Discussion
bleeding, myocardial infarction, unstable coronary artery disease, death, coronary microembolization, myocardial biomarker-negative, coronary microvascular circulation disorder, impaired vasomotion, capillary obstruction, capillary rupture, atherosclerotic, vasospasm, hemorrhage, rupture, platelet aggregation
ACUTE MI, BLEEDING, MYOCARDIAL INFARCTION, VASOSPASM, HEMORRHAGE, PLAQUE, EVENTS
A multicenter, randomized, double-blind, placebo-controlled trial (The ISAR-REACT 3 trial) has shown that although bivalirudin treatment significantly reduced the incidence of in-hospital bleeding, it did not provide a net clinical benefit (defined as the quadruple endpoint of death, myocardial infarction, TVR, or in-hospital major bleeding) at 30 days in myocardial biomarker-negative patients with stable and unstable coronary artery disease undergoing PCI after pre-treatment with 600-mg clopidogrelIn the present study, we found that infusion of a full dose of bivalirudin after ePCI for 4 h exerted a cardioprotective effect, as indicated by significantly reduced levels of cardiac biomarkers (CK-MB and cTnI), even though the incidence of PMI was not markedly decreased compared with bivalirudin use during operation. Furthermore, prolonged use of bivalirudin did not increase the risk of bleeding. It is reported that a post-PCI full dose of bivalirudin (1.75 mg/kg/h for ≤ 4 h) could reduce the incidence of myocardial infarction or major bleeding when compared with no or low-dose post-PCI infusion or heparin in ACS patients with or without ST-segment elevationIn the observational study of Sheikh-Taha et al., using bivalirudin as a bolus followed by infusion for the duration of the intervention did not significantly reduce the incidence of the primary endpoints (a composite of death, acute MI, or an urgent need for TVR during hospitalization) but significantly increased bleeding events in patients undergoing ePCI compared with the bolus only groupDuring plaque rupture resulting from PCI, the coronary arterial endothelial barrier is damaged, and connective tissue elements, atherosclerotic materials, and subendothelial matrix proteins (von Willebrand factor, collagen) are exposed and released into the blood. Platelets adhere to collagen and von Willebrand factor through specific cell receptors (glycoprotein [GP] Ia/IIa, GP Ib-IX, GP VI) and then become activated. Clotting factors, chemotaxins, and activated platelets de-granulate and secrete agonists and vasoconstrictors, which can promote thrombin generation, platelet aggregation, and vasospasm. Eventually, these pathophysiological changes lead to coronary microvascular circulation disorder (capillary obstruction, impaired vasomotion, pletelet-leukocyte aggregation, coronary microembolization, capillary rupture and hemorrhage), which is closely associated with PMI