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

Marcus Fischer, Wolfgang Lieb, Daniel Marold, Matthias Berthold, Andrea Baessler, Hannelore Lowel, Hans Werner Hense, Christian Hengstenberg, Stephan Holmer, Heribert Schunkert, Jeanette Erdmann

Research output: Contribution to journalArticlepeer-review

10 Scopus citations

Abstract

The BK (bradykinin) B2 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.

Original languageEnglish
Pages (from-to)505-511
Number of pages7
JournalClinical Science
Volume107
Issue number5
DOIs
StatePublished - Nov 2004
Externally publishedYes

Keywords

  • Bradykinin receptor
  • Genetic association study
  • Myocardial infarction
  • Polymorphism

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