Abstract

Abstract Introduction The protease activated receptor (PAR) 2 is a G protein-coupled receptor and expressed in cardiomyocytes, vascular cells, and leukocytes. Experimental studies demonstrated that PAR2 signaling is associated with adverse cardiac remodeling, heart failure, vascular inflammation and atherosclerosis. Recently, we and others demonstrated that subclinical myocardial damage is associated with cardiovascular mortality in general population. However, the impact of single nucleotide polymorphisms (SNPs) of PAR2 gene on subclinical myocardial damage in general population is unclear. Purpose The aim of this study was to investigate whether SNPs of PAR2 gene is associated with subclinical myocardial damage in general population. Methods The present study included 2,926 apparently healthy subjects (aged ≥40) who participated in a community-based health checkup. We investigated 639 SNPs and measured serum heart-type fatty acid binding protein (H-FABP) as markers of subclinical myocardial damage. Results We found the association of SNPs rs616235 within a PAR2 gene with subclinical myocardial damage. The homozygous A-allele (AA), heterozygous (AG), and homozygous G-allele (GG) carriers of rs616235 were identified in 2084 (71%), 791 (27%), and 51 (2%) subjects, respectively. The prevalence rates of subclinical myocardial damage were 29% in AA carriers, 23% in AG carriers, and 18% in GG carriers. Multivariate logistic analysis showed that the homozygous (AA) of rs616235 was independently associated with subclinical myocardial damage (odds ratio: 1.330, 95% confidence interval: 1.077–1.641, P=0.0080) after adjustment for conventional cardiovascular risk factors. Conclusions Genetic variant of PAR2 gene was independently associated with subclinical myocardial damage in the general population.

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