American Journal of Epidemiology Vol. 143, No. 9: 845-859
Copyright © 1996 by The Johns Hopkins University School of Hygiene and Public Health
research-article |
Homocysteine Metabolism and Risk of Myocardial Infarction: Relation with Vitamins B6, B12, and Folate
1Department of Epidemiology and Public Health, Agricultural University Wageningen, Netherlands
2Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School Boston, MA
3Departments of Epidemiology and Nutrition, Harvard School of Public Health Boston, MA
4Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School Boston, MA
5Division of Ambulatory Care and Prevention, Brigham and Women's Hospital and Harvard Medical School Boston, MA
6Department of Medicine, Division of Hematology, University of Colorado Health Sciences Center Denver, CO
7Department of Human Nutrition and Dietetics, University of Illinois Chicago, IL
8Department of Epidemiology, Harvard School of Public Health Boston, MA
Reprint requests to Dr. M. J. Stampfer, Channing Laboratory, 180 Longwood Ave., Boston, MA 02115
Elevated plasma homocyst(e)ine levels are an independent risk factor for vascular disease. In a case-control study, the authors studied the associations of fasting plasma homocyst(e)ine and vitamins, which are important cofactors in homocysteine metabolism, with the risk of myocardial infarction. The cases were 130 Boston area patients hospitalized with a first myocardial infarction and 118 population controls, less than 76 years of age, enrolled in 1982 and 1983. Dietary intakes of vitamins B6, B12, and folate were estimated from a food frequency questionnaire. After adjusting for sex and age, the authors found that the geometric mean plasma homocyst(e)ine level was 11% higher in cases compared with controls (p = 0.006). There was no clear excess of cases with extremely elevated levels. The age- and sex-adjusted odds ratio for each 3-µmol/liter (approximately 1 standard deviation) increase in plasma homocyst(e)ine was 1.35 (95% confidence interval 1.05–1.75; p trend = 0.007). After further control for several other risk factors, the odds ratio was not affected, but the confidence interval was wider and the p value for trend was less significant. Dietary and plasma levels of vitamin B6 and folate were lower in cases than in controls, and these vitamins were inversely associated with the risk of myocardial infarction, independently of other potential risk factors. Vitamin B12 showed no clear association with myocardial infarction, although methylmalonic acid levels were significantly higher in cases. Comparing the mean levels of several homocysteine metabolites among cases and controls, the authors found that impairment of remethylation of homocyst(e)ine (dependent on folate and vitamin B12 rather than on vitamin B6-dependent transsulfuration) was the predominant cause of high homocyst(e)ine levels in cases. Accordingly, plasma folate and, to a lesser extent, plasma vitamin B12, but not plasma vitamin B6, correlated inversely with plasma homocyst(e)ine, even for concentrations at the high end of normal values. These data provide further evidence that plasma homomocyst(e)ine is an independent risk factor for myocardial infarction. In this population, folate was the most important determinant of plasma homocyst(e)ine, even in subjects with apparently adequate nutritional status of this vitamin. Am J Epidemiol 1996;143:845–59.
folic acid; homocysteine; myocardial infarction; pyridoxine; vitamin B 12
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D. A. J. Brouwer, H. T. M. E. Welten, D.-J. Reijngoud, J. J. van Doormaal, and F. A. J. Muskiet Plasma folic acid cutoff value, derived from its relationship with homocyst(e)ine Clin. Chem., July 1, 1998; 44(7): 1545 - 1550. [Abstract] [Full Text] [PDF]
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J. H. Stein and P. E. McBride Hyperhomocysteinemia and Atherosclerotic Vascular Disease: Pathophysiology, Screening, and Treatment Arch Intern Med, June 22, 1998; 158(12): 1301 - 1306. [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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E. B. Rimm, W. C. Willett, F. B. Hu, L. Sampson, G. A. Colditz, J. E. Manson, C. Hennekens, and M. J. Stampfer Folate and Vitamin B6 From Diet and Supplements in Relation to Risk of Coronary Heart Disease Among Women JAMA, February 4, 1998; 279(5): 359 - 364. [Abstract] [Full Text] [PDF]
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R. W. Evans, B. J. Shaten, J. D. Hempel, J. A. Cutler, and L. H. Kuller Homocyst(e)ine and Risk of Cardiovascular Disease in the Multiple Risk Factor Intervention Trial Arterioscler Thromb Vasc Biol, October 1, 1997; 17(10): 1947 - 1953. [Abstract] [Full Text]
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O. Nygard, J. E. Nordrehaug, H. Refsum, P. M. Ueland, M. Farstad, and S. E. Vollset Plasma Homocysteine Levels and Mortality in Patients with Coronary Artery Disease N. Engl. J. Med., July 24, 1997; 337(4): 230 - 237. [Abstract] [Full Text] [PDF]
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S. M. Schwartz, D. S. Siscovick, M. R. Malinow, F. R. Rosendaal, R. K. Beverly, D. L. Hess, B. M. Psaty, W. T. Longstreth Jr, T. D. Koepsell, T. E. Raghunathan, et al. Myocardial Infarction in Young Women in Relation to Plasma Total Homocysteine, Folate, and a Common Variant in the Methylenetetrahydrofolate Reductase Gene Circulation, July 15, 1997; 96(2): 412 - 417. [Abstract] [Full Text]
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M. D. Phillips Interrelated Risk Factors for Venous Thromboembolism Circulation, April 1, 1997; 95(7): 1749 - 1751. [Full Text]
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C. Schmitz, K. Lindpaintner, P. Verhoef, J. M. Gaziano, and J. Buring Genetic Polymorphism of Methylenetetrahydrofolate Reductase and Myocardial Infarction: A Case-Control Study Circulation, October 15, 1996; 94(8): 1812 - 1814. [Abstract] [Full Text]
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M. J. Stampfer and E. B. Rimm Folate and Cardiovascular Disease: Why We Need a Trial Now JAMA, June 26, 1996; 275(24): 1929 - 1930. [Abstract] [PDF]
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