An average serum sodium level of less than 130 mEq/L during cardiopulmonary bypass is independently associated with an increased risk of postoperative stroke in patients who undergo primary coronary artery bypass grafting.

Acute preoperative plateletpheresis (APP), cell salvage (CS) technique, and the use of aprotinin have been individually reported to be effective in reducing blood loss and blood component transfusion while improving hematological profiles in patients undergoing cardiac surgery with cardiopulmonary bypass (CPB). In this prospective randomized clinical study, the efficacy of these combined approaches on reducing blood loss and transfusion requirements was evaluated. Seventy patients undergoing primary coronary artery bypass grafting (CABG) were randomly divided into four groups: a control group (group I, n = 10) did not receive any of the previously mentioned approaches. An APP and CS group (group II, n = 20) experienced APP in which preoperative platelet-rich plasma was collected and reinfused after reversal of heparin, along with the cell salvage technique throughout surgery. The third group (group III, n = 22) received aprotinin in which 5,000,000 KIU Trasylol was applied during surgery, and a combination group (group IV, n = 18) was treated with all three approaches, i.e., APP, CS, and aprotinin. Compared with group I (896 ± 278 mL), the postoperative total blood loss was significantly reduced in groups II, III, and IV (468 ± 136,388 ± 122,202 ± 81 mL, respectively, p < 0.05). The requirements of packed red blood cells in the three approached groups (153 ± 63,105 ± 178,0 ± 0 mL, respectively) also were reduced when compared with group I (343 ± 118 mL, p < 0.05). In group I, six patients (6/10) received fresh-frozen plasma and three patients (3/10) received platelet transfusion, whereas no patients in the other three groups required fresh-frozen plasma and platelet. In conclusion, both plateletpheresis concomitant with cell salvage and aprotinin contribute to the improvement of postoperative hemostasis, and the combination of these two approaches could minimize postoperative blood loss and requirement.

Platelets play a major role in the thromboembolic diseases and upon vascular injury, especially arterial vascular injury. These platelets rapidly adhere to the exposed subendothelial area, where they become activated by contacting with stimulants. Antiplatelet therapy remains extremely important in treatment and prophylaxis of arterial thromboembolic disorders such as coronary arterial diseases and stroke. The antiplatelet drugs (APDs) are among the most widely used in the world. Based on the molecular targets, APDs are classified as Thromboxane A2 pathway blockers, ADP receptor antagonists, GPIIa/IIIb antagonists, adenosine reuptake inhibitors, phosphodiesterase inhibitors, thrombin receptor inhibitors, and others. Coronary artery bypass graft (CABG) surgery is an important therapeutic approach to treat coronary artery disease. Long-term success after CABG depends on the patency of the bypass vessels. Since platelets play a crucial role in the pathogenesis of thrombosis in the blood vessels, APDs are broadly used to reduce serious cardiovascular events. Platelets also are an integral part of inflammation and APDs have demonstrated to reduce the inflammation mediators in the healthy volunteers and coronary artery disease patients; it will be an interesting topic to determine if platelet inhibition will attenuate CPB-induced systemic inflammatory response syndrome. Due to concerns of post-op bleeding with use of APDs, it is a common practice to withhold APDs prior to surgery; however, recent studies have demonstrated that continuation of APDs prior to surgery (even until the day of surgery) does not increase the risk of post-op bleeding. With extensive use of APDs in cardiovascular thromboembolic events, APD resistance becomes problematic in clinical antiplatelet therapy. Since there is no standardized or universal definition available to quantify APDs resistance, a clinically meaningful definition of APD resistance needs to be developed based on data linking laboratory tests to clinical outcomes in patients.