Circulation, Vol 88, 2762-2770, Copyright © 1993 by American Heart Association
NR Phillips, D Waters and RJ Havel
BACKGROUND. There is considerable evidence that remnants of
triglyceride-rich lipoproteins may be particularly atherogenic. METHODS AND
RESULTS. Levels of lipoprotein lipids and of apolipoprotein B in
low-density lipoproteins were measured in 335 men and women enrolled in a
study in which quantitative coronary angiography was carried out at 2- year
intervals. Clinical events related to coronary disease occurred in 129
patients during the trial and in the subsequent follow-up period of 4 to 6
years. In multivariate analysis controlled for a number of nonlipid risk
factors, high-density lipoprotein cholesterol was inversely related to the
mean percentage increase in coronary artery stenosis in both men and women.
Neither plasma triglycerides nor low- density lipoprotein cholesterol,
triglycerides, or apolipoprotein B was related to change in stenosis, but a
measure of remnants of triglyceride-rich lipoproteins, which included
cholesterol in intermediate-density lipoproteins, was directly related to
lesion progression. The same relations for these measures of plasma
lipoprotein concentrations were found to hold for clinical events related
to coronary artery atherosclerosis. CONCLUSIONS. In patients with
established coronary heart disease, increased levels of remnants of
triglyceride-rich lipoproteins and decreased levels of high-density
lipoproteins appear to promote progression of coronary artery
atherosclerosis, which in turn may lead to an untoward clinical event. No
such relation could be shown for the level of components of low- density
lipoproteins. These and other observations call for reevaluation of
relations between particular species of lipoproteins containing
apolipoprotein B and the pathogenesis of coronary artery atherosclerosis
and coronary heart disease.
ARTICLES
Plasma lipoproteins and progression of coronary artery disease evaluated by angiography and clinical events
Cardiovascular Research Institute, University of California, San Francisco 94143-0130.
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