Platelet transfusion enhances pro‐aggregatory status shortly after coronary artery bypass grafting (CABG) while modulating platelet pro‐inflammatory state 1‐week post‐surgery

Abstract

During coronary artery bypass grafting (CABG), the surgical procedure, particularly the manipulation of the major arteries of the heart, induces a significant inflammatory state that may compromise platelet function to the extent that platelet transfusion is required. Given stored platelets as a major source of biological mediators, this study investigates the effects of platelet transfusion on the major pro‐aggregatory, pro‐inflammatory and immunomodulatory markers of platelets. Platelets from 20 patients, 10 who received platelet transfusion and 10 without, were subjected to flow cytometery where P‐selectin and CD40 ligand (CD40L) expressions and PAC‐1 binding (activation‐specific anti GPIIb/GPIIIa antibody) analysed at five‐time points of 24 h before surgery, immediately, 2 h, 24 h and 1 week after surgery. Analysis of intra‐platelet transforming growth factor‐beta‐1 (TGF‐β1) was also conducted using western blotting. Patients with platelet transfusion showed increased levels of P‐selectin, CD40L and intra‐platelet TGF‐β1 2‐h after surgery compared to those without transfusion (p < 0.05). PAC‐1 binding was increased 24 h after surgery in transfused patients (p < 0.05). Given the significant post‐transfusion elevation of platelet TGF‐β1, P‐sel/CD40L reduction in transfused patients a week after was of much interest. This study showed for the first time the significant effects of platelet transfusion on the pro‐inflammatory, pro‐aggeregatory and immunomodulatory state of platelets in CABG patients, which manifested with immediate, midterm and delayed consequences. While the increased pro‐inflammatory conditions manifested as an immediate effect of platelet transfusion, the pro‐aggregatory circumstances emerged 24 h post‐transfusion. A week after surgery, attenuations of pro‐inflammatory markers of platelets in transfused patients were shown, which might be due to the immunomodulatory effects of TGF‐β1.