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A smoking–dependent risk of coronary artery disease associated with a polymorphism of the endothelial nitric oxide synthase gene

Abstract

Endothelium–dependent vasodilatation is mediated by release of nitric oxide formed by constitutively expressed endothelial nitric oxide synthase (ecNOS). We explored the distribution of polymorphism ecNOS4a/b in 549 subjects with, and 153 without, coronary artery disease in relation to smoking. In current and ex–cigarette smokers, but not nonsmokers, there was a significant excess of homozygotes for the rare ecNOS4a allele in patients with severely stenosed arteries, compared with those with no or mild stenosis. This genotype was also associated with a history of myocardial infarction. This smoking–dependent excess coronary risk in ecNOS4a homozygotes is consistent with predisposition to endothelial dysfunction.

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Wang, X., Sim, A., Badenhop, R. et al. A smoking–dependent risk of coronary artery disease associated with a polymorphism of the endothelial nitric oxide synthase gene. Nat Med 2, 41–45 (1996). https://doi.org/10.1038/nm0196-41

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