Association analysis of the IL-17F His161Arg polymorphism in myocardial infarction

There is growing evidence that coronary atherosclerosis and its most severe phenotype, myocardial infarction (MI), are chronic inflammatory diseases. Interleukins are important mediators and modulators of inflammation. The His161Arg polymorphism in the gene encoding of IL-17F has recently been consistently found to be associated with chronic inflammatory disorders. In this study, we explored the hypothesis that the variant also affects the risk of MI.

We conducted a case-control association study on a cohort of 513 unrelated MI patients and 477 age-matched and sex-matched controls in a Chinese Han population.

Differences in the genotype distributions and allele frequencies of this polymorphism between cases and controls were insignificant (P = 0.38 and 0.57, respectively). Further stratification for age, sex, the number of diseased coronary arteries, and other cardiovascular risk factors did not affect the negative findings.

This study indicates for the first time that, unlike other chronic inflammatory diseases, the IL-17F His161Arg polymorphism is unlikely to be a major contributor to the pathogenesis of MI.