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ǥ : ǥ ȣ - 550541   101 
Effect of Glycoprotein IIb/IIIa Antagonist on the Levels of Circulating Microparticles in Patients with Acute Myocardial Infarction Treated by Primary Angioplasty
연세의대 강남세브란스병원 심장내과¹ 심혈관제품유효성평가센터² 차의과학대학교³
민필기¹ , 이다령² 홍성유² 김종윤¹ 최의영¹ 윤영원¹ 이병권¹ 홍범기¹ 임세중¹ 정광회³ 권혁문¹
Backgrounds Recently, it has been reported that high levels of procoagulant microparticles (MPs) are present in the circulating blood of patients with acute myocardial infarction (AMI). In this study, we evaluated the effect of PCI with or without glycoprotein (Gp) IIb/IIIa inhibitor on the level of procoagulant MPs in patients with AMI who underwent primary PCI. Methods In this study, we studied 86 patients with AMI (72 men, age 58 ± 13) who underwent primary PCI. The decision to administer the GpIIb/IIIa inhibitor just before PCI was left to the discretion of the physician based on clinical and angiographic findings. Blood samples for analysis of MPs were obtained from the femoral artery before and after PCI. MPs were isolated by capture with annexin A5 and determined their procoagulant potential with a prothrombinase assay using commercial kit. The cell origins of MPs were determined by antigenic capture with specific antibodies. Results Procoagulant MPs captured onto annexin A5 were not changed significantly after PCI (13.4 ± 13.2 vs. 13.2 ± 16.1 nM phosphatidylserine equivalent, P=0.875). However, endothelial derived CD146+ MPs were significantly reduced after PCI by 48% (P=0.020). GpIIb/IIIa inhibitor was used in 30 of 86 patients (35%) just before PCI. Between the two groups, no differences were observed in clinical and angiographic findings. In patients who underwent PCI without GpIIb/IIIa inhibitor, no significant change in the level of MPs was observed after PCI, regardless of their cellular origins. However, in GpIIb/IIIa group, pre-intervention CD31+ MPs and CD42b+ MPs were significantly reduced after PCI by 53% and 70%, respectively (P=0.027). Conclusion PCI with GpIIb/IIIa inhibitor significantly reduced procoagulant MPs of endothelial and platelet origin in patients with AMI.


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