硝酸甘油在不稳定性心绞痛及急性心肌梗塞中的抗血小板聚集作用…

硝酸甘油在不稳定性心绞痛及急性心肌梗塞中的抗血小板聚集作用（摘要）杨杰孚邢宝利许晓东潘洁陈爱萍郑天林近年的国外研究发现，硝酸甘油还具有抗血小板聚集作用。本研究探讨国人冠心病不稳定型心绞痛及急性心肌梗塞静脉滴入小剂量的硝酸甘油的抗血小板聚集效应。一、研...     

二硝酸异山梨醇酯对冠心病患者血小板聚集功能的影响

本文就二硝本酸异山梨醇酯(ISDN)体内外给药对冠心病患者血小板聚集功能的影响作了探讨.然果表明,以5mg/h速度静滴ISDN对患者血压、心率均无明显影响,但可明显抑制血小板聚集功能,此可为应用ISDN治疗冠心病提供新的理论依据.体外应用ISDN亦可使患者血小板聚集功能受抑,但所需ISDN量远较体内用量大,推测此体内外作用差别与ISDN体内外释放一氧化氮不同有关.     

小剂量乌拉地尔与硝酸甘油注射液治疗重度心力衰竭短期临床疗效的对比观察

目的 :观察经静脉小剂量乌拉地尔与硝酸甘油注射液治疗重度心力衰竭短期临床疗效。方法 :重度心力衰竭患者 30例 ,NYHA心功能均Ⅳ级。被随机分为乌拉地尔组 15例 ,硝酸甘油组 15例。两组心率、血压无显著性差异。在心力衰竭处理 (吸氧、利尿剂、洋地黄 )同时 ,两组分别持续静脉使用乌拉地尔 10 0 μg/min或硝酸甘油 2 0 μg/min 2 4h ,期间暂不用其他血管扩张剂。用药前、后检查心率、血压、血气分析、超声心动图。结果 :两组患者用药后心率、舒张期血压和血气分析参数均无显著性差异 ;硝酸甘油组患者用药后 2h、6h收缩期血压减低较明显 ,收缩功能指标射血分数明显增大、舒张功能指标二尖瓣血流E峰减速时间明显延长 ,与用药前比较均有显著性差异 (P <0 0 5～ 0 0 1)。乌拉地尔组患者用药后超声心动图收缩功能指标每搏输出量、射血分数均明显增大、主动脉瓣最大血流速度明显增快 ,与用药前比较均有显著性差异 (P <0 0 5～ 0 0 1)。结论 :小剂量静脉泵入乌拉地尔可有效用于重度心力衰竭短期治疗 ,能明显改善心力衰竭患者心脏收缩功能 ,同时患者耐受性好 ,较为安全     

硝酸甘油治疗冠心病抗血小板聚集耐药性观察

硝酸甘油治疗冠心病抗血小板聚集耐药性观察德州市立医院（２５３０１２）李世军近来发现，硝酸甘油除扩张血管外，还有抗血小板聚集作用，但连续用药后此作用减弱或消失，即产生了耐药性。对此，我们进行了临床观察，现报告如下。资料与方法：本组男１２例，女６例；年龄...     

高龄冠心病患者双联抗血小板长期治疗的安全性

虽然介入治疗在冠心病治疗中占重要位置,但在多方面因素作用下,我国仍有绝大部分高龄冠心病患者采用保守治疗控制病情.血小板活化、聚集、血栓形成是冠状动脉闭塞的中心病理环节[1],因此抗血小板聚集治疗是冠心病的主要用药之一,但高龄患者往往是出血高危人群[2],长期双联抗血小板治疗时两种药物剂量如何选择,安全性如何?国内外循证医学方面证据不多.本研究拟回顾性分析高龄冠心病患者单用阿司匹林及阿司匹林+小剂量氯吡格雷双联抗血小板的安全比较,为高龄冠心病患者安全有效的抗血小板聚集治疗提供依据.     

阿司匹林抑制老年冠心病患者血小板聚集的疗效观察

目的:观察阿司匹林治疗老年冠心病患者24周对血小板聚集功能的影响。方法:选择临床需要服用阿司匹林抗血小板治疗,且ADP诱导的血小板聚集率增高的老年冠心病患者122例,给予阿司匹林100mg口服24周。用药前及用药6、12、24周后分别测定血小板聚集率。结果:服用阿司匹林后,患者的血小板聚集率显著降低,6、12、24周测定血小板聚集率与基线比较均差异有统计学意义(均P<0.01),血小板聚集抑制率分别为-(21.13±21.66)%,-(29.25±21.67)%,-(22.87±21.92)%。12周的血小板聚集率较6周进一步下降,但24周较12周则明显升高,两个差值均差异有统计学意义(均P<0.05)。结论:阿司匹林可明显降低患者的血小板聚集功能,但抗血小板聚集作用在24周后较12周有明显下降。     

西洛他唑对老年冠心病不稳定心绞痛患者血小板功能的影响

目的探讨西洛他唑对老年冠心病不稳定心绞痛患者血小板聚集功能及蛋白激酶B(PKB)的活性变化。方法老年冠心病不稳定心绞痛(UAP)患者48例,随机分2组,即西洛他唑(cilostazol,CS)组和阿斯匹林(aspirine,AS)组;26例健康老年人作对照组(NC组)。UAP组在常规抗凝治疗的同时给予抗血小板治疗,即CS组给予CS100mg口服;AS组给予AS300mg口服。于用药前10min及用药后35h、6h、24h测定血小板聚集率、血小板PKB的活性变化。结果所有老年UAP患者血小板最大聚集率均较NC组明显增加(P<001);胞膜PKB表达较对照组明显增高(P<001);而胞浆PKB表达则显著降低(P<001)。口服CS、AS后6h血小板最大聚集率较用药前降低最明显(P<001),但24h时CS对血小板聚集仍有较强的抑制作用,而AS已不明显。口服CS6h后UAP组患者血小板胞膜PKB活性较用药前明显下降(P<001);而胞浆PKB表达则已明显升高。AS组二指标虽有所变化,但用药前后比较无显著差异。结论老年UAP患者体内血小板处于活化状态,CS能有效抑制血小板活化,作用优于AS,为抗血小板治疗提供新的理论基础。     

曲美他嗪治疗冠心病合并糖尿病疗效评价

将96例冠心病(CHD)伴糖尿病患者随机分成两组,对照组给予常规口服药物,治疗组在此基础上加用曲美他嗪(TMZ).比较两组治疗前后心绞痛发作频率、发作持续时间、含化硝酸甘油量、心率、血压、平板运动耐量指标.结果 治疗组治疗后心绞痛发作次数与硝酸甘油用量减少,心绞痛发作持续时间缩短,平板运动耐量提高,疗效明显优于对照组(P＜0.05或＜0.01).两组治疗前后心率和血压均无明显改变,无药物相关性不良反应发生.认为冠心病伴糖尿病患者在常规药物治疗的基础上加用TMZ可显著提高心肌收缩和舒张功能,具有明显的心脏保护作用.     

小剂量尿激酶治疗无ST段抬高的急性冠脉综合征疗效观察

目的:探讨在充分抗凝及抗血小板基础上应用小剂量尿激酶治疗无ST段抬高的急性冠脉综合征(ACS)的疗效。方法:对于入院确诊为无ST段抬高的ACS患者按随机数字表分为A、B两组。B组为常规抗凝组:低分子肝素钙5000IU,皮下注射,1次/12h,共1周,阿斯匹林0.3g,口服,1次/d,10天后改为100mg,1次/d,长期服用。A组为尿激酶治疗组:尿激酶50万IU30分钟静脉滴入,连用2天,每次尿激酶均在上述药物应用2小时滴入。其余治疗同B组。结果:A组48小时内胸痛完全消失率93.55％,3月内心脏事件复发率6.45％,与B组48h胸痛完全消失率63.49％,3月内心脏事件复发率23.81％相比有显著性差异(分别为P<0.01,P<0.01)。而二组轻度出血发生率无显著性差异(P>0.05)。结论:在充分抗凝及抗血小板基础上加用小剂量尿激酶,治疗无ST段抬高的ACS疗效优于常规抗凝治疗。     

择期行CABG术患者中抗血小板药物对血小板聚集率的影响

目的：探讨择期行冠状动脉旁路移植手术(Coronary artery bypass graft,CABG)的冠心病(Coronary artery diseas,CAD)患者停用阿司匹林和氯吡格雷后,抗血小板药物作用持续时间。方法： 24例经冠状动脉造影(Coronary arteriography,CAG)提示需行CABG术的冠心病患者,连续口服100 mg肠溶阿司匹林和75mg氯吡格雷一周,观察停药后1,2,3,4,5,6,7,9天血小板聚集率的变化。采用光学血小板聚集仪(light transmission aggregometer, LTA)测定花生四烯酸诱导的血小板聚集率(arachidonic acid induced platelet aggregation, PL-AA)和二磷酸腺苷诱导的血小板聚集率(adenosine diphosphate induced platelet aggregation,PL-ADP)。结果：停药后第一天AA诱导的血小板聚集抑制效应最强(5.4±1.6%),血小板功能在停药后第四天恢复至正常水平(76.6±4.0%);停药后第一天ADP诱导的血小板聚集抑制效应最强(29.5±12.1%),在停药后第七天恢复至正常水平(69.7±3.5%)。结论：冠心病患者口服100mg阿司匹林和75mg氯吡格雷一周后,停药后AA诱导的血小板聚集功能第四天恢复至正常;ADP诱导的血小板聚集功能在第七天恢复至正常。     

Antianginal effects of intravenous nitroglycerin over 24 hours

To determine the constancy of hemodynamic and antianginal effects of the constant infusion of intravenous nitroglycerin (NTG) and their relationship to infusion rate and plasma NTG concentration, we administered maximal tolerated doses of intravenous NTG (range 10 to 120 micrograms/min, mean = 52 +/- 33 micrograms/min) and placebo to 10 patients with chronic stable angina for 25 hr each in a randomized, double-blind fashion. Sublingual NTG (0.4 mg) was given at 24.5 hr of infusion as a positive control. Bicycle exercise time (NIH protocol), blood pressure, heart rate, exercise ST response, and venous plasma NTG were determined before and at 1, 4, 8, 24, and 24.5 hr. Plasma NTG was linearly related to infusion rate, reached a steady state within 15 min and was unchanged over 24 hr (mean = 5.5 +/- 1.2 ng/ml). Mean plasma NTG clearance was 9.3 liters/min. However, during dose titration, patients demonstrated different relationships between plasma NTG and hemodynamic effects, with widely varying slopes and intercepts. Intravenous NTG produced a sustained reduction in blood pressure and a rise in heart rate at rest, and a reduction in blood pressure during submaximal exercise at as late as 24 hr, associated with reduced submaximal ST segment abnormality. In contrast, exercise tolerance to onset of angina showed a marked initial increase on intravenous NTG but fell progressively and did not differ from that with placebo at 24 hr. Increased exercise tolerance was associated with an increase in maximal heart rate and double product (heart rate X blood pressure), suggesting that direct coronary vasodilation and/or reduced left ventricular volume were the principal determinants of increased exercise tolerance.(ABSTRACT TRUNCATED AT 250 WORDS)     

Combined use of nitroglycerin and N-acetylcysteine in the management of unstable angina pectoris

The vasodilator effects of nitroglycerin (NTG) are mediated via activation of guanylate cyclase; this process is believed to require the availability of free sulfhydryl groups. Previous studies in man have shown that the sulfhydryl donor N-acetylcysteine (NAC) potentiates the systemic and coronary vasodilator effects of NTG. Furthermore, interaction of NTG and NAC may lead to the formation of S-nitroso-NAC, which strongly inhibits platelet aggregation. The effects of intravenous NTG combined with intravenous NAC (5 g 6 hourly) were compared with those of intravenous NTG alone in a double-blind trial in 46 patients with severe unstable angina pectoris unresponsive to conventional treatment, which included calcium antagonists and cutaneous nitrates in all but one patient. Treatment with NTG/NAC (24 patients) and that with NTG alone (22 patients) was associated with a similar frequency of episodes of chest pain and of increments in NTG infusion rate for pain control (10 vs 17; p = NS). The NTG/NAC group had a significantly lower incidence of acute myocardial infarction than the NTG/placebo group (three vs 10 patients; p = .013). Symptomatic hypotension occurred frequently in the NTG/NAC group (seven vs 0 patients; p = .006). Lactate-pyruvate ratios and venous NTG concentrations were not significantly affected by NAC. Subsequently, another 20 consecutive patients were treated with intravenous NTG and continuously infused NAC (10 g/day). Seven remained pain free during the first 24 hr of NTG infusion; 11 required increments in NTG infusion rate for pain control. Acute myocardial infarction occurred in one patient, while none developed symptomatic hypotension.(ABSTRACT TRUNCATED AT 250 WORDS)     

Nitroglycerin rebound associated with vascular, rather than platelet, hypersensitivity

OBJECTIVES

The purpose of this study was to determine whether acute withdrawal of nitroglycerin (NTG) during hemodynamic tolerance is associated with platelet hypersensitivity.

BACKGROUND

Nitroglycerin is an effective antianginal medication but its use is limited by the development of tolerance and rebound. We have previously demonstrated a sustained inhibition of platelet function during continued use of NTG, but whether cessation of NTG is associated with an increase in platelet function that may contribute to rebound is unknown.

METHODS

Normal porcine aortic media were exposed to flowing arterial blood from pigs (n = 8) treated continuously with NTG patches (Nitrodur 0.8 mg/h) for 48 h. Platelet function, blood pressure and the responses to angiotensin II infusion were evaluated before, during and after NTG treatment.

RESULTS

Mean arterial pressure fell by 15% after 3 h of treatment compared with control, returned to baseline by 48 h and increased significantly 2 h after drug removal. Autologous ⁵¹Cr-labelled platelet deposition on the aortic media was reduced by 30% after 48 h of continuous NTG administration compared with baseline (p = 0.02) and remained decreased 2 h after cessation of NTG therapy. Platelet aggregation to thrombin decreased in parallel to the decrease in platelet deposition. Blood pressure increase after intravenous injection of 10 μg of angiotensin II was blunted during treatment with NTG but increased significantly 2 h after cessation of nitrate therapy when compared with baseline.

CONCLUSIONS

Supersensitivity of the vessel wall to vasoconstrictors such as angiotensin 11, but not platelet hyperactivity, may contribute to the rebound phenomenon after acute nitrate withdrawal.     

急性脑梗死静脉溶栓/桥接治疗24 h内血小板活化的研究进展

急性脑梗死目前最理想的治疗是尽快使闭塞的血管再通,静脉溶栓治疗是急性脑梗死确证有效的开通闭塞动脉的急救措施,桥接治疗提高了闭塞血管的再通机率,但仍有一部分患者存在残余血管狭窄。已知血小板在急性脑梗死的发生和发展中起着重要作用。溶栓/桥接治疗后导致血管再通后再闭塞的关键因素之一是溶栓后24 h内禁止抗血小板聚集药物的使用,血小板的聚集与活化使一部分残余动脉狭窄患者发生了动脉再闭塞。本文针对血小板活化机制及近年来关于急性脑梗死静脉溶栓/桥接治疗后血小板活化状态及抗血小板治疗联合静脉溶栓/桥接治疗的研究进行综述,以探讨在静脉溶栓/桥接治疗后24 h内使用抗血小板聚集药物的可行性及安全性,从而改善患者的预后。     

Development of tolerance in continuous nitroglycerin infusion

For treatment of unstable angina pectoris or recent myocardial infarction, intravenous NTG is frequently employed, beginning with doses of 3 mg/h or more; thereafter, dependent on the clinical course, in particular, if the blood pressure is lowered notably, the dose may be reduced to 1 or 2 mg/h. Reports published in recent years have documented to the development of tolerance to nitrates when given orally in higher doses three times daily or administered by the transdermal mode. Accordingly, we suspected that tolerance development would be the inevitable outcome during a continuous intravenous infusion of NTG. Consequently, this placebo-controlled study was undertaken to determine whether tolerance develops during a continuous 28-hour infusion of NTG and whether tolerance is reversible on interruption of the treatment with a twelve-hour infusion-free interval. The studies were performed in ten male patients ranging in age from 49 to 65 years, mean age 53 years. All patients had recovered from myocardial infarction (mean interval since infarction 42 days) and had reproducible, asymptomatic ST-segment depression of at least 0.2 mV during exercise testing after discontinuation of all antiischemic drugs with a washout period of three days. Exercise testing was performed at four hours after beginning the infusion of 1.5 mg/h NTG or placebo (2 p.m.), at 28 hours after beginning the infusion (2 p.m. on the second day) and, after having discontinued the infusion for a twelve-hour period (from 10 p.m. to 10 a.m.), at four hours after having re-started the infusion (2 p.m. on the third day).(ABSTRACT TRUNCATED AT 250 WORDS)     

Timing of anti-platelet effect after oral aspirin administration in patients with sympathetic excitement.

Aspirin is used in percutaneous coronary interventions (PCI) for acute myocardial infarction (AMI) to prevent thrombosis. It is reported that the aspirin concentration in blood reaches its peak approximately 20 min after oral administration in healthy volunteers, but the absorption and bioavailability of aspirin in AMI may be quite different. In the present study patients undergoing coronary angiogram for the first time were enrolled as a model of sympathetic excitement and the timing of the antiplatelet effect after oral aspirin administration was investigated. Aspirin (162 mg) was administered to the patients in a catheter laboratory. Platelet count, aspirin concentration, and platelet aggregation were measured at scheduled timepoints before and up to 120 min. Ticlopidine was administered in the same procedure, and platelet count and platelet aggregation were evaluated at 0 and 120 min. There was no significant change in the platelet count. Aspirin concentration in blood had not reached its peak by 120 min. Platelet aggregation induced by collagen or ADP began to be inhibited 45 min after aspirin administration. No significant inhibition of platelet aggregation was observed up to 120 min following ticlopidine administration. During sympathetic excitement, aspirin absorption and its antiplatelet effect were significantly delayed in these patients. Ticlopidine did not show any antiplatelet effect by 120 min. For PCI performed in a patient with a high level of sympathetic excitement, aspirin should be administered at least 45 min before the first balloon dilatation.     

替罗非班在支架辅助栓塞颅内动脉瘤中的初步应用

目的评价替罗非班在支架辅助栓塞治疗颅内动脉瘤时的效果和安全性。方法 2010年1月—2011年12月,采用支架辅助弹簧圈栓塞或单纯行载瘤动脉内支架置入治疗颅内宽颈动脉瘤42例（46个动脉瘤）。在成功置入支架后,应用替罗非班（8～10μg/kg,静脉推注,3～5 min,继而以0.1～0.15μg.kg-1.min-1持续泵入24 h,然后降为0.05～0.07μg.kg-1.min-1,持续泵入24～48 h）行抗血小板聚集治疗。术后次日逐渐过渡到常规剂量口服阿司匹林和氯吡格雷。对其临床资料进行回顾性分析。结果①46个动脉瘤中,破裂动脉瘤18个,未破裂动脉瘤28个;在支架辅助下用弹簧圈栓塞40个,单纯行载瘤动脉内支架置入6个。术中出现支架内血栓形成3例,均经导引导管动脉内注射替罗非班（150～250μg,3～5 min）后恢复再通;术中微导丝穿破动脉瘤1个,为次全栓塞动脉瘤,术后患者苏醒,但2h后突发脑疝死亡。②本组34例患者血小板计数在术前、术后3 d的平均值分别为（150±53）×109/L和（142±43）×109/L（t=1.738,P=0.092）;部分活化凝血酶时间（APTT）在术前、术后3 d的平均值分别为（25±6）s和（26±4）s（t=-1.087,P=0.285）,差异均无统计学意义。有41例患者在术后48～72 h成功过渡到口服抗血小板聚集药物。在应用替罗非班期间无出血并发症、出血倾向及脑血栓、短暂性脑缺血发作等。结论选择性使用替罗非班,对支架辅助栓塞颅内动脉瘤的患者,较为便捷、有效;但对动脉瘤出血急性期患者应用时需慎重,其安全性有待进一步观察。     

Effects of intravenous atrial natriuretic peptide and nitroglycerin on coronary vasodilation and flow velocity determined using 3 T magnetic resonance imaging in patients with nonischemic heart failure

Although atrial natriuretic peptide (ANP) is widely used in patients with congestive heart failure (CHF), little is known about its effect on epicardial coronary arteries. Magnetic resonance imaging (MRI) enables precise measurement of coronary vasodilation and flow velocity. In this study, we examined the changes in epicardial coronary artery size and flow velocity in response to intravenous infusion of ANP or nitroglycerin (NTG) by using 3 T MRI in patients with CHF. The study cohort contained a total of 14 subjects: 8 patients with CHF and 6 healthy volunteers as controls, randomly divided into two groups: the ANP group (0.03 μg/kg/min) and the NTG group (0.3 μg/kg/min). Cross-sectional MR angiography and phase-contrast flow velocity of the right coronary artery in the same in-plane slice were obtained at the baseline, during drug infusion, and at two subsequent time points after stopping drug infusion. A significant increase was observed in the coronary cross-sectional area at 15 min after drug infusion in both groups compared with that at baseline; however, a late peak was observed at 15 min after stopping infusion in the ANP group. No significant differences were detected in the flow velocity in both groups. Furthermore, although NTG increased the heart rate, this change was not found in the ANP group. Coronary vasodilation and flow velocity can be measured simultaneously using 3 T MRI. Using this method, we showed that the effects of ANP on the coronary artery vasodilation and flow velocity were not inferior to those of NTG, with no significant alteration in heart rate.     

Prolonged fenoldopam infusions in patients with mild to moderate hypertension: Pharmacodynamic and pharmacokinetic effects

Thirty-three patients with mild-to-moderate essential hypertension received either placebo or fenoldopam, a selective dopamine-1 agonist, by intravenous infusion at a fixed infusion rate ranging from 0.1 to 0.8 μg/kg/min for 48 h during a double-blind, placebo-controlled, randomized inpatient clinical trial. Blood pressure and heart rate were measured every 15 min for 24 h before, during, and 24 h after the 48-h drug infusion. Plasma concentrations of racemic fenoldopam were measured at frequent intervals during and for 24 h after fenoldopam infusion.In the 26 patients who received fenoldopam, there were dose-dependent reductions in systolic and diastolic blood pressure, which usually reached a nadir within 2 h of beginning infusion and were significant even at the lowest dose studied (−9 and −9 mm Hg for systolic and diastolic blood pressure, respectively, at 24 h for the dose of 0.04 μg/kg/min, P < .05). There were associated increases in heart rate that were greater in the first than in the last 24 h of drug infusion. Compared to the average 24-h control blood pressure, maximum mean reductions in systolic and diastolic blood pressures of 33 and 21 mm Hg, respectively, were noted in patients receiving fenoldopam at 0.8 μg/kg/min and occurred 4 and 1 h, respectively, after beginning infusion. Tolerance to the blood pressure lowering effects of the drug developed slowly during the 48 h of drug infusion; the half-life for this effect was 60 h. No serious adverse clinical effects were noted in any patient.These results demonstrate that fenoldopam is effective in reducing blood pressure of patients with mild-to-moderate hypertension at doses as low as 0.04 μg/kg/min, is well tolerated at doses up to 0.8 μg/kg/min, maintains most of its antihypertensive efficacy throughout 48 h of continuous, constant rate infusion, and produces neither prolonged pharmacodynamic effects nor rebound hypertension when discontinued. The pharmacodynamic effects of the drug are best predicted by pharmacokinetics of racemic and R-fenoldopam.     

Pharmacodynamic and clinical trials of glycoprotein IIb/IIIa inhibitors and potential relationship of results to dosing

Glycoprotein IIb/IIIa inhibitors have become the standard of care for patients undergoing percutaneous coronary intervention (PCI) and for those presenting with non-ST-segment elevation myocardial infarction (NSTE-ACS). Clinical effects of GP IIb/IIIa inhibitors in PCI and NSTE-ACS strongly correlate with potency, consistency, and durability of platelet aggregation inhibition. Under standardized conditions [light transmission aggregometry (LTA), 20 micromol adenosine diphosphate (ADP) as an agonist, and D-phenylalanyl-L-propyl-L-arginine chloromethyl ketone (PPACK) as an anticoagulant], we demand consistent platelet aggregation inhibition >80% during the time of PCI (initial balloon inflation), and during the entire duration of therapy in NSTE-ACS. The benefit of abciximab (bolus 0.25 mg/kg plus infusion 10 microg/kg/min) correlates with >80% inhibition of platelet aggregation during the intervention (PCI) and immediately thereafter (<6 hours). The absence of a benefit with abciximab in NSTE-ACS is most likely due to <80% inhibition during the major part of the infusion period (>6 hours). Tirofiban does not achieve >80% inhibition at the time of PCI at a dose of 10 microg/kg bolus plus 0.15 microg/kg/min infusion, and at a dose of 0.4 lg/kg/min loading infusion for 30 minutes plus 0.1 microg/kg/min maintenance infusion, the target value is only reached after 18 h. Eptifibatide (double-bolus 180 microg/kg 10 min apart, followed immediately by a 2.0 microg/kg/min infusion) provided an instant, consistent, and durable antiplatelet effect for the entire duration of infusion, and a significant clinical benefit in both PCI (non-ACS patients) and medically managed NSTE-ACS patients.