血栓弹力图评价经皮冠脉介入治疗患者服用抗血小板药物效果的研究

目的评价采用血栓弹力图观察经皮冠脉介入治疗（PCI）患者服用抗血小板药物后血小板抑制效果。方法选择住院的135例冠心病患者,其中120例接受PCI治疗并联合服用阿司匹林与氯吡格雷的患者作为联合用药组,15例未接受PCI治疗的患者（单独用药组）分别单独服用阿司匹林（阿司匹林组,8例）或氯吡格雷（氯吡格雷组,7例）。采用血栓弹力图检测花生四烯酸（AA）和磷酸腺苷（ADP）途径诱导的血小板抑制率,并比较两组抗血小板治疗的效果。结果阿司匹林组AA途径诱导的血小板抑制率为（61．66±21．44）％,高于氯吡格雷组ADP途径诱导的血小板抑制率[（55．23±13．44）％],但差异无统计学意义（P〉0．05）;联合用药组AA和ADP途径诱导的血小板抑制率分别为（65．52±24．61）％和（58．67±22．75）％,高于阿司匹林组AA途径和氯吡格雷组ADP途径,但差异无统计学意义（P均〉0．05）;联合用药组抗血小板治疗的疗效（良好率）均优于单独应用阿司匹林或氯吡格雷组（40．00％郴12．50％,26．67％ vs 0,P均〈0．01）。结论阿司匹林与氯吡格雷均能起到很好的抗血小板作用,但氯吡格雷稍差,联合服用阿司匹林和氯吡格雷能起到更强的抗血小板作用。血栓弹力图是评价血小板抑制率的有效工具,可根据AA／ADP抑制率的情况发现对阿司匹林和／或氯吡格雷抵抗的患者,进而调整用药方案。     

氯吡格雷对急性冠脉综合征患者阿司匹林抵抗的影响

【目的】研究氯吡格雷对急性冠脉综合征（ACS）阿司匹林抵抗患者的治疗价值。【方法】将79例ACS病人分为两组,阿司匹林组39例,入院后3d内口服阿司匹林300mg／d,后改为100mg／d至两周;联合用药组40例,阿司匹林服用如前,同时加用氯吡格雷75mg／d。于两周时采静脉血,应用比浊法分别测定二磷酸腺苷（ADP）和花生四烯酸（AA）诱导的血小板集聚率。【结果】联合用药组与阿司匹林组相比,两种不同诱导剂诱导的血小板平均集聚率均明显下降（P〈0．05或P〈70．01）,其中以ADP诱导的血小板平均集聚率下降更显著,联合用药组阿司匹林抵抗（AR）与阿司匹林半抵抗（ASR）总发生率较单用阿司匹林组明显为低（P〈0．05）。【结论】氯吡格雷用于ACS可明显减少阿司匹林抵抗,从而减少不良心血管事件的发生。     

Prasugrel hydrochloride for the treatment of acute coronary syndrome patients

Introduction: Dual antiplatelet therapy (DAPT) with aspirin combined with either a thienopyridine (clopidogrel or prasugrel) or acyclopentyl-triazolo-pyrimidine (ticagrelor) plays a vital role in the management of acute coronary syndrome (ACS) especially in those undergoing percutaneous coronary intervention (PCI) but even those being managed medically. Observational studies and some formal studies have shown patients on the standard dual antiplatelet regimen (clopidogrel and aspirin) continue to have further ischemic events and can suffer stent thrombosis. It has been demonstrated that clopidogrel is associated with a delayed onset of action with a considerable inter-individual variation to treatment thus making it difficult to achieve an optimal level of platelet inhibition.

Areas covered: This article will review the current evidence that is available regarding the effectiveness and safety of prasugrel in ACS patients undergoing percutaneous coronary intervention (PCI).

Expert commentary: Prasugrel is an oral third-generation inhibitor of platelet activation and aggregation. Laboratory studies and early phase clinical trials show prasugrel has a faster onset of action, is more potent and has reduced inter-patient response variability compared to clopidogrel. The published studies so far demonstrated that prasugrel when compared to clopidogrel also shows a higher degree of effectiveness in the prevention of platelet-initiated thrombotic events in patients with ACS undergoing PCI, however these benefits are offset somewhat by an increased bleeding risk.     

急性冠状动脉综合征患者介入术后抗血小板药物抵抗的临床研究

目的 探讨急性冠状动脉综合征(ACS)患者经皮冠状动脉介入术(PCI)后阿司匹林和氯吡格雷抵抗的发生率及相关影响因素;根据血栓弹力图(TEG)结果指导ACS患者抗血小板药物的使用.方法 用TEG方法检测ACS患者服用阿司匹林和氯吡格雷的血小板抑制率.比较性别、年龄、吸烟、家族史、使用质子泵抑制剂(PPI)、高血压病、高脂血症、糖尿病等对PCI术后阿司匹林和氯吡格雷抵抗的影响,以及对阿司匹林和氯吡格雷抵抗的预测意义.结果 67例ACS患者中13例(19.4％)存在阿司匹林反应低下,9例(13.4％)患者存在氯吡格雷反应低下,3例(4.5％)同时存在阿司匹林反应低下和氯吡格雷反应低下.血小板药物反应低下者44.0％(11/25)合并糖尿病,血小板药物反应正常者11.9％(5/42)合并糖尿病,两者比较差异有统计学意义(P＜0.05);血小板药物反应正常者女性比例(60.0％)明显高于血小板药物反应低下者(19.1％),两者比较差异有统计学意义(P＜0.05).随着年龄的增长抗血小板药物的反应性会降低(P＜0.05).而两者在吸烟、家族史、使用PPI、合并高血压病、高脂血症比例等方面比较差异无统计学意义(P＞0.05).二分变量线性回归分析结果表明,PCI术后阿司匹林和氯吡格雷抵抗的影响因素包括性别、年龄、糖尿病.结论 对不同性别、年龄的ACS合并糖尿病的患者采用个性化抗血小板治疗,可以减少临床缺血事件的发生.     

血栓弹力图测定老年急性冠脉综合征患者氯吡格雷抵抗的临床观察

【目的】通过血栓弹力图（TEG）分析仪检测血小板聚集率,观察接受标准双联抗血小板治疗的住院老年急性冠脉综合征（ACS）患者的氯吡格雷抵抗发生率及可能的影响因素。【方法】选取109例老年（年龄≥60岁）ACS患者,在常规服用阿司匹林100mg／d基础上,口服氯吡格雷75mg／d,5d以后采血,通过TEG方法测定患者服用氯吡格雷和阿司匹林的血小板聚集率。以二磷酸腺苷诱导的血小板聚集率≥70％为氯吡格雷抵抗,花生四烯酸诱导的血小板聚集率〉50％为阿司匹林抵抗。【结果】氯吡格雷抵抗发生率为31．2％（34例）,有10．1％（11例）发生阿司匹林和氯吡格雷双抵抗。氯吡格雷抵抗组与非抵抗组间阿司匹林抵抗的发生率有非常显著的统计学意义（P〈0．01）。两组患者在年龄、高血压、糖尿病、应用药物等方面差异无统计学意义（P〉0．05）;但氯吡格雷抵抗组中无吸烟史的患者更多,差异具有统计学意义（P=0．045）;此外还观察到女性（P=0．052）患者有容易发生氯吡格雷抵抗的趋势。【结论】接受标准抗血小板治疗的老年ACS患者中,31．2％存在氯吡格雷抵抗现象。这一现象不受年龄、合并疾病、服用药物等影响,而阿司匹林抵抗或从未吸烟的患者更易发生氯吡格雷抵抗。     

The Residual Platelet Aggregation after Deployment of Intracoronary Stent (PREDICT) score.

BACKGROUND: Recent studies suggest a high interindividual variability of response to clopidogrel associated with adverse cardiovascular outcome. Different clinical factors are considered to influence a persistent residual platelet aggregation (RPA) despite conventional antiplatelet therapy. OBJECTIVES: To investigate clinical factors that affect RPA after 600-mg clopidogrel loading in a large unselected cohort of patients with symptomatic CAD. METHODS: The study population included a consecutive cohort of 1,092 patients treated with coronary stenting for stable angina and acute coronary syndromes (ACS). Residual platelet activity was assessed by ADP (20 micromol L(-1))-induced platelet aggregation >or= 6 h after LD. Eleven clinical factors were included in the primary analysis. RESULTS: In multivariate regression analysis increased RPA was significantly influenced by ACS, reduced LV-function, diabetes mellitus, renal failure (creatinine > 1.5 mg dL(-1)), and age > 65 years. In a factor-weighed model the risk for high RPA increased with higher score levels (OR for patients with a score of 1-3, 1.21, 95% CI 0.7-2.1; score 4-6, OR 2.0, 95% CI 1.17-3.5; P = 0.01; score 7-9, OR 3.3, 95% CI 1.8-6.0). During a 30-day follow-up the incidence of major adverse events was higher in patients with RPA in the upper tertile (4.8% vs. 2.5% in the 2nd and 1.5% in the 1st tertile; P < 0.05). CONCLUSIONS: The PREDICT score provides a good tool to estimate residual platelet activity after clopidogrel LD by easily available patient details. Additionally, we demonstrate its association with short-term outcome. Thus, patients with a high score may benefit from intensified antiplatelet therapy by improved platelet inhibition and risk reduction for thromboischemic events.     

Prasugrel in acute coronary syndrome patients undergoing percutaneous coronary intervention

Currently, dual antiplatelet therapy with aspirin and clopidogrel represents the key treatment strategy for the prevention of ischemic events in patients with acute coronary syndrome (ACS) and/or undergoing percutaneous coronary intervention (PCI). However, there is a broad inter-individual response variability to such treatment strategy, and a considerable number of patients persist with inadequate platelet inhibition, which has been associated with an increased risk of ischemic events. Overall, these findings underscore the need for novel antiplatelet agents able to achieve greater platelet inhibition; this can potentially reduce ischemic event rates. Prasugrel (CS-747; LY 640315), a novel third-generation oral thienopyridine, is a specific, irreversible antagonist of the platelet adenosine diphosphate P2Y₁₂ receptor. Laboratory studies have shown prasugrel to be associated with more prompt, potent and predictable degrees of platelet inhibition compared with clopidogrel. In a large-scale clinical study, which was comprised of high-risk ACS patients undergoing PCI, prasugrel was shown to significantly reduce the short- and long-term risk of ischemic events, including stent thrombosis. However, such significant reduction in ischemic events occurred at the expense of a higher risk of bleeding. Recent clinical trial data analyses have led to a better understanding of the efficacy and safety of prasugrel. This article reviews the currently available data regarding the efficacy and safety of prasugrel in ACS patients.     

替格瑞洛治疗氯吡格雷低反应患者的有效性及安全性分析

目的 观察替格瑞洛对氯吡格雷低反应急性冠状动脉综合征(acute coronary syndromes,ACS)患者治疗的有效性及安全性。方法 选择2013年1月至2014年6月应用氯吡格雷75 mg/d治疗的ACS经皮冠状动脉介入治疗(PCI)术后患者493例,用血栓弹力图测定血小板聚集率,根据血小板聚集率筛选出氯吡格雷低反应患者173例,采用数字随机法分为氯吡格雷组(n=87)和替格瑞洛组(n=86)。氯吡格雷组继续服用氯吡格雷(75 mg/d),替格瑞洛组将氯吡格雷替换为替格瑞洛(90 mg,2次/d)。主要终点事件为治疗3天、7天、30天二磷酸腺苷(ADP)诱导的血小板聚集率变化情况,次要终点事件为主要不良心脑血管事件(MACCE)及出血的发生率。结果 替格瑞洛组3天、7天、30天血小板聚集率分别为(56.7±12.5)%、(54.1±12.3)%、(53.2±15.3)%显著低于氯吡格雷组(87.7±14.3)%、(85.4±12.7)、(84.9±10.7)%,差异有统计学意义(P<0.01)。对所有患者随访12个月,替格瑞洛组MACCE及出血的发生率显著低于氯吡格雷组(P<0.05)。而两组出血发生率差异无统计学意义(P＞0.05)。结论 对于经皮冠状动脉介入治疗的氯吡格雷低反应患者接受替格瑞洛治疗后能获得理想的抗血小板效果,且替格瑞洛是有效、安全可信赖的药物。     

Oral antiplatelet agents in ACS: from pharmacology to clinical differences

Antiplatelet agents play an essential role in the treatment of acute coronary syndrome (ACS). Numerous clinical trials have established the value of antiplatelet therapies for ACS. Aspirin (ASA), thienopyridines and GP IIb/IIIa antagonists comprise the major classes of antiplatelet therapies demonstrated to be of benefit in the treatment of ACS. Thienopyridines are a class of drugs that function via inhibition of the adenosine diphosphate (ADP) P2Y12 platelet receptors. Currently, clopidogrel, a second generation thienopyridine, is the main drug of choice and the combination of aspirin and clopidogrel is administered orally for the treatment of ACS. Recently, a third generation of thienopyridines has been introduced represented by prasugrel that has demonstrated promising results in ACS patients treated with percutaneous coronary intervention (PCI). A number of nonthienopyridine oral antiplatelet drugs are under development, and one of them, ticagrelor has already been tested in a major phase III clinical trial, PLATO, with the inclusion of a broad spectrum of patients with ACS. The present review aims to discuss the present knowledge about the safety and efficacy of oral antiplatelet treatment of patients with ACS.     

The future of platelet function testing to guide therapy in clopidogrel low and enhanced responders

Dual oral antiplatelet therapy with aspirin and clopidogrel is the therapy of choice in patients with acute coronary syndromes and in patients undergoing coronary stent placement to lower the risk of thrombotic events. Responsiveness to aspirin and especially to clopidogrel is not uniform and is subject to considerable interindividual variability. Furthermore, there is a broad consensus that clopidogrel low response or so-called high on-treatment platelet reactivity is linked to the occurrence of ischemic events. On the other hand, evidence is accumulating that enhanced clopidogrel responders are at increased risk of bleeding. Newer antiplatelet drugs, such as prasugrel and ticagrelor, are more potent and produce more consistent inhibition of platelet aggregation via the P2Y(12) ADP platelet receptor. A variety of methods of platelet function testing are available for evaluating platelet inhibition in percutaneous coronary intervention-treated patients in order to help determine the individual risk for ischemic and bleeding complications. Although not yet routinely undertaken, platelet function testing offers the potential to tailor antiplatelet therapy for individual patients. Whether alteration of therapy based on platelet function testing improves patients' outcomes remains unclear and is currently under investigation. This article reviews the impact of antiplatelet drug responsiveness on clinical outcomes with a focus on P2Y(12) receptor inhibition as well as on current and future concepts for personalized antiplatelet strategies.     

PCI术前测定血小板表面P-选择素的意义

目的探讨经皮冠状动脉介入(PCI)术前血小板表面P-选择素表达情况及与血小板聚集功能的关系。方法选择拟行PCI的冠心病患者51例,其中ST段抬高急性冠状动脉综合征(STE ACS)9例、非ST段抬高急性冠脉综合征(NSTE ACS)36例、稳定型心绞痛(SA)6例,另设对照组14名。分别采用全血法流式细胞术和光学法血小板聚集仪对各组血小板表面P-选择素和血小板聚集功能进行测定。结果各组间血小板表面P-选择素比较差异有统计学意义(F=16.915,P=0.001),其中STE ACS组明显高于其他组(P<0.05);NSTE ACS组、SA组与对照组比较差异无统计学意义(P>0.05)。血小板表面P-选择素与二磷酸腺苷、花生四烯酸诱导的血小板聚集功能无关(r分别为-0.038、0.165,P>0.05)。结论血小板表面P-选择素高表达与STE ACS相关,血小板P-选择素测定可结合血小板聚集法评价抗血小板治疗后残余血小板活性。     

Unmet needs in oral antiplatelet therapy with ADP receptor blocking agents

Antiplatelet agents like aspirin and clopidogrel are treatment cornerstones for acute coronary syndromes (ACS). Drawbacks of dual therapy with these agents include slow onset and offset of effect and wide response variability. Clopidogrel may provide little benefit if administered too close to percutaneous coronary intervention (PCI) and increase major bleeding risk if given too close to coronary artery bypass grafting (CABG) or other surgery. It may not provide sufficient antiplatelet coverage prior to CABG if stopped too long before intervention and leave patients without antiplatelet coverage due to hyporesponsiveness. Prasugrel has made steps towards addressing these limitations by exhibiting more efficient metabolism, more rapid onset of effect, and greater and more consistent platelet inhibition than clopidogrel. The TRITON-TIMI38 trial in ACS patients undergoing PCI showed prasugrel produced greater ischemic event protection than clopidogrel but significantly increased major bleeding risk. AZD6140, the first reversible oral P2Y₁₂ inhibitor, provides more rapid onset of effect and greater and more consistent platelet inhibition than clopidogrel. In DISPERSE2, a phase II trial in ACS patients, AZD6140 did not increase bleeding risk, reduced bleeding risk among CABG patients, and produced numerical reductions in myocardial infarction risk. AZD6140 is being compared with clopidogrel in PLATO, a phase III trial in approximately 18000 ACS patients.     

Differential impacts of CYP2C19 gene polymorphisms on the antiplatelet effects of clopidogrel and ticlopidine

We examined the influence of CYP2C19 polymorphisms on the antiplatelet effects of clopidogrel and ticlopidine. The platelet aggregation induced by 20 μmol/l adenosine diphosphate (ADP) and CYP2C19 single-nucleotide polymorphisms (*2 and *3) was determined in patients with coronary artery disease (CAD) who were taking aspirin alone (n = 21), aspirin plus clopidogrel (n = 97), or aspirin plus ticlopidine (n = 47). The degree of platelet aggregation in the clopidogrel group, although not in the ticlopidine group, depended on the CYP2C19 polymorphism, and the maximal platelet aggregation in poor metabolizers (PMs) taking clopidogrel was equivalent to that in the group taking aspirin alone. After being switched from clopidogrel to ticlopidine, all seven of the PMs showed markedly lower platelet aggregation. These results suggest that CYP2C19 polymorphisms have a profound impact on the antiplatelet effect of clopidogrel but not on that of ticlopidine. Ticlopidine may be an effective therapeutic option for CYP2C19 PMs.     

经皮冠状动脉介入治疗术后应用泮托拉唑的临床效果观察

目的探讨泮托拉唑对经皮冠状动脉介入治疗(PCI)术后氯吡格雷抗血小板聚集和临床效果的影响。方法选取本院行PCI术的患者共92例,按随机原则将其分为治疗组和对照组,术前与术后均接受氯吡格雷及阿司匹林治疗,治疗组加用泮托拉唑。检测2组患者的血小板聚集率、血常规等指标,术后对患者进行随访。结果治疗组和对照组血小板聚集率分别为(29.93±10.48)%和(26.32±8.53)%,心肌缺血的发生率分别为8.7%和4.3%,2组间比较均无统计学差异,且均未发生严重的心血管以及出血等不良临床事件。结论泮托拉唑不会降低PCI术后氯吡格雷抗血小板聚集作用,不会增加临床心血管事件的发生率,同时能够明显降低消化道出血事件发生率。     

Clopidogrel discontinuation and platelet reactivity following coronary stenting

See also Lordkipanidzé M, Harrison P. Beware of being caught on the rebound. This issue, pp 21–3. Summary. Aims: Antiplatelet therapy with aspirin and clopidogrel is recommended for 1 year after drug‐eluting stent (DES) implantation or myocardial infarction. However, the discontinuation of antiplatelet therapy has become an important issue as recent studies have suggested a clustering of ischemic events within 90 days of clopidogrel withdrawal. The objective of this investigation was to explore the hypothesis that there is a transient ‘rebound’ increase in platelet reactivity within 3 months of clopidogrel discontinuation. Methods and Results: In this prospective study, platelet function was assessed in patients taking aspirin and clopidogrel for at least 1 year following DES implantation. Platelet aggregation was measured using a modification of light transmission aggregometry in response to multiple concentrations of adenosine diphosphate (ADP), epinephrine, arachidonic acid, thrombin receptor activating peptide and collagen. Clopidogrel was stopped and platelet function was reassessed 1 week, 1 month and 3 months later. Thirty‐two patients on dual antiplatelet therapy were recruited. Discontinuation of clopidogrel increased platelet aggregation to all agonists, except arachidonic acid. Platelet aggregation in response to ADP (2.5, 5, 10, and 20 μm ) and epinephrine (5 and 20 μm ) was significantly increased at 1 month compared with 3 months following clopidogrel withdrawal. Thus, a transient period of increased platelet reactivity to both ADP and epinephrine was observed 1 month after clopidogrel discontinuation. Conclusions: This study demonstrates a transient increase in platelet reactivity 1 month after clopidogrel withdrawal. This phenomenon may, in part, explain the known clustering of thrombotic events observed after clopidogrel discontinuation. This observation requires confirmation in larger populations.     

Antiplatelet therapy in acute coronary syndromes: the emergency physician's perspective

The platelet plays a central role in the pathogenesis of coronary thrombosis after atherosclerotic plaque rupture, and its active inhibition forms a cornerstone of the management of acute coronary syndromes (ACS). Early treatment with clopidogrel in addition to aspirin is more effective than aspirin alone in reducing recurrent ischemic events in patients presenting with ACS, and is a useful adjunct to percutaneous coronary intervention, especially with stenting. There is a potential for increased bleeding complications in patients on clopidogrel therapy who subsequently undergo urgent coronary artery bypass graft surgery. Consequently, many emergency physicians withhold clopidogrel treatment until it is clear that urgent coronary artery bypass graft surgery will not be required. The potential untoward effects seem to be minimized by withholding antiplatelet therapy 3-5 days before surgery. Intravenous glycoprotein (GP) IIb/IIIa receptors inhibitors are also particularly useful in patients who undergo percutaneous coronary intervention, and may have some utility in the medical management of patients with high-risk non-ST-segment elevation ACS, starting in the emergency department. For patients presenting to the emergency department with ACS, the benefits and risks of initiating clopidogrel or GP IIb/IIIa inhibitor therapy need to be considered on an individual basis.     

The platelet in diabetes: focus on prevention of ischemic events

Accelerated atherosclerosis and the increased risk of thrombotic vascular events in diabetes may result from dyslipidemia, endothelial dysfunction, platelet hyperreactivity, an impaired fibrinolytic balance, and abnormal blood flow. There is also a correlation between hyperglycemia and cardiovascular (CV) events. The importance of platelets in the atherothrombotic process has led to investigation of using antiplatelet agents to reduce CV risk. A meta-analysis conducted by the Antiplatelet Trialists' Collaboration demonstrated that aspirin reduced the risk of ischemic vascular events as a secondary prevention strategy in numerous high-risk groups, including patients with diabetes. Based on results from placebo-controlled randomized trials, the American Diabetes Association recommends low-dose enteric-coated aspirin as a primary prevention strategy for people with diabetes at high risk for CV events. Clopidogrel is recommended if aspirin allergy is present. There is occasionally a need for an alternative to aspirin or for additive antiplatelet therapy. Aspirin in low doses inhibits thromboxane production by platelets but has little to no effect on other sites of platelet reactivity. Agents such as ticlopidine and clopidogrel inhibit ADP-induced platelet activation, whereas the platelet glycoprotein (Gp) IIb/IIIa complex receptor antagonists block activity at the fibrinogen binding site on the platelet. These agents appear to be useful in acute coronary syndromes (ACSs) in diabetic and nondiabetic patients. A combination of clopidogrel plus aspirin was more effective than placebo plus standard therapy (including aspirin) in reducing a composite CV outcome in patients with unstable angina and non-ST segment elevation myocardial infarction. In a meta-analysis of six trials in diabetic patients with ACSs, intravenous GpIIb-IIIa inhibitors reduced 30-day mortality when compared with control subjects. Results from controlled prospective clinical trials justify the use of enteric-coated low-dose aspirin (81-325 mg) as a primary or secondary prevention strategy in adult diabetic individuals (aged >30 years) at high risk for CV events. Recent studies support the use of clopidogrel in addition to standard therapy, as well as the use of GpIIb-IIIa inhibitors in ACS patients.     

Antiplatelet options for secondary prevention in acute coronary syndromes

Current guidelines recommend dual antiplatelet therapy, a combination of aspirin and a P2Y(12) inhibitor, for 6?12 months after percutaneous coronary intervention with drug-eluting stent implantation in all patients and for 1 year in all patients after an acute coronary syndrome (ACS), irrespective of revascularization strategy. Clopidogrel has a pharmacokinetic and pharmacodynamic profile that results in a delayed and/or subtherapeutic antiplatelet effect, and wide variability in antiplatelet response. New P2Y(12) inhibitors, such as prasugrel and ticagrelor, have favorable pharmacodynamics and clinical efficacy over clopidogrel and offer an alternative antiplatelet treatment strategy in specific patients. Prasugrel has more potent, rapid, and consistent effects on inhibiting ADP-induced platelet aggregation than clopidogrel. Ticagrelor also appears to have more rapid and consistent antiplatelet effects than clopidogrel. The higher levels of antiplatelet inhibition provided by prasugrel and ticagrelor compared with standard-dose clopidogrel result in improved ischemic outcomes in patients with ACS. Despite an increase in bleeding risk, prasugrel and ticagrelor appear to have a better net clinical benefit, especially in higher-risk patients with ACS.     

冠心病患者发生阿司匹林抵抗的有关研究

目的探讨冠心病患者发生阿司匹林抵抗的概率以及相关影响因素方法79名冠心病患者服用阿司匹林（100mg/d）7天以上，分别用ADP和从作诱导剂，检测血小板聚集功能。结果用光学法（广为使用的方法）测定血小板聚集功能，阿司匹林抵抗发生率为11．4％（n=9）。阿司匹林抵抗组高血压患者的比率（44．4％）与阿司匹林敏感组（25．0％）比较有显著差别（P=0．01）。结论对服用阿司匹林的患者要检测其血小板聚集功能。高血压患者易发生阿司匹林抵抗，这提示这类患者要调整抗血小板药物，加大阿司匹林的剂量或换用其他抗血小板药物。     

Long-term care after percutaneous coronary intervention: focus on the role of antiplatelet therapy

Arterial wall injury caused by percutaneous coronary intervention (PCI) triggers transient platelet activation and mural thrombosis; these effects are superimposed on the preexisting platelet hyperreactivity associated with underlying atherothrombosis. Platelet activation has been implicated in the major complications of PCI: acute and subacute thrombosis and restenosis. Antithrombotic and anticoagulant therapy minimizes thrombotic complications after PCI. Aspirin plus a thienopyridine (ticlopidine or clopidogrel) is more effective than aspirin plus heparin and extended warfarin therapy in preventing periprocedural ischemic events and subsequent stent thrombosis and results in less major and minor bleeding. Dual antiplatelet therapy with aspirin and clopidogrel (the preferred thienopyridine because of its superior hematologic safety) is recommended for at least 4 weeks to prevent subacute stent thrombosis with bare-metal stents and 3 to 6 months to prevent late-stent thrombosis with drug-eluting stents. Coronary atherothrombosis is a diffuse vascular disease, and reduction of the risk of future ischemic events requires strategies that extend beyond the focal treatment of stenotic lesions. Optimal long-term care after PCI requires aggressive systemic pharmacotherapy (antiplatelet agents, statins, beta-blockers, and angiotensin-converting enzyme Inhibitors) in conjunction with therapeutic lifestyle changes (smoking cessation, weight reduction, dietary measures, and exercise). In this context, dual antiplatelet therapy (aspirin plus clopidogrel) is recommended for at least 12 months after PCI for prophylaxis of future atherothrombotic events.