Abstract 6103: Effect of Lipid or Antioxidant Vitamin Therapy on Three Year Progression of Electron Beam Tomography (EBT) Coronary Calcium Scores
LDL-C and HDL-C are strongly correlated with coronary artery calcium (CAC) which progresses slowly in observational studies of subjects with low LDL-C compared to those with coronary heart disease (CHD) or elevated cholesterol. We therefore hypothesized that lipid-altering therapy would also slow the progression of CAC scores in direct relation with the slowing of angiographic CHD. The relationship of change in CAC score to stenosis change has yet to be examined. Ninety-five of the original 160 participants with clinically manifest CHD and low HDL-C in the HDL Atherosclerosis Treatment Study (HATS) had coronary EBT scans at baseline, 1, 2 and 3 years. Participants were randomly assigned in a 2 × 2 factorial design to receive simvastatin plus niacin [SN(+)] or their placebos [SN(−)], and to receive antioxidant vitamins [AOx(+)] or their placebos [AOx(−)]. Multivariate analysis was performed to assess the percent or absolute CAC score change over 1, 2, and 3 years for each treatment assignment. Coronary stenoses (S) were measured angiographically in 9 proximal segments per patient, averaging 39%S. The average age of participants was 55 years, 5.3% were women. Baseline Agaston score averaged 541 (84.6 percentile general population). Agaston scores progressed 43% of baseline score in the first year, 13% in the second year, and 6% in the third year. There was no difference between SN(+) and SN(−) for Agaston score or CAC volume score for any time point, nor between AOx(+) or AOx(−). As previously reported, quantitative coronary arteriography demonstrated halting of proximal coronary stenosis progression (delta %S = +0.1%S) among those given SN(+) as compared with substantial progression (delta %S = +2.8%S) among those given SN(−) (p<0.001). There was no significant effect of AOx(+) on stenosis progression. Although lipid-altering therapy vs. placebo raised HDL-C by 30%, lowered LDL-C by 42% and halted progression of coronary arterial obstruction, CAC score was not slowed. We hypothesize that lipid-altering therapy results in depletion of plaque lipid core, plaque stabilization, and slows progressive obstruction. Calcification, however, continues unabated for at least three years as part of the plaque aging process.