Articles |
From the Departments of Epidemiology (R.W.E., L.H.K.) and Biological Sciences (J.D.H.), University of Pittsburgh, Pittsburgh, Penn; the MRFIT Coordinating Center, Division of Biostatistics, University of Minnesota, Minneapolis, Minn (B.J.S.); and the Division of Epidemiology and Clinical Applications, National Heart, Lung, and Blood Institute, Bethesda, Md (J.A.C.).
Correspondence to R.W. Evans, PhD, University of Pittsburgh, Graduate School of Public Health, Department of Epidemiology, 503 Parran Hall, 130 DeSoto St, Pittsburgh, PA 15261. E-mail RWE2{at}vms.cis.pitt.edu.
Abstract A nested case-control study was undertaken involving men participating in the Multiple Risk Factor Intervention Trial (MRFIT). Serum samples from 712 men, stored for up to 20 years, were analyzed for homocyst(e)ine. Cases involved nonfatal myocardial infarctions (MIs), identified through the active phase of the study, which ended on February 28, 1982, and deaths due to coronary heart disease (CHD), monitored through 1990. The nonfatal MIs occurred within 7 years of sample collection, whereas the majority of CHD deaths occurred more than 11 years after sample collection. Mean homocyst(e)ine concentrations were in the expected range and did not differ significantly between case patients and control subjects: MI cases, 12.6 µmol/L; MI controls, 13.1 µmol/L; CHD death cases, 12.8 µmol/L; and CHD controls, 12.7 µmol/L. Odds ratios versus quartile 1 for CHD deaths and MIs combined were as follows: quartile 2, 1.03; quartile 3, 0.84; and quartile 4, 0.92. Thus, in this prospective study, no association of homocyst(e)ine concentration with heart disease was detected. Homocyst(e)ine levels were weakly associated with the acute-phase protein (C-reactive protein). These results are discussed with respect to the suggestion that homocyst(e)ine is an independent risk factor for heart disease.
Key Words: homocyst(e)ine cardiovascular disease MRFIT prospective
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A. R. Folsom, F. J. Nieto, P. G. McGovern, M. Y. Tsai, M. R. Malinow, J. H. Eckfeldt, D. L. Hess, and C. E. Davis Prospective Study of Coronary Heart Disease Incidence in Relation to Fasting Total Homocysteine, Related Genetic Polymorphisms, and B Vitamins : The Atherosclerosis Risk in Communities (ARIC) Study Circulation, July 21, 1998; 98(3): 204 - 210. [Abstract] [Full Text] [PDF] |
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N. J. Wald, H. C. Watt, M. R. Law, D. G. Weir, J. McPartlin, and J. M. Scott Homocysteine and Ischemic Heart Disease: Results of a Prospective Study With Implications Regarding Prevention Arch Intern Med, April 27, 1998; 158(8): 862 - 867. [Abstract] [Full Text] [PDF] |
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G. S. Omenn, S. A. A. Beresford, and A. G. Motulsky Preventing Coronary Heart Disease : B Vitamins and Homocysteine Circulation, February 10, 1998; 97(5): 421 - 424. [Full Text] [PDF] |
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J. C. Chambers, P. M. Ueland, M. Wright, C. J. Dore, H. Refsum, and J. S. Kooner Investigation of Relationship Between Reduced, Oxidized, and Protein-Bound Homocysteine and Vascular Endothelial Function in Healthy Human Subjects Circ. Res., July 20, 2001; 89(2): 187 - 192. [Abstract] [Full Text] [PDF] |
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P. M. Ridker, J. Shih, T. J. Cook, M. Clearfield, J. R. Downs, A. D. Pradhan, S. E. Weis, A. M. Gotto Jr, and for the Air Force/Texas Coronary Atherosclerosis P Plasma Homocysteine Concentration, Statin Therapy, and the Risk of First Acute Coronary Events Circulation, April 16, 2002; 105(15): 1776 - 1779. [Abstract] [Full Text] [PDF] |
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