Abstract
The 894G>T polymorphism of the endothelial constitutive nitric oxide synthase gene consists of the substitution of a guanine base by a thymine at the 894th nucleotide of the gene. An association of this polymorphism with acute coronary syndromes has been described, only when in combination with other polymorphisms of this gene. The aim of the present study was to search for an association between this polymorphism and unstable angina in a southern Brazilian population. In a case-control study, 156 patients (group 1 (N = 83): unstable angina, group 2 (N = 73): stable angina) were genotyped by PCR and digestion of the product. Univariate analysis demonstrated that the minimal luminal diameter and the degree of stenosis of the culprit lesion differed between groups (P = 0.006 and 0.005, respectively). In addition, the frequencies of the T allele and of the T allele carriers (combined TT and TG genotypes) were significantly higher in the group with unstable angina (41.6 vs 28.8%; P = 0.025, Pearson chi-square test, and 73.5 vs 45.2%; P = 0.001, Pearson chi-square test, respectively). Multivariate logistic regression showed that the frequency of the T allele carriers was the only variable with a predictive value for unstable angina, when controlled for the other variables (6.1 (95% CI = 2.55-14.43); P < 0.001). Thus, in a homogenous group of patients, the endothelial constitutive nitric oxide synthase 894G>T polymorphism was associated with unstable angina. We suggest that this polymorphism may be a genetic risk factor for unstable angina.
Highlights
The leading mechanism of unstable angina is the transitory interruption of myocardial perfusion by a subocclusive thrombus, superposed on a fissured or eroded coronary atherosclerotic plaque [1]
The 894G>T polymorphism has been described in exon 7 of the endothelial constitutive NO synthase (ecNOS) gene, and consists of the substitution of a guanine base by a thymine at nucleotide 894 of the gene; this mutation results in the substitution of the amino acid glutamate by aspartate at the 298th position of the ecNOS protein (Glu298Asp) [14]
We investigated the possible association between 894G>T polymorphism of the ecNOS gene and unstable angina in a Southern Brazilian population mostly of European ancestry (97.44%)
Summary
The leading mechanism of unstable angina is the transitory interruption of myocardial perfusion by a subocclusive thrombus, superposed on a fissured or eroded coronary atherosclerotic plaque [1]. The endothelium plays a fundamental role in the regulation of the thrombotic process by releasing, among other substances, endothelial-derived relaxing factor (EDRF), synthesized by the endothelial cell [2] and identified as nitric oxide (NO) [3,4]. EDRF is synthesized in the endothelial cell from L-arginine by endothelial constitutive NO synthase (ecNOS), a constitutive enzyme coded by a gene located at locus 7q35-36, containing 26 exons that occupy 21 kb [13]. Some polymorphisms of this gene have been described, as well as their possible association with diverse cardiovascular pathologies. The 894G>T polymorphism has been described in exon 7 of the ecNOS gene, and consists of the substitution of a guanine base by a thymine at nucleotide 894 of the gene; this mutation results in the substitution of the amino acid glutamate by aspartate at the 298th position of the ecNOS protein (Glu298Asp) [14]
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