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Lipids, Apolipo..

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Cardiovascular (CV) disease is a major cause of death worldwide. There are strong epidemiologic data supporting the relationship between cholesterol and cardiovascular events. Most clinical practice guidelines recommend the measurement of traditional lipid values or their ratios (total cholesterol, LDL-cholesterol, HDL-cholesterol, total/HDL cholesterol, LDL/HDL cholesterol) as a measure of CV risk. More recently however some guidelines allow clinicians to use apolipoprotein B (ApoB) in place of LDL-cholesterol. Ingelsson and colleagues explored the relationship between apolipoprotein ratios, traditional lipid ratios and the prediction of coronary heart disease (CHD).1 Their data did not support the measurement of apolipoproteins in clinical practice. However data from the INTERHEART study indicated that the nonfasting Apo B to apolipoprotein A1 (ApoA1) ratio was superior to any of the cholesterol ratios for estimating the risk of an acute myocardial infarction.2 

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In an effort to further clarify the relationship between lipids, apolipoproteins, and vascular disease risk, the Emerging Risk Factors Collaboration (ERFC) completed a meta-analysis of 68 long-term studies.3 Trials were selected from a central database containing over 100 prospective population-based studies. Inclusion criteria required an absence of CHD history (myocardial infarction, angina, or stroke) at baseline, the presence of complete information regarding total cholesterol, HDL-cholesterol (HDL-C), and triglyceride levels, as well as information regarding vascular risk factors (i.e. age, sex, smoking status, history of diabetes, systolic blood pressure, and BMI). Of these 68 studies, 22 studies contained additional information concerning ApoB and ApoA1, while 8 contained directly measured LDL-C. The primary outcome was CHD, defined as first instance myocardial infarction (MI) or fatal CHD. Stroke was also viewed as an alternate outcome.

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The mean age of participants at entry was 59 years, 43% were women, 60% were in Western Europe, and 32% were in North America. There were 2.79 million person-years at risk of follow-up during which time there were first-ever 8857 nonfatal MIs, 3928 CHD deaths, 2534 ischemic strokes, 513 hemorrhagic strokes, and 2536 unclassified strokes. The adjusted hazard ratios for CHD with triglyceride was 0.99 (95% CI, 0.94-1.05), with HDL-C 0.78 (95% CI, 0.74-0.82), and with non-HDL-C 1.50 (95% CI, 1.39-1.61). The hazard ratios for CHD of TC/HDL were 1.50 (95% CI, 1.38-1.62) and for ApoB/ApoA1 1.49 (95%CI, 1.39-1.60). These findings were also similar for stroke. Additionally, hazard ratios for vascular disease were just as strong in participants who did not fast as in those who did fast.

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The authors concluded that lipid measurements in vascular risk assessment could be simplified by using either cholesterol levels or apolipoproteins without the need to fast and without regard for triglyceride. The implications of these findings are significant. The practical advantage of obtaining random lipid measurements that accurately predict vascular risk could improve our ability to identify more high risk individuals.

1. Ingelsson E, Schaefer EJ, Contois JH, et al. Clinical utility of different lipid measures for prediction of coronary heart disease in men and women. JAMA 2007;298:776-785.  [PubMed: 17699011]
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