Abstract
Abstract Aims Junctional adhesion molecule A (JAM-A/F11R) is a cell adhesion molecule. Membrane associated JAM-A mediates platelet aggregation, secretion, adhesion, and spreading. Plasma levels of JAM-A are elevated in hypertension and atherosclerosis. This study was designed to investigate the impact of JAM-A single nucleotide polymorphisms (SNPs) on circulatory JAM-A levels and prognosis in patients with symptomatic coronary artery disease (CAD). Methods and results JAM-A SNP analysis (JAM-A F11R rs2774276 and rs790056) was performed in 943 patients with symptomatic CAD. All patients were tracked for all-cause death (ACD), myocardial infarction (MI), and ischemic stroke (IS) for 1080 days. The primary combined endpoint (CE) was defined as a composite of ACD and/or MI and/or IS. Secondary endpoints were defined as the single events of ACD and MI. Homozygote carriers of the minor allele (F11R rs2774276 and rs790056) showed significantly worse event-free survival for MI when compared with major allele carriers (Log rank = 0.011 and log rank = 0.031, respectively). No significant differences could be shown for the CE and ACD. Of note, in multivariate analysis, both SNPs were significantly and independently associated with MI. Furthermore, serum levels of soluble JAM-A were elevated in homozygote carriers of minor allele when compared to major allele carriers. Finally, serum levels of soluble JAM-A were significantly elevated in patients with MI when compared to stable CAD (p=0.036). Figure 1 Conclusion JAM-A SNPs are associated with prognosis in patients with symptomatic coronary artery disease. Furthermore, JAM-A SNPs might influence serum concentration of soluble JAM-A. Finally, serum concentration of soluble JAM-A is higher in patients with myocardial infarction when compared to stable coronary artery disease. These findings suggest JAM-A as a valuable biomarker for risk stratification and tailoring therapies in patients with coronary artery disease. Acknowledgement/Funding DFG-KFO274, CRC/Transregio 240
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