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  Vol. 163 No. 9, May 12, 2003 TABLE OF CONTENTS
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Relation of Triglyceride Levels, Fasting and Nonfasting, to Fatal and Nonfatal Coronary Heart Disease

Lynn E. Eberly, PhD; Jeremiah Stamler, MD; James D. Neaton, PhD; for the Multiple Risk Factor Intervention Trial Research Group

Arch Intern Med. 2003;163:1077-1083.

Background  It remains unclear whether hypertriglyceridemia is an independent risk factor for coronary heart disease (CHD), and whether fasting and nonfasting triglyceride (TG) levels are equally predictive.

Methods  A total of 2809 (of 12 866) men randomized during 1973 through 1975 into the Multiple Risk Factor Intervention Trial with fasting and nonfasting TG levels measured at baseline were followed up for CHD incidence and death. Proportional hazards regression models were used to assess associations of fasting and nonfasting TG levels with CHD.

Results  Average fasting and nonfasting TG levels were 187 and 284 mg/dL (2.11 and 3.21 mmol/L), respectively. Prevalence of hypertriglyceridemia (200 mg/dL [2.26 mmol/L] or more) was 31% for fasting and 61% for nonfasting. There were 175 nonfatal or fatal CHD events during 8 years and 328 CHD deaths during 25 years. Compared with TG levels less than 200 mg/dL, risk factor–adjusted hazard ratios for CHD mortality for hypertriglyceridemia were 1.24 (P = .09) for fasting and 1.26 (P = .07) for nonfasting. For nonfatal or fatal CHD, fasting and nonfasting TG levels were similarly predictive with hazard ratios of 1.64 (P = .004) for fasting and 1.46 (P = .03) for nonfasting. These associations for fasting TG levels were assessed to be underestimated by 56% because of regression dilution bias, with attenuation likely greater for nonfasting TG levels.

Conclusions  Greater ease of obtaining nonfasting than fasting measurements, greater prevalence of hypertriglyceridemia with nonfasting than fasting values, and similarly increased risk with each indicate that nonfasting TG levels may be more useful than fasting ones for risk stratification.


From the Division of Biostatistics, School of Public Health, University of Minnesota, Minneapolis (Drs Eberly and Neaton); and Department of Preventive Medicine, Northwestern University Medical School, Chicago, Ill (Dr Stamler). The principal investigators and senior staff of the Multiple Risk Factor Intervention Trial clinical, coordinating, and support centers and the National Heart, Lung, and Blood Institute project office were published previously (JAMA. 1982;248:1476-1477). The authors have no relevant financial interest in this article.



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