A smoking–dependent risk of coronary artery disease associated with a polymorphism of the endothelia

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.

Cite this article

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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