Evaluation of Hypercoagulable Status after Off-Pump Coronary Artery Bypass Using Platelet-Derived Microparticles

(Department of Cardiovascular Surgery, Obihiro Kousei General Hospital, Obihiro, Japan and Department of Cardiovascular Surgery, Hokkaido University Hospital*, Sapporo, Japan)
Hidetoshi Yamauchi Masamichi Ito Toru Watanabe
Hiroyuki Satoh Yoshiro Matsui*
Thromboembolic events after cardiac surgery, including ischemic strokes, can be devastating complications, however only a few studies manifest the platelet activation and coagulation state after off-pump coronary artery bypass (OPCAB). Platelet-derived microparticles (PMP) are observed as released vesicles from platelets following platelet activation, and are believed to play a role in some clinical diseases because of their procoagulant activity. The aim of the present study was to evaluate the hypercoagulant state after OPCAB using PMP and other indices. Data were obtained from 15 patients (aged 69±7 years; only men) undergoing elective OPCAB surgery. One hundred milligrams of aspirin were used as postoperative antiplatelet drugs. Preoperative risk factors, operation time, postoperative hospital stay, transfusion and blood samples of CBC, PMP, βTG, PF4, platelet aggregation, FDP, D-dimer and TAT of pre- and postoperative days (POD) 3 and 7 were studied. There was no difference between the PMP level with or without risk factor. The PMP levels of POD 3 and 7 were significantly higher compared to the preoperative levels (pre-op, POD 3, 7: 9.1±5.1, 15.2±10.3, 28.4±24.5/104plt respectively, p＜0.05). The levels of FDP, D-dimer and TAT rose significantly on POD 3 and 7 and significantly correlated with the PMP levels. Beta TG, PF4 and platelet aggregation did not change after OPCAB surgery, and no correlation was found with the PMP levels. Elevated levels of PMP, TAT, FDP and D-dimer persisted until POD 7 and suggested not only platelet activation, but also activation of the coagulation and fibrinolytic system. The findings suggest that 100mg of aspirin may not be adequate for the inhibition of platelet activation after OPCAB surgery.
　Jpn. J. Cardiovasc. Surg. 36: 121-126 (2007)