Levels of sCD40, sCD40L, TNFα, and TNF-RI in the culprit coronary artery during myocardial infarction

Abstract

Background: Inflammatory processes are involved in the pathogenesis of coronary artery disease and acute myocardial infarction (AMI). Yet there is little known about concentrations of pro-inflammatory mediators in the cardiac milieu of patients suffering from AMI. The aim of this study was to evaluate blood samples directly obtained from the culprit coronary artery during AMI. Materials and Methods: Serum samples were obtained from the culprit coronary artery of AMI patients (n=39) using a X-sizer thrombectomy system. Sera from patients with stable angina (SA, n=34) and unstable angina (UA, n=37) served as controls. Levels of sCD40, sCD40L, TNFα, and sTNF-RI were determined by enzyme-linked immunosorbent assays. Results: Levels of sCD40L and sCD40 were increased in the AMI group when compared to patients suffering from SA and UA. Levels of both inflammatory markers were highest in the culprit coronary artery. Increased concentrations of TNFα and sTNF-RI evidenced a further inflammatory response at the site of infarction. Conclusions: We conclude that mediators of inflammation are heightened in the coronary blood flow during myocardial infarction. Our observations extend the current knowledge of the inflammatory cascade during myocardial infarction.