替罗非班对急性冠状动脉综合征肝素剂量及血小板的影响

目的探讨替罗非班对急性冠状动脉综合征患者肝素剂量及血小板计数和功能的影响。方法选择因急性冠状动脉综合征入院患者64例,分为常规治疗组36例和替罗非班组28例,常规治疗组使用抗血小板药和肝素抗凝;替罗非班组在上述基础上联合使用替罗非班,以达到肝素抗凝使激活的部分凝血时间延长2倍为标准,比较两组肝素用量、二磷腺苷（ADP）诱导的血小板聚集及血小板数。结果替罗非班组肝素用量（500±120）U／h显著低于常规组（760±148）U／h,差异有统计学意义（t=7.558,P〈0．01）,用药后两组的血小板聚集率均显著低于用药前（P〈0．01）,但替罗非班组降低更显著（P〈0．01）,替罗非班组用药后血小板数降低（P〈0.05）。结论联合应用替罗非班可降低抗凝肝素剂量,显著抑制血小板聚集,并呈降低血小板数的趋势。     

盐酸替罗非班对非ST段抬高急性冠脉综合征患者血小板聚集率、sCD40L水平及预后的影响

目的观察盐酸替罗非班对非ST段抬高急性冠脉综合征（NSTEACS）患者血小板聚集率、sCD40L水平及预后的影响。方法入选60例NSTE-ACS患者,随机分为常规治疗组（n=30）和替罗非班组（n=30）。常规治疗组给予抗凝、抗血小板、调脂等常规药物治疗;替罗非班组在常规治疗的基础上,联合应用盐酸替罗非班持续治疗48 h。在应用替罗非班治疗前、后,分别测定血浆ADP诱导的血小板聚集率、血清sCD40L水平。同时记录两组患者30 d随访期间发生心血管事件情况。结果用药前基线水平时常规治疗组、替罗非班组血小板聚集率分别为（49.88±11.81）%及（47.73±10.31）%,两组差异无统计学意义（P〉0.05）。常规治疗及应用替罗非班48 h后,两组血小板聚集率均有下降,分别为（36.27±15.89）%及（9.04±6.16）%,与基线水平相比均有统计学差异（P〈0.05～0.01）,替罗非班组血小板聚集率下降幅度显著高于常规治疗组。常规治疗组、替罗非班组sCD40L基线水平分别为（1.63±1.04）ng/mL及（1.69±1.16）ng/mL,两组间差异无统计学意义（P〉0.05）。常规治疗及应用替罗非班48 h后,两组sCD40L均有下降,分别为（1.27±1.14）ng/mL及（0.54±0.48）ng/mL,但与基线水平相比,仅替罗非班组具有显著统计学差异（P〈0.01）。两组患者出血不良反应以及30 d再发心血管事件没有统计学差异。结论 NSTE-ACS患者中应用盐酸替罗非班可产生更迅速、有效的抑制血小板聚集及降低sCD40L水平的作用。     

经皮冠状动脉介入术中辅助应用替罗非班的效果观察

目的评价急性冠状动脉综合征(ACS)患者行经皮冠状动脉介入术(PCI)中辅助应用替罗非班的临床疗效和安全性。方法随机选取ACS行PCI治疗的患者119例,根据术中是否应用替罗非班和给药方式分为静脉组(42例,术中替罗非班静脉推注)、联合组(42例,术中替罗非班静脉和冠状动脉内推注)和常规组(35例,术中予常规用药,不给予替罗非班)。观察记录三组患者PCI术后冠脉血流TIMI分级、校正的TIMI帧数(CTFC)、血清肌酸激酶同工酶(CK-MB)水平、左室射血分数(LVEF)和用药前后血清血小板活化标志物膜糖蛋白CD63,CD62p及不良反应发生情况。结果用药后,静脉组和联合组冠状动脉血流TIMI分级明显高于、CTFC及CK-MB和血小板活化标志物明显低于用药前和常规组用药后(P均<0.05),联合组较静脉组改善更明显(P<0.05)。与常规组用药后比较,联合组LVEF增加明显(P<0.05),静脉组与常规组近似(P>0.05)。结论对于行PCI治疗的ACS患者术中宜采用替罗非班静脉联合冠状动脉推注辅助治疗。     

替罗非班在急性心肌梗死患者急诊冠状动脉介入治疗无复流中的应用

目的评价冠状动脉内应用血小板膜糖蛋白(GP)Ⅱb/Ⅲa受体拮抗剂盐酸替罗非班,对急性心肌梗死患者梗死相关动脉行直接PCI后无复流现象的效果及对血小板活化功能的影响。方法选择330例急性心肌梗死患者直接行PCI出现无复流者48例,根据其用药情况分为硝酸甘油组(24例)和替罗非班组(24例)。两组均行冠状动脉造影,分别于术前和术后24 h检测血小板GPⅠb、GPⅡb/Ⅲa、GPⅢa。结果与用药前比较,两组术后均能改善冠状动脉血流,硝酸甘油组患者TIMI血流为(1.61±0.38)级vs(1.85±0.42)级(P<0.05),替罗非班组患者TIMI血流为(1.59±0.40)级vs(2.15±0.65)级(P<0.01)。替罗非班组患者术后24 h血小板GPⅠb、GPⅡh/Ⅲa、GPⅢa较术前明显降低(P<0.01)。结论冠状动脉内应用GPⅡb/Ⅲa受体拮抗剂替罗非班较安全。能更有效改善TIMI血流,并能在一定程度上抑制血小板活化。     

早期应用替罗非班对冠心病PCI术后患者血小板功能的影响

目的探究早期替罗非班应用对经皮冠状动脉介入治疗(PCI)术后的冠状动脉粥样硬化性心脏病(冠心病)患者血小板功能的影响。方法连续入选2016年2月~2017年3月于深圳市第三人民医院行PCI治疗的冠心病患者78例,在PCI术前随机分为替罗非班组和对照组,替罗非班组在术前静脉推注10ug/kg替罗非班,术后继续以0.15 ug/kg/min静脉滴注18 h,术后两组均以氯吡格雷片、阿司匹林肠溶片进行常规抗凝治疗,比较两组治疗前后血小板功能的差异。结果治疗前两组的血小板粘附率、血小板聚集率、最大聚集时间及P选择素浓度无统计学意义(P0.05);治疗后替罗非班组血小板粘附率、血小板聚集率、最大聚集时间及P选择素浓度低于对照组(P0.05)。且两组出血并发症的发生率(17.1%vs.16.2%)无统计学意义(P0.05);治疗组心血管事件包括急性血栓、术中慢血流/无复流及再闭塞的发生率显著低于对照组(P0.05),但两组再发心绞痛的发生率无统计学意义(5.4%vs.17.1%,P0.05)。结论早期推注替罗非班可有效地抑制PCI患者血小板功能,且安全性较高。     

替罗非班应用于急性冠状动脉综合征患者不同时机的安全性和有效性

目的:探讨急性冠状动脉综合征(ACS)患者择期经皮冠状动脉支架置入术前、术中、术后应用国产盐酸替罗非班的疗效和安全性.方法:ACS患者280例,随机分为替罗非班组和对照组,其中替罗非班组分为术前组(68例)、术中组(70例)、术后组(72例).用比浊法测定ADP诱导的血小板聚集率,观察4组术后30 d内主要不良心血管事件(MACE)的发生率;出血并发症及拔管后压迫止血15 min后出血率;术后3 d血小板计数.结果:与对照组比较,替罗非班组30 d内MACE(包括顽固性心绞痛、新发心肌梗死、心源性死亡、再次血运重建)发生率显著降低, 血小板聚集率明显降低(P＜0.05).拔管后压迫止血15 min后出血率术前、术中组较术后、对照组明显增高(P＜0.05).替罗非班组间血小板聚集率差异无统计学意义(P＞0.05).4组出血并发症、术后血小板计数差异无统计学意义(P＞0.05).结论:替罗非班术后应用也能降低血小板聚集率和术后MACE发生率,拔管后压迫止血15 min后出血率下降.     

替罗非班在药物治疗非ST段抬高型心肌梗死中的疗效及安全性观察

对未进行介入治疗的急性非ST段抬高型心肌梗死(NSTEMI)患者,在同时应用抗血小板和抗凝治疗的情况下应用替罗非班治疗,观察其临床疗效和安全性.发现在用药后30 d内,替罗非班组与对照组比较,发生心血管事件的几率显著降低;用药后48 h替罗非班组ST段下降幅度和T波倒置幅度平均值的降幅显著高于对照组.认为在未接受介入治疗的急性NSTEMI患者中联合应用替罗非班、阿司匹林、波立维和克赛可有效降低心血管事件的发生率和改善心肌供血,同时没有增加出血或血小板减少症等并发症.     

复杂冠状动脉病变择期介入治疗中使用替罗非班的临床研究

目的观察在复杂冠状动脉病变患者择期介入治疗中使用替罗非班对患者术后心脏标记物、血小板聚集率和不良心脏事件的影响,探讨其安全性和有效性。方法选择2006年8月至2007年12月首都医科大学附属北京安贞医院收治的676例复杂冠状动脉病变患者分入常规治疗组和替罗非班组。两组患者术前均常规使用阿司匹林和氯吡格雷治疗,替罗非班组患者于术中给予替罗非班并持续至少24h。观察院内实验室检查结果和术后6个月主要不良心脏事件(再发心绞痛、再次血管重建、非致死性心肌梗死、心源性死亡)的发生。结果两组间基线危险无明显差别。术后24h替罗非班组血小板聚集率(12%对41%,P=0.015)、肌钙蛋白I(21%对68%,P=0.033)和CK-MB(14%对52%,P=0.016)均明显低于常规治疗组。随访6个月时,替罗非班组再发性心绞痛(9.3%对14.3%,P=0.046)和不良心脏事件(17.3%对23.6%,P=0.043)的发生低于常规治疗组,再次血管重建、非致死性心肌梗死和心源性死亡的发生无明显差别。替罗非班组血小板数量无明显降低[(238±57)×109/L对(224±46)×109/L,P=0.328]。替罗非班组小出血事件增多(8.2%对3.7%,P=0.024),1例患者出现胃肠道出血事件,无颅内出血事件。结论使用替罗非班可以明显降低血小板聚集率,减少冠状动脉复杂病变介入治疗术后心肌标记物(TnI、CK-MB)的升高,减少患者术后6个月不良心脏事件的发生,且安全性良好。     

替罗非班并依诺肝素对糖尿病伴非ST段抬高急性冠脉综合征的疗效

目的：探讨替罗非班与依诺肝素联合应用对糖尿病合并非ST段抬高急性冠脉综合征（NSTEACS）的有效性和安全性。方法：选择我院2009年3月～2011年3月确诊为糖尿病合并NSTEACS患者90例,随机分为常规治疗组（44例,主要采用阿司匹林、依诺肝素等治疗）;替罗非班组（46例,在常规治疗基础上加用国产替罗非班）。观察48h、30d时主要不良心血管事件（MACE）的发生率,活化部分凝血激酶时间（APTT）、血小板计数变化,以及有无出血等并发症。结果：替罗非班组48h、30d的MACE发生率明显低于常规治疗组（48h：4.3%比20.5%,30d：13.0%比29.5%,P〈0.05）;两组治疗前,治疗后48h、7d时APTT、血小板计数无显著差异（P〉0.05）,两组出血并发症无显著差异（P〉0.05）。结论：替罗非班与依诺肝素联合治疗糖尿病合并非ST段抬高急性冠脉综合征患者是有效和安全的。     

替罗非班联合益气活血化瘀方对冠心病慢性心力衰竭合并2型糖尿病患者经皮冠状动脉介入术后冠状动脉血流参数和血液流变学指标的影响

目的 探讨替罗非班联合益气活血化瘀方对冠心病慢性心力衰竭(CHF)合并2型糖尿病(T2DM)患者经皮冠状动脉介入(PCI)术后冠状动脉血流参数和血液流变学指标的影响。方法 选取行PCI术的160例气滞血瘀型冠心病CHF合并T2DM患者,随机将其分为替罗非班组(n=80)和联合用药组(n=80)。两组均采用常规对症支持联合替罗非班治疗,联合用药组在此基础上加用益气活血化瘀方。比较两组治疗前、治疗14 d后中医证候总积分、冠状动脉血流参数、血管内皮功能和血液流变学指标,以及两组术中、治疗14 d内不良反应的发生情况。结果 治疗14 d后,联合用药组冠状动脉舒张期峰流速、收缩期峰流速、血流速度储备、舒张期速度-时间积分和血清一氧化氮水平均高于替罗非班组,中医证候总积分、全血高切黏度、全血低切黏度、全血红细胞压积与全血纤维蛋白原水平,以及血清内皮素-1水平均低于替罗非班组(均P<0.05);两组术中、治疗14 d内不良反应发生率差异无统计学意义(P>0.05)。结论 替罗非班联合益气活血化瘀方能有效地改善冠心病CHF合并T2DM患者冠状动脉血流情况和血管内皮功能,降低血液黏度,具有...     

不同维持量替罗非班治疗高危不稳定型心绞痛患者的疗效

目的：评价不同维持量替罗非班治疗高危不稳定型心绞痛（UAP）的临床疗效及安全性。方法：41例已给予标化阿司匹林、氯吡格雷抗血小板治疗,低分子肝素抗凝治疗,冠心病常规治疗的高危UAP患者,行急诊冠状动脉造影检查无法进行介入治疗,仍频发心绞痛,按替罗非班维持剂量随机分为半剂量组（21例）和常规剂量组（20例）,两组均给予负荷剂量替罗非班,维持剂量持续应用48h。结果：两组总有效率均为100%,与治疗前比较,两组心电图ST段下移幅度均有明显减小[常规剂量组：（1.52±0.72）mm比（0.71±0.54）mm,半剂量组：（1.49±0.81）mm比（0.69±0.72）mm,P均〈0.01],半剂量组的不良反应（轻度出血）的发生率明显低于常规剂量组（14.3%比20.0%,P〈0.05）。结论：常规或半维持剂量替罗非班治疗高危不稳定型心绞痛,均可进一步缓解心绞痛症状和改善心电图,但半剂量组不良反应较常规剂量组显著减少。     

Effect of tirofiban on C-reactive protein in non-ST-elevation myocardial infarction

Objectives

C-reactive protein (CRP) is a prototypic marker of inflammation. The effect of tirofiban on CRP levels in patients with non-ST-elevation myocardial infarction (NSTEMI) was investigated.

Methods

The present study was prospective and randomized. Patients with NSTEMI received aspirin, clopidogrel, statin, and unfractionated heparin. Patients with NSTEMI were enrolled into either the tirofiban + heparin group (group 1: n = 25) or the heparin group (group 2: n = 32). Levels of CRP were determined at baseline and after 48 and 72 hours. Heparin and tirofiban were discontinued after 48 hours.

Results

Levels CRP of were similar in two groups at baseline; they increased significantly at 48 hours and 72 hours in the control group but not in the tirofiban group. The differences on and after treatment were statistically significant. In group 1, CRP elevation was attenuated after tirofiban infusion compared with group 2.

Conclusions

Products of platelet activation may aid neutrophil accumulation and enhance inflammation. Activated leukocytes and platelets potentate each others' effects. Tirofiban strongly inhibits the platelet aggregation. The decreased platelet aggregation can suppress the inflammatory protein, chemokine, and adhesion molecule expression. After the tirofiban infusion, CRP elevation was atteunated in patients with NSTEMI.     

替罗非班对急性冠脉综合征经皮冠状动脉介入术后无复流现象的影响

目的观察盐酸替罗非班对急性冠脉综合征（ACS）患者经皮冠状动脉介入术（PCI）后无复流现象的影响。方法纳入ACS患者行PCI治疗术后无复流患者72例,随机分为替罗非班组36例和对照组36例。对照组经冠状动脉给予硝普钠0.9μg/kg,替罗非班组经冠状动脉给予盐酸替罗非班负荷剂量10μg/kg,3min内注完,随后以0.15μg/（kg·min）微量泵持续静脉泵入24h。观察两组患者冠脉给药前、给药后20min靶血管前向血流的TIMI血流分级、心电图改变及术后2周内主要不良心脏事件及药物的不良反应。结果冠状动脉内给药20min后造影显示,两组患者梗死相关动脉TIMI血流分级均较给药前有改善,替罗非班组IRA的TIMI血流0级、1级发生率显著低于对照组,TIMI血流3级发生率显著高于对照组,差异均有统计学意义（P〈0.01）;冠状动脉给药2h后与给药前比较,对照组心电图改善不明显,而替罗非班组患者心电图获得显著改善,两组冠脉给药2h后ST抬高及压低程度、缺血损伤导联数差异均有显著统计学意义（P〈0.01）;术后2周内替罗非班组主要不良心脏事件显著低于对照组（P〈0.01）;术后2周内两组不良反应的发生率差异无统计学意义（P〉0.05）。结论经冠状动脉给予盐酸替罗非班治疗可有效地改善ACS患者术后无复流现象,并减少术后2周内主要不良心脏事件。     

小剂量替罗非班治疗高原非ST段抬高型急性冠脉综合征的临床观察

目的:观察小剂量替罗非班治疗高原非ST段抬高型急性冠脉综合征(NSTE-ACS)患者的疗效及安全性。方法: 将75例NSTE-ACS患者随机分为对照组(n=37)和观察组(n=38)。两组均常规使用阿司匹林、氯吡格雷、低分子肝素等药物治疗,观察组加用小剂量替罗非班［负荷量0.3 μg/（kg·min）×30 min,维持量0.05 μg/（kg·min）×72 h］微量泵静脉泵入。检测治疗前后血小板计数和血小板聚集率;观察30 d内心血管事件和出血事件的发生率。结果: 对照组30 d内心血管事件的发生率为22%,观察组为5%,两组间有显著差异(P<0.05);对照组30 d内出血事件的发生率为5%,观察组为8%,两组间无显著差异;对照组血小板聚集率治疗前后无显著变化,观察组治疗后血小板聚集率显著降低(P<0.05)。两组患者中均未观察到血小板减少的发生。结论: 小剂量替罗非班联合阿司匹林、氯吡格雷和低分子肝素治疗高原NSTE-ACS是安全和有效的。     

替罗非班对急性冠脉综合征伴糖尿病患者介入术后心肌灌注及心肌损伤的影响

目的探讨替罗非班对急性冠脉综合征（ACS）伴糖尿病（DM）患者冠状动脉介入（PCI）术后心肌灌注及及心肌损伤的影响。方法选择ACs合并DM患者92例,随机分为两组,对照组（n=45）应用阿司匹林、氯吡格雷、低分子肝素钙抗凝等常规治疗;替罗非班组（n=47）在常规治疗基础上加用替罗非班。观察两组患者冠脉内注药20min后梗死相关动脉（IRA）的TIMI及心肌灌注血流分级,术后8h、12h、24h的心肌肌钙蛋白T（cTnT）、超敏C反应蛋白（hs—CRP）,主要不良心血管事件及出血发生率。结果术后8h、12h、24h替罗非班组的cTnT、hs—CRP均显著低于对照组（P〈O．05或P〈0．01）。冠脉内注药后20min行冠脉造影,替罗非班组IRA的TIMI及心肌灌注血流分级均显著优于对照组（P〈0．05）。替罗非班组心血管事件发生率显著低于对照组（P〈0．05）;术后30d内两组出血并发症的发生率差异无统计学意义（P〉0．05）。结论在常规抗凝基础上合用盐酸替罗非班治疗ACS合并糖尿病患者,可明显改善心肌灌注,减少心肌损伤．减少心血管事件。     

Comparison of enoxaparin versus heparin during elective percutaneous coronary intervention performed with either eptifibatide or tirofiban (the ACTION Trial)

Limited data are available with regard to the pharmacodynamics and safety of combining enoxaparin with glycoprotein IIb/IIIa inhibition during elective percutaneous coronary interventions (PCIs). We randomized 200 patients to receive open-label enoxaparin (0.75 mg/kg intravenous bolus) or unfractionated heparin (60 U/kg intravenous bolus) and eptifibatide or tirofiban during PCI. This yielded 4 groups of combination therapy (50 patients/group). The first 10 patients per group had anti-Xa activity and inhibition of platelet aggregation measured at baseline, and at 5 minutes, 10 minutes, 4 hours, and 24 hours. All patients received aspirin and clopidogrel therapy before PCI. Patients who received enoxaparin and heparin achieved therapeutic peak anti-Xa activity observed shortly after drug administration. At 4 hours, a differential anticoagulant effect was observed, with patients who received enoxaparin having a more gradual decrease in anti-Xa activity. Patients who received eptifibatide achieved >80% inhibition of platelet aggregation soon after initiation of therapy more often than did those who received tirofiban. Type of heparin did not affect inhibition of platelet aggregation. Compared with patients who received heparin, periprocedural myocardial infarction and bleeding events occurred less frequently among those who received enoxaparin (14% vs 8% and 10% vs 5%); however, these differences were not statistically significant. Three cases of intraprocedural thrombus occurred among patients who received enoxaparin. Two patients received concomitant tirofiban therapy. Compared with unfractionated heparin, similar levels of anticoagulation and platelet inhibition are achieved with enoxaparin when concomitant therapy with eptifibatide or tirofiban is used during elective PCI, without an observed increase in early bleeding events or periprocedural ischemic complications.     

Combination therapy with tirofiban and enoxaparin in acute coronary syndromes

BACKGROUND: Tirofiban, an intravenous glycoprotein IIb/IIIa antagonist, and enoxaparin, a low molecular weight heparin, have each been shown to be effective at reducing cardiac ischemic events compared to unfractionated heparin alone in separate trials of patients with unstable angina and non-Q-wave myocardial infarction. The combination of these agents may offer further therapeutic benefit. MATERIALS AND METHODS: Fifty-five patients with non-Q-wave myocardial infarction were randomized to receive double-blind treatment with tirofiban (0.1 microgram/kg/min i.v.) for 48-108 h coadministered with either enoxaparin (1 mg/kg sc q 12 h) (n=26) or unfractionated heparin (i.v. adjusted to activated partial-thromboplastin time) (n=27) to evaluate pharmacokinetics, pharmacodynamics, and safety. The primary objective of the study was to investigate the effect of unfractionated heparin versus enoxaparin on the plasma clearance of tirofiban. RESULTS: Coadministration of tirofiban and enoxaparin was generally well tolerated. Plasma clearance of tirofiban was 176.7+/-59.8 and 187.5+/-81.8 ml/min, respectively, for enoxaparin and unfractionated heparin-treated patients (P=NS). The mean difference was well within the prespecified criterion for comparability. Administration of tirofiban with enoxaparin vs. unfractionated heparin resulted in lesser variability and a trend towards greater inhibition of platelet aggregation using 5 microM adenosine phosphate agonist. More patients achieved target inhibition of platelet aggregation >70% in the tirofiban and enoxaparin group (84% vs. 65%, P=0.19). Median bleeding time was 21 min for tirofiban and enoxaparin vs. > or =30 min for tirofiban and unfractionated heparin (P=NS). For a given level of inhibition of platelet aggregation, bleeding time was less prolonged with tirofiban and enoxaparin than tirofiban and unfractionated heparin (adjusted mean bleeding time 19.6 vs. 24.9 min, P=0.02). Tirofiban plasma concentration and clearance were comparable whether coadministered with enoxaparin or unfractionated heparin. There were no major or minor bleeding events in either group by the TIMI criteria. INTERPRETATION: The more consistent inhibition of platelet aggregation and lower adjusted bleeding time of tirofiban and enoxaparin vs. tirofiban and unfractionated heparin support the therapeutic potential of combining these two agents. These data from the first clinical report of coadministration of a glycoprotein IIb/IIIa receptor antagonist and a low molecular weight heparin are consistent with prior data which show differential pharmacodynamic effects of enoxaparin and unfractionated heparin on platelet aggregation.     

Safety and Feasibility of a Novel Dosing Regimen of Tirofiban Administered in Patients with Acute Myocardial Infarction with ST Elevation Before Primary Coronary Angioplasty: A Pilot Study

BACKGROUND: Intravenous glycoprotein GP IIb/IIIa receptor antagonists administered to patients with acute coronary syndromes limit platelet-dependent thrombus formation and vasoconstriction and lower the complication rate of PCI. The efficacy of glycoprotein IIb/IIIa inhibitors critically depends on appropriate suppression of platelet aggregation. A growing body of evidence indicates that regimen of tirofiban used in several recent trials may be suboptimal. We investigated if a novel regimen of dosage of tirofiban administered to patients with acute myocardial infarction with ST elevation (STEMI) before primary angioplasty is safe, feasible and whether such treatment improves coronary flow in infarct-related artery. METHODS: It was an open-label, non-randomized, prospective observational study. 253 consecutive patients with STEMI, qualified to PCI were included. 104 of patients (group 1) received heparin plus tirofiban at a novel regimen (10 microg/kg bolus, followed by 0.4 microg/kg/min for 30 min and then 0.1 microg/kg/min for 12-24 hours) and the remaining 149 of the patients (group 2) received a standard dose of heparin prior to PCI. Bleeding complications were recorded. The primary end point of the study was combined TIMI 1 + 2 + 3 grade flow at the time of first contrast medium injection during angiography for primary PCI. RESULTS: Heparin was administered 50.3 +/- 58.1 minutes (group 1) or 62.3 +/- 67.3 minutes (group 2) ( p = 0.205). Tirofiban was administered for an average of 14.5 +/- 14.4 minutes before TIMI assessment (group 1). In patients treated with heparin + tirofiban the rate of combined TIMI 1 + 2 + 3 coronary flow was higher (38.4% vs. 24.8%, p = 0.020) as compared to patients treated with heparin alone. The difference in the rate of TIMI > or = 2 coronary blood flow between the groups 1 and 2 (24.0% vs. 20.1%) has not reached statistical significance ( p = 0.459). At the same time the significant difference in the rate of TIMI 1 coronary blood flow between the groups 1 and 2 was noted (14.4 vs. 4.7%, p = 0.007). In hospital mortality in the groups 1 and 2 was similar (5.3 vs. 4.8%, p = 0.838). Significant difference was noted between the groups 1 and 2 with regard to minor bleeding complications (17.3 vs. 8.7%, p = 0.041). CONCLUSION: In patients undergoing primary angioplasty for acute myocardial infarction the novel regimen of tirofiban is well tolerated and feasible, and is associated with improvement in coronary blood flow in the infarct related artery. Larger studies assessing the effects of tirofiban on clinical outcomes of patients with AMI undergoing primary angioplasty seem worthwhile.