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"Genes, Vitamins, Homocyst(e)ine And Cardiovascular Diseases"

y in 587 men and women with coronary heart disease. After a median follow-up of 4.6 years, 3.8% of patients with initial homocyst(e)ine levels below 9 pmol/L have died, as compared with 24.7% of those with initial homocyst(e)ine levels > 15 pmol/L (Nygaard, et al. N Engl J Med 1997; 337:230).

Figure 3. Results of an observation conducted in Northern France in 229 subjects with history of myocardial infarction and in 315 controls. The odds ratios for having had a myocardial infarction in those with homocyst(e)ine levels > 17.2 pmol/L were 6.06 times higher than in those with homocyst(e)ine < 9.8 pmol/L. The graph shows that the risk was progressive across the entire distribution of homocyst(e)ine concentration, i.e., without a threshold (adapted from Malinow et at, Atherosclerosis 1996;125:27).

Figure 4. Changes in homocyst(e)ine levels brought about by daily doses of 1 or 2 mg of folic acid during 3 weeks. Subjects were habitual users of multivitamins (n=99) or non-users of multivitamins (n=143). Subjects were sorted by the genotypes of an enzyme [methylenetetrahydrofolate reductase (MTHFR)], which catalyzes the synthesis of the active form of circulating folic acid in blood. The frequency of homozygotes "wild type" (C/C in nucleotide 677 of the gene) was about 40%, of heterozygotes (C/T) about 50%, and of homozygotes for the mutation (T/T) about 10% (not shown in the figure). C=cytosine; T=thymine. The basal levels of homocyst(e)ine levels due to the intake of folic acid was larger in the homozygotes for the mutation compared to the other genotypes.

Note to reporters: This is one of four fact sheets about the symposium presentation. News release also available. Contact: 214-706-1340.


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Contact: Cathy Yarbrough
cathyy@amhrt.org
214-706-1340
American Heart Association
14-Feb-1998


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