4.7 Article

Lack of association of a 9 bp insertion/deletion polymorphism within the bradykinin 2 receptor gene with myocardial infarction

Journal

CLINICAL SCIENCE
Volume 107, Issue 5, Pages 505-511

Publisher

PORTLAND PRESS LTD
DOI: 10.1042/CS20040129

Keywords

bradykinin receptor; genetic association study; myocardial infarction; polymorphism

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The BK (bradykinin) B-2 receptor is the major cellular mediator of the effects of BK. A 9 bp deletion in the promoter of the receptor gene represents an allelic variant that is associated with enhanced mRNA expression levels. We tested whether this polymorphism is associated with the prevalence of MI (myocardial infarction) or with echocardiographically determined left ventricular function in post-MI patients. Patients with documented MI (n=484), matched controls and controls without evidence of coronary heart disease (n = 1363) constituted cases and controls. MI patients and controls were carefully matched for age, gender and cardiovascular risk factors. Genotype distributions of the 9 bp insertion/deletion polymorphism were similar across the groups: -9/-9, -9/+9 and +9/+9 were 22.1, 49.5 and 28.5 % in MI patients, and 23.0, 44.6 and 32.5 % in matched control subjects respectively. The lack of association was also observed in selected subgroups, stratified by age, gender and cardiovascular risk factors. Furthermore, there was no relation between this polymorphism and left ventricular systolic function in post-MI patients. These findings indicate that the 9 bp insertion/deletion polymorphism of the BK B-2 receptor gene is neither related to the prevalence of MI nor to left ventricular function after MI.

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