Increased platelet reactivity and platelet–leukocyte aggregation after elective coronary bypass surgery

Abstract

Inflammatory mechanisms are activated, and thrombotic complications occur during the initial months after coronary artery bypass grafting (CABG). Therefore, changes over time of platelet activation and platelet-leukocyte interactions after CABG are of interest. Whole-blood flow cytometry was performed before, and 4-6 days, one month, and three months after elective CABG in 54 men with stable coronary artery disease treated with acetylsalicylic acid (ASA). Single platelets and platelet-leukocyte aggregates (PLAs) among monocytes (P-Mon), neutrophils (P-Neu), and lymphocytes (P-Lym) were studied without and with stimulation by submaximal concentrations of ADP, thrombin, and the thromboxane analog U46619. White blood cell counts were increased during the initial postoperative course, and platelet counts were increased after one month. Platelet P-selectin expression was significantly enhanced at one month when stimulated by thrombin and U46619 and at three months with ADP and thrombin. All PLAs subtypes were increased at one month without stimulation in vitro. P-Mon and P-Neu stimulated by ADP, thrombin, or U46619 were significantly increased one month after the operation but decreased compared to baseline at three months. Agonist stimulated P-Lyms were increased at one month and remained increased at three months after ADP stimulation. There was significant platelet activation and formation of PLAs unstimulated and after agonist stimulation by ADP, thrombin, and a thromboxane analog after CABG in patients with stable coronary artery disease irrespective of ASA treatment. Changes observed up to three months after CABG support further studies of the clinical implications of protracted increases in platelet activation and platelet-leukocyte interactions.

Effect of the expression of CD62P and thrombin generation on patients using central venous catheters for hemodialysis

“…2 The results revealed that P-selectin expression was significantly increased (P < .005) from 1 to 3 months. 3 This finding strongly suggests that the contact of medical devices with blood can continuously increase platelet reactivity. Thus, activated platelets may contribute to the increased risk of thrombus formation due to the insertion of medical devices such as CVCs.…”

“…Another study investigated platelet activation by evaluating CD62P after 4‐6 days, 1 and 3 months of myocardial revascularization surgery . The results revealed that P‐selectin expression was significantly increased ( P < .005) from 1 to 3 months . This finding strongly suggests that the contact of medical devices with blood can continuously increase platelet reactivity.…”

“…Thrombus formation in blood-contacting medical devices is a common cause of morbidity and mortality. [1][2][3] Thrombosis is initiated by the platelet-coagulation interplay, and is the precipitating event in 30%-40% of central venous catheter (CVC) malfunctions and is responsible for up to two-thirds of CVC failures. 1 The coagulation system can be triggered by the intrinsic or extrinsic pathway.…”

“…1 The coagulation system can be triggered by the intrinsic or extrinsic pathway. [2][3][4] Contact between factor XII and the CVC surface can stimulate the intrinsic pathway, while the extrinsic pathway can be stimulated by contact between CVCs and the subendothelial layer of the vein. [3][4][5] This latter pathway occurs when the endothelium is injured, allowing plasma factor VIIa to form a complex with the tissue factor (TF) of the exposed subendothelial layer.…”

“…[2][3][4] Contact between factor XII and the CVC surface can stimulate the intrinsic pathway, while the extrinsic pathway can be stimulated by contact between CVCs and the subendothelial layer of the vein. [3][4][5] This latter pathway occurs when the endothelium is injured, allowing plasma factor VIIa to form a complex with the tissue factor (TF) of the exposed subendothelial layer. 5 Activation of the coagulation system leads to platelet activation and the expression of glycoprotein complexes such as integrin αIIbβ3 (CD41a) or P-selectin (CD62P), which in turn regulate coagulation reactions that lead to thrombin generation (TG).…”