Key result
Elective CABG in men with stable coronary artery disease on ASA was associated with significantly increased platelet activation and platelet-leukocyte aggregates up to 3 months postoperatively.
Why the study?
Does elective CABG increase platelet activation and platelet-leukocyte aggregation over time in men with stable CAD on ASA?
Observational (n=54)
Does elective CABG increase platelet activation and platelet-leukocyte aggregation over time in men with stable CAD on ASA?
Elective CABG induces protracted increases in platelet activation and platelet-leukocyte interactions up to three months post-surgery, which may contribute to late thrombotic complications.
Persistent platelet activation post-CABG on ASA should not yet change practice; leaves open whether intensified regimens improve outcomes in stable CAD.
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.
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Ivert et al. (2018) conducted an observational in Stable coronary artery disease (n=54). Elective coronary artery bypass grafting (CABG) vs. Baseline (pre-operative) was evaluated on Platelet activation and platelet-leukocyte interactions. Elective CABG in men with stable coronary artery disease on ASA was associated with significantly increased platelet activation and platelet-leukocyte aggregates up to 3 months postoperatively.
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