13% (all 2P<.0001) and increased apolipoprotein A1 and HDL
cholesterol levels by 4% (both 2P<.0005), in comparison with placebo. Carotid
atherosclerosis was assessed from B-mode ultrasound measurements of the
common carotid artery. After 4 years, mean carotid wall thickness had
increased by 0.048 mm (SE=0.01) in the placebo group and declined by 0.014 mm
in the pravastatin-treated group (SE=0.01) (2P for difference <.0001). The
effect of treatment on wall thickness was similar in three groups classified
by tertiles of total cholesterol at baseline, with mean levels of 4.8, 5.7,
and 6.6 mmol/L, respectively (2P for interaction >.8). CONCLUSIONS: Treatment
with pravastatin reduced the development of carotid atherosclerosis among
patients with coronary heart disease and a wide range of pretreatment
cholesterol levels. Treatment with this agent prevented any detectable
increase in carotid wall thickening over 4 years of follow-up.
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