NEW YORK (Reuters Health) – Lipid assessment of vascular disease risk can be simplified by measuring either cholesterol levels or apolipoproteins, without fasting and without looking at triglyceride levels.

That’s according to an analysis of data from 68 prospective studies, with more than 300,000 participants, reported in the November 11th Journal of the American Medical Association by the Emerging Risk Factors Collaboration.

Among the implications of the study, its authors say, is that “current discussions about whether to measure cholesterol levels or apolipoproteins in vascular risk assessment should hinge more on practical considerations (e.g., cost, availability, and standardization of assays) than on major differences in strength of epidemiological associations.”

According to the paper, which was written by Dr. John Danesh from the University of Cambridge, UK, and colleagues, none of the 302,430 study subjects had vascular disease at baseline (mean age at entry, 59 years). During 2.79 million person-years at risk there were 8857 first-time nonfatal myocardial infarctions, 3928 deaths due to coronary heart disease, and 2534 first-time ischemic strokes.

Non-high-density lipoprotein-cholesterol (non-HDL-C) and apolipoprotein B (apo B) were similar in the shape and magnitude of their associations with coronary heart disease, according to the article. Also similar to each other in their associations with heart disease were HDL-C and apo AI.

Hazard ratios for coronary heart disease were 1.50 for the ratio of non-HDL-C to HDL, and 1.49 for the apo B-to-apo AI ratio.

Furthermore, “hazard ratios were at least as strong in participants who did not fast as in those who did.” For example, for HDL-C, hazard ratios in non-fasting and fasting subjects were 0.75 and 0.79, respectively.

The adjusted hazard ratios were more modest in their association with ischemic stroke.

“In contrast with previous findings based on much less data,” triglyceride concentrations were not independently associated with coronary heart disease risk after controlling for HDL-C, non-HDL-C, and other risk factors, the researchers say.

“The current findings encourage large coronary heart disease studies of therapies and genotypes that specifically affect each of these lipid measures to help judge etiological relevance,” the research team concludes.

Reference:
JAMA 2009;302:1993-2000.