Platelets and Complement Activation in Coronary Artery Bypass Graft Surgery (CABG)

Patients undergoing coronary artery bypass graft surgery (CABG) frequently exhibit postoperative bleeding complications which are still a major cause for morbidity and mortality. One major contributing factor is the loss of platelets and impaired platelet function. During cardiopulmonary bypass (CPB) blood comes in close contact with foreign surfaces which induces a series of reactions; especially the complement system as part of the innate immunity is highly activated. Due to the strong crosslink between complement system, platelet function and the plasmatic coagulation it is likely that complement activation during CPB has an impact on the overall process of clot formation. Besides the activation of the complement system there is growing evidence that the occurrence of mitochondrial DNA (mtDNA) during CPB might be related to further platelet activation . Activated platelets may enhance micro-thrombosis leading to organ failure and thereby contributing to postoperative morbidity. One major complication during and after CABG surgery is bleeding requiring transfusion and even reoperation in about 2%- 8% of patients. As bleeding complications increase patient morbidity and mortality, this study is designed to investigate the possible mechanisms of platelet loss during CABG. The hypothesis is that increased complement activation during CPB leads to platelet activation and loss of platelets. Further the degree of complement activation and levels of mtDNA might correlate with postoperative bleeding, transfusion requirements and clinical outcome.