Relationship of the Glu298Asp polymorphism of the endothelial nitric oxidesynthase gene and early-onset coronary artery disease

Citation
Ba. Nassar et al., Relationship of the Glu298Asp polymorphism of the endothelial nitric oxidesynthase gene and early-onset coronary artery disease, AM HEART J, 142(4), 2001, pp. 586-589
Citations number
29
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
AMERICAN HEART JOURNAL
ISSN journal
00028703 → ACNP
Volume
142
Issue
4
Year of publication
2001
Pages
586 - 589
Database
ISI
SICI code
0002-8703(200110)142:4<586:ROTGPO>2.0.ZU;2-N
Abstract
Background The Glu298Asp polymorphism of endothelial nitric oxide synthase (eNOS) gene has been associated with coronary artery disease (CAD) in some but not all studies. To determine the impact of the mutant Asp298 eNOS alle le on the development of premature CAD, we examined the prevalence of this mutation in patients with early-onset CAD compared with those manifesting C AD later in life. If this mutation confers an increased risk of premature C AD, we hypothesized that the frequency of the homozygous mutation (Asp298As p298) would be greater among the younger patient group. Methods A total of 299 patients with a history of myocardial infarction (MI) or angina pectori s plus angiographically documented CAD were studied. Patients were divided into 2 groups: group 1 (149 patients) included patients with CAD before the age of 50 years and group 2 (150 patients) included patients with a first presentation of CAD at > 65 years old. Prevalence of eNOS Glu298 and Asp298 alleles was assessed by molecular analysis and compared for the 2 groups. Results There was no significant difference in the frequency of the mutant Asp298 allele between the 2 groups (G1: 42% vs G2: 42.7%, P = .79). The fre quencies of the Glu298Glu298, Glu298Asp298, and Asp298Asp298 genotypes were Similar in both groups (34.9%, 46.3%, and 18.8% for G1 and 29.3%, 56%, and 14.7% for G2, respectively, P = .29). Conclusions Our study does not suppo rt the conclusion that the eNOS Asp298 allele contributes to the developmen t of premature CAD.