ObjectiveTo evaluate effects of glyeoprotein II b/IIIa receptor blockade with tirofiban (intraeoronary artery and vein injection) on myocardial blush perfusion recovery, cardiac function and clinical outcome in patients with acute myocardial infarctionMethods66 patients, that got emergency PCI in the Red Cross Hospital of Guangzhou from Oct 2008 to Jan 2010, were divided randomly into 2 groups (tirofiban vein application group,n=30; tirofiban coronary artery and vein application joint group, n=36).The joint group patients in the emergency department (or outpatient) that were diagnosed as ST-elevation myocardial infarction (STEMI) were accepted tirofiban intravenous 10ug/Kg, in 1 to 3mins before PCI, then at 0.15 ug/Kg. min intravenous drip. Tirofiban were injected intracoronary lOug/Kg when godet or balloon got to the vascular occlusion and infarct related artery (IRA) where blood emerged, then maintain the intravenous drip speed, tirofiban was used for 36 hours totally. The vein group patients were treated as the joint group patients without tirofiban application intracoronary. The postoperative IRA TIMI grade, myocardial perfusion TMP grade and electrocardiogram ST-segment variations 2 hours in the 2 groups patients after PCI; NT-pro BNP,CK—MB,Hs—CRP and cTnT levels were detected after PCI 6 hours and 24 hours; cardiac ejection fraction (LVEF) and left ventricular end-diastolic dimension (LVEDD) were detected by ultrasonic cardiogram (UCG) 1 week after PCI; major cardiovascular events (MACE) were observed in hospital and the next 1 month out of hospital; the bleeding and thrombocytopenia were compared in 2 group patients.Results1. The ratio of IRA TIMI 3 and TMPG 3 in joint group patients were significantly higher than the venous group patients. ST-segment restore in patients after PCI 2 hours in joint group were apparently more than that in vein group; in joint group patients, postoperative CK-MB, cTnT peak appeared ahead; LVEF and LVEDD in joint group patients were superior than that in the vein group; There was no statistical significant difference of NT-pro BNP between 2 groups after PCI 6 hours and 24 hours, but the significant difference may be observed in a long time; There was no statistical significant difference of Hs—CRP between 2 groups after PCI 6 hours and 24 hours.2. There was no significant difference of the MACE (Heart Failure, MI, target-vessel revascularizations and death) incidence in hospital and the next 1 month out of hospital between the 2 groups, but the total MACE ratio in joint group patients was lower than that in vein group patients.3. There was no significant difference in mild bleeding and serious bleeding complications between the 2 groups.Conclusions1. The myocardial injury markers cTnT and CK-MB peak appeared ahead in the STEMI patients treated with tirofiban lOug/Kg intravenous and intracoronarylOug/Kg followed with tirofiban at 0.15 ug/Kg.min in intravenous drip for 36 hours accepted emergency PCI2. The treatment of the STEMI patients treated with tirofiban lOug/Kg intravenous and intracoronarylOug/Kg followed with tirofiban at 0.15 ug/Kg.min intravenous drip for 36 hours accepted emergency PCI was safe and effective. Compared to the treatment without tirofiban intracoronary application, it can improve the level of myocardial reperfusion.3. The LVEF and LVEDD 1 week later were improved in patients treated with tirofibanlOug/Kg intravenous and intracoronary lOug/Kg followed with tirofiban at 0.15 ug/Kg.min intravenous drip for 36 hours accepted emergency PCI; the advantage of NT-pro BNP in patients treated with the above treatment may be observed in a long time.4. The total MACE incidence in the patients treated with tirofiban intravenous and intracoronary application was lower than that in tirofiban intravenous application alone.5. Compared to the vein group patients, the treatment of the STEMI patients treated with tirofibanlOug/Kg intravenous and intracoronarylOug/Kg followed with tirofiban at 0.15 ug/Kg.min intravenous drip for 36 hours accepted emergency PCI resulted in no more apparent reduction of the Hs—CRP.
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