Observational Study of Platelet Dysfunction Assessed by Thromboelastography in Cardiovascular Surgery (DISPLATEG)

Overview

Perioperative bleeding requiring blood transfusion is common during cardiovascular surgery, especially in procedures requiring cardiopulmonary bypass. Adenosine diphosphate (ADP) plays a fundamental role in platelet function. Several studies have shown that some patients not receiving antiplatelet therapy undergoing cardiovascular surgery have decreased platelet ADP receptor activity; the prevalence of this condition can be as high as 36%. Furthermore, extracorporeal circulation itself has been shown to cause a reduction in platelet function. Platelet dysfunction due to reduced platelet receptor activity after cardiac surgery is potentially a common cause of bleeding, perioperative blood transfusion, and surgical reexploration in patients not receiving antiplatelet agents. However, these studies are conducted with few patients and present some contradictory results, so the evidence is still scarce. The study hypothesis is that preoperative platelet dysfunction for ADP measured by TEG® Platelet Mapping™ is associated with a higher incidence of moderate-severe bleeding after CPB in patients undergoing cardiovascular surgery.

Perioperative bleeding requiring blood transfusion is common during cardiovascular surgery, especially in procedures requiring cardiopulmonary bypass. Cardiac surgery is one of the groups that uses the most blood products, with 20% to 40% of patients requiring transfusions for routine procedures. Various publications have shown that these types of procedures consume between 10% and 15% of the blood supply in Western countries. The etiology of bleeding and coagulopathy is generally multifactorial and may result from hemodilution, surgical losses, residual effects of anticoagulant and antiplatelet drugs, activation of tissue factor in the extrinsic system, contact activation of the intrinsic system in components of the extracorporeal circulation (ECC) circuit, and the presence of residual heparin after CPB. This process can lead to hyperfibrinolysis, reduced platelet count and function, decreased fibrinogen concentration, and depletion of coagulation factors, culminating in impaired thrombin generation. Surgical trauma and the CPB circuit itself produce an increase in inflammatory cytokines, interleukins, and tumor necrosis factor, which in turn contribute to increased release and activation of coagulation factors, as well as dysregulated fibrinolysis. Adenosine diphosphate (ADP) plays a fundamental role in platelet function. When secreted from the platelet-dense granules where it is stored, it amplifies platelet responses induced by other platelet agonists and stabilizes platelet aggregates. Several studies have shown that some patients not receiving antiplatelet therapy undergoing cardiovascular surgery have decreased platelet ADP receptor activity; the prevalence of this condition can be as high as 36%. In healthy blood donors, an average reduction in this activity of 18% has been shown, as measured by TEG® Platelet Mapping™ (Haemoscope Corporation, Niles, Illinois, USA) (0-58%). Furthermore, extracorporeal circulation itself has been shown to cause a reduction in platelet function, as measured by both the TEG® Platelet Mapping™ technique and aggregometry (Multiplate®). Platelet dysfunction due to reduced platelet receptor activity after cardiac surgery is potentially a common cause of bleeding, perioperative blood transfusion, and surgical reexploration in both patients not receiving antiplatelet agents and those treated with clopidogrel. However, these studies were conducted with small numbers of patients and presented some contradictory results, so the evidence is still scarce.