The Etiology And Influential Factor Of Myocardial Injury After Elective Percutaneous Coronary Intervention

Objective: The use of Percutaneous Coronary Intervention (PCI) in patients with ischemic coronary artery disease had expanded dramatically over the past two decades. With the evolution of operator experience and equipment design, procedural mortality and the need of emergency coronary artery bypass graft surgery (CABG) was occasional, but postprocedural myocardial injury was still the common complication. Frequent (5.0 to 20.0 percent) elevations in creatine kinase isoenzymes (CK-MB) had been reported. With the more detectable sensibility of myocardial injury, the rate of postprocedural increase of Troponin was between 30% and 40%. There was evidence that postprocedural myocardial injury after PCI was associated with a worse long-term prognosis. Therefore, it was very important to clarify the etiology of postprocedural myocardial injury. However, the etiology of post procedural myocardial injury is still not clear. Side branch occlusion, transient coronary spasm or intimal dissection was reported to be responsible for increased levels of cardiac injury markers. But there were lack of study about the relation of coronarymicroembolization with postprocedure cardiac injury marker increase. During PCI, release of thrombotic material from damaged endothelial cells activated the platelet,induced thrombus formation in the treated lesion；or debris that was washed out of the plaque could not only dislodg into the microcirculation but also activate the platelet to form platelet-rich thrombus in the microcirculation. So myocardial injury could be induced by the plaque debris and the following platelet-rich thrombus. In recent years, with the routine use of platelet inhibitors and thrombin inhibitors and wide-scale availability of stents, the incidence of abrupt vessel closure had decreased to 1％-2％, and there was almost completely no-occlusive thrombus formation in the treated lesion. Therefore, it was clinically significant to recognize the relationship of coronary microembolization and postprocedural myocardial injury. Platelet membrane glycoprotein CD62P and GPⅡb/Ⅲa were the specific markers of platelet activation. D－dimer was one molecular marker of ongoing thrombus and lysis. CK－MB and Cardiac troponin I ( cTnI) were the specific markers of myocardial infraction. The purpose of the present study was to find out the relationship between activated platelet, microthrombus formation and postprocedural myocardial injury by measuring platelet membrane protein CD62P and membrane glycoprotein GPⅡb/Ⅲa,D-dimer,CK-MB and cTnI. Another purpose of this current study was, with theroutine adjunctive drug therapy before and during PCI, whether it was needed or not to strengthen the antiplatelet therapy and anticoagulation therapy. Thirdly, we also tried to evaluate whether the increase of CK－MB and cTnI was the predictor of major adverse cardiac events (MACE) during hospitalization . Methods: 68 patients who underwent PCI were enrolle...