急性冠脉综合征抗血小板治疗进展

急性冠脉综合征(acute coronary syndrome,ACS)是由于局部血管炎症、内皮功能不良、血管痉挛、血流剪切力等因素造成的不稳定斑块(易损斑块)的纤维帽破裂,激活血小板进而引起冠状动脉内血栓形成所致心肌缺血的一组进展性疾病谱,包括不稳定性心绞痛(UA)、非ST段抬高性心肌梗死(NSTEMI),ST段抬高性心肌梗死(STEMI).从上述特点可以看出,ACS发病的核心病理基础是冠状动脉内血栓形成,其中血小板活化是血栓形成的关键和始动因素.     

急性冠脉综合征的抗血小板治疗

急性冠状动脉综合征（ACS）包括不稳定性心绞痛（UA）、非ST抬高的心肌梗死（NSTEMI）和ST抬高的心肌梗死（STEMI）。动脉粥样硬化斑块破裂后,随之触发的血小板激活和凝血酶形成,最终导致血栓形成是ACS主要发病机制。     

抗血小板药物在治疗急性冠脉综合征中的作用

抗血小板治疗是对抗血小板粘附,聚集,是抗心肌缺血治疗中的一个重要内容。本文简述抗血小板药物在治疗急性冠脉综合征中的作用。1 血小板粘附、聚集在急性冠脉综合征发病机制中的作用 急性冠脉综合证是指冠状动脉内血流量急剧减少引起的一系列临床情况,主要包括不稳定型心绞痛,Q波型心肌梗死和非     

血小板功能检测指导急性冠脉综合征抗血小板治疗的研究

目的探索血小板功能检测在未行血运重建术治疗的急性冠脉综合征(ACS)患者中抗血小板治疗的临床应用价值。方法 60例ACS患者根据血小板功能分为四组予相应的个体化抗血小板治疗,并随访1年,比较四组患者血栓/出血事件发生率。结果高剂量氯吡格雷治疗组及加用西洛他唑治疗组血小板聚集率比标准治疗组明显下降(P<0.05),但四组患者主要心血管事件发生率及出血率无统计学差异(P>0.05)。结论血小板功能检测在指导急性冠脉综合征患者抗血小板治疗中未获得预期临床获益,其应用价值仍需大规模、前瞻性及更严谨的研究去验证。     

急性冠脉综合征双重抗血小板联用质子泵抑制剂150例临床观察

目的：探讨急性冠脉综合征双重抗血小板联用质子泵抑制剂的临床效果。方法：选择近年因急性冠脉综合征在笔者所在医院治疗的患者150例,根据治疗方法的不同分为治疗组和对照组。结果：治疗组患者只有1例发生胃肠道事件,占1．3％,明显低于对照组4．0以3／75）,差异有统计学意义（P〈0．05）;治疗组患者3例发生心血管事件,占4．O％,明显低于对照组9．3％（7／60）,差异有统计学意义（P〈0．05）。结论：急性冠脉综合征患者应用双重抗血小板联用质子泵抑制剂治疗,在不增加心血管终点事件发生率的同时,能够减少胃肠道终点事件的发生率。     

急性冠脉综合征药物治疗进展

在急性冠状动脉综合征的治疗进展中，目前广泛使用阿司匹林、氯吡格雷和低分子肝素联合应用血小板糖蛋白Ⅱb／Ⅲa受体抑制剂、倍他乐克、ACEI制剂、硝酸酯类等，笔者对其在急性冠状动脉综合征治疗中的作用作一阐述。     

靶向性护理对增强急性冠脉综合征患者双联抗血小板治疗依从性的评价

目的 探讨科学的靶向性护理措施对增强急性冠脉综合征（ACS）患者双联抗血小板药物使用依从性的临床护理效果。方法 将本院治疗的ACS患者120例依据随机原则分为研究组60例（予以靶向性护理措施）和对照组60例（予以常规护理措施）。疗程均为9个月,应用改良Morisky服药依从量表及服药依从性影响因素问卷评分评估依从性。比较两组焦虑程度及生活质量。结果 与对照组相比,研究组的药物依从性的比例与评分显著较高（P<0.05）,生活质量评分以及心理焦虑程度显著改善（P<0.05）。结论 靶向性护理能够有效地增强ACS患者双联抗血小板药物服药依从性,缓解焦虑情绪,提高患者生活质量。     

幽门螺杆菌根除治疗对急性冠脉综合征上消化道出血的疗效

目的探讨幽门螺杆菌感染对急性冠脉综合征患者抗血小板治疗后上消化道出血的影响。方法选择自2014年1月-2018年1月在天津市第五中心医院接受治疗的急性冠脉综合征患者392例,其中幽门螺杆菌感染阳性患者260例,幽门螺杆菌感染阴性患者132例为阴性组,阳性患者选择进行幽门螺杆菌根除治疗的患者165例为试验组,未进行幽门螺杆菌根除治疗的患者95例为对照组。392例患者均使用氯吡格雷联合阿司匹林进行抗血小板治疗。患者在治疗后1年进行电话随访或来院复诊时随访,观察三组患者的血红蛋白(Hemoglobin,Hb)表达水平、血浆凝血酶原时间(Prothrombin time,PT)、血肌酐(Serum creatinine, Scr)水平、谷丙转氨酶(Alanine aminotransferase,ALT)水平和幽门螺杆菌感染阳性转阴性情况;同时记录患者治疗1年后临床症状发生及预后情况。结果对照组患者的上消化道出血、贫血和黑便症状较试验组患者和阴性组患者重(P<0.05);对照组患者的Hb表达水平为(118.51±4.53)g/L,低于试验组患者(131.75±4.96)g/L和阴性组患者(132.06±5.22)g/L(P<0.05);试验组患者治疗后1年幽门螺杆菌感染阳性转阴性患者135例,感染消除率达到了81.8%,而对照组未出现幽门螺杆菌感染阳性转阴性患者(P<0.05);对照组复发心绞痛和消化道不适不良事件发生例数多于试验组和阴性组患者(P<0.05)。结论幽门螺杆菌感染根除治疗能够改善急性冠脉综合征患者抗血小板治疗后上消化道出血情况和贫血情况,减少心脏、消化道不良事件的发生率,改善患者预后。     

非ST段抬高急性冠脉综合征的治疗进展

非ST段抬高急性冠脉综合征（ ACS）包括不稳定性心绞痛（ UAP）和非ST段抬高心肌梗死（ NSTEMI）,是由不稳定性动脉粥样硬化斑块梗死相关动脉导致的急性心脏病,它属于不完全闭塞型冠状动脉血栓栓塞,且以血小板为主的“白血栓”,不同于 STEMI冠脉内闭塞性的“红血栓”,故两者的治疗策略有很大差异。本文就非 ST段抬高型急性冠脉综合征治疗的一些进展作一综述。     

急性冠脉综合征治疗进展(综述)

不稳定型心绞痛(UA)、无Q波心肌梗死(NQ—MI)和Q波心肌梗死(QMI)为冠心病(CAD)最常见的临床特征,它们有着共同的病理生理学基础,即冠状动脉内粥样斑块松动、裂纹或破裂,使斑块内高度致血栓形成的物质暴露于血流中,引起血小板在受损表面黏附、活化、聚集,形成血栓,最终使心肌血流灌注受损,因而常将三者归为统一的急性冠状动脉综合征(ACS)已成共识。本文重点探讨ACS治疗进展．为临床治疗提供参考依据。     

急性冠脉综合征抗凝与抗血小板治疗

近年来 ,人们已知急性冠脉综合征 (ACS)发病机制是不稳定斑块即易损斑块的破裂 ,由易损斑块的破裂引起血小板聚集并激活血凝系统 ,形成血栓。根据血栓是否自溶 ,是否完全阻塞血管而在临床上形成急性冠脉综合征中的不稳定性心绞痛 (UA)、非ST段抬高心肌梗死 (NSTEMI)和ST段抬高心肌梗死(STEMI)。所以 ,在临床治疗上 ,抗凝和抗血小板治疗则成为急性冠脉综合征治疗中最重要措施之一。1　抗凝治疗肝素是一种平均分子质量为 (1 1 90 4～ 1 4 880 )× 1 0 3 u粘多糖类物质的混合物。肝素与抗凝血酶Ⅲ作用后抑制凝血因子Ⅹa和Ⅸa特别是凝血…     

Latest evidence in personalized antiplatelet therapy in patients with acute coronary syndromes undergoing percutaneous coronary intervention

In patients with acute coronary syndromes undergoing percutaneous coronary intervention, the combination of aspirin and clopidogrel, a P2Y12 adenosine diphosphate (ADP) receptor antagonist, is the gold standard of antiplatelet therapy. Two more potent P2Y12 ADP receptor antagonists are now available. Pharmacodynamic studies have revealed a large interindividual variability in the biological response to clopidogrel that is primarily related to variable active metabolite generation, depending on clinical factors, drug-drug interactions, and genetic polymorphisms. Several assays to measure platelet function are available and have revealed a high prevalence of high on-treatment platelet reactivity (HTPR). Patients exhibiting HTPR after a clopidogrel loading dose have a higher risk of thrombotic recurrence after percutaneous coronary intervention. A recent consensus has defined HTPR for the main platelet assays available (using receiver operating characteristic curve analysis) to define the optimal cutoff value for each assay in order to predict thrombotic recurrences. In this article, we present several lines of evidence that suggest a therapeutic window of platelet reactivity inhibition with P2Y12 ADP receptor antagonists. Such a paradigm shift is supported by the results of the Platelet Inhibition and Patient Outcomes (PLATO) trial and the Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition with Prasugrel-Thrombolysis in Myocardial Infarction (TRITON-TIMI) 38, which showed the superiority of ticagrelor and prasugrel on thrombotic events compared with clopidogrel; however, these 2 medications had an increased bleeding rate. With the results of these trials, in addition to the evidence of a therapeutic window with P2Y12 ADP receptor antagonists, we summarize the potential of platelet reactivity monitoring and pharmacogenomics to tailor therapy.     

Emerging oral antiplatelet therapies for acute coronary syndromes

Emergency department physicians, along with hospitalists and interventional cardiologists, provide first-line care for patients experiencing symptoms potentially associated with acute coronary syndromes (ACS). Because these health care providers encounter and manage patients with varying degrees of risk, a clear understanding of the modes of action, benefits, and limitations of various therapeutic options is crucial for achieving optimal outcomes in the acute-care setting. Oral antiplatelet therapy has a major role in the acute care of patients with suspected ACS due to the critical role of platelets in the pathophysiology of disease. The current standard-of-care oral antiplatelet therapy for ACS is aspirin in combination with a P2Y12 adenosine diphosphate (ADP) receptor antagonist, most commonly clopidogrel. Aspirin and P2Y12 antagonists have both demonstrated efficacy in reducing morbidity and mortality in patients with ACS, but are also associated with increased bleeding risk compared with controls. Additionally, despite dual oral antiplatelet therapy, patients remain at substantial residual risk for ischemic events due to thrombotic episodes driven by platelet activation pathways that are not inhibited by these agents, including the protease-activated receptor (PAR)-1 platelet activation pathway, stimulated by thrombin. Novel oral antiplatelet agents in advanced clinical development include a direct and more readily reversible P2Y12 antagonist, ticagrelor, as well as a new class of PAR-1 antagonists, which includes vorapaxar and atopaxar. Ticagrelor has shown a significant ischemic benefit and an increase in non-surgical bleeding over clopidogrel in the large phase 3 Platelet Inhibition and Patient Outcomes trial. Results of phase 2 trials with PAR-1 antagonists suggest that these agents may provide incremental reduction in ischemic events without a bleeding liability. This hypothesis is being evaluated in 2 large ongoing phase 3 trials with vorapaxar, including the Thrombin Receptor Antagonist for Clinical Event Reduction in Acute Coronary Syndrome (TRA*CER) trial in patients with non-ST-segment elevation ACS.     

The cost-effectiveness of dual oral antiplatelet therapy following percutaneous coronary intervention

The CREDO trial demonstrated the clinical efficacy of 12-month antiplatelet therapy with clopidogrel compared to standard 28-day treatment with a 27% relative reduction in the combined risk of death, myocardial infarction, or stroke in patients undergoing percutaneous coronary intervention (PCI) and being treated with aspirin. This study evaluated the long-term cost-effectiveness of 12-month vs. 28-day therapy with clopidogrel in Sweden. A Markov model was developed which assumed a hypothetical cohort of patients in a post-PCI state to have certain risks of suffering one of the endpoints of the CREDO trial: stroke, myocardial infarction, or death. The model predicted a mean survival of 12.098 years in the 12-month arm vs. 12.026 in the 28-day arm, an incremental gain of 0.072 life-years. The gain in survival came at a predicted incremental cost of €217, resulting in an incremental cost-effectiveness ratio of €3,022. Thus the predicted cost-effectiveness ratio of long-term treatment with clopidogrel in patients undergoing PCI is well below the threshold values currently considered cost-effective.     

Antiphospholipid antibodies in acute coronary syndrome

The authors examined the presence of antiphospholipid antibodies in acute coronary syndrome. As their results show the frequency of antibodies against B2-glycoprotein I is significantly higher (14.4%) than the presence of these antibodies in a healthy control group (2%). Occurrence of antibodies against B2-glycoprotein I is much more higher than the occurrence of IgG- or IgM type antibodies against cardiolipin or lupus anticoagulant. CONCLUSIONS: The authors emphasize the possible role of anti-B2-glycoprotein I antibodies in thrombotic process of acute coronary syndrome. The previous ischaemic stroke was significantly more frequent in those patients medical history in whose serums antibodies against B2-glycoprotein I were present, so the presence of this thrombophil factor in acute coronary syndrome points out the importance of secunder antithrombotic prevention.     

急性冠脉综合征冠状动脉造影特点

目的了解急性冠脉综合征(ACS)冠脉血管病变情况,为临床分析病情、制定治疗方案提供客观依据.方法对其造影显示的冠脉病变支数、部位、狭窄程度、危险分层及相关因素进行分析.结果 148例确诊ACS患者纳入研究范围,不稳定型心绞痛(UAP)66例,急性心肌梗死(AMI)82例.单支病变94例,占63.5%,双支42例,占28.4%,三支11例,占7.4%;犯罪血管分布中左前降支(LAD)81例,占54.7%,左回旋支(LCX)13例,占8.7%,右冠状动脉(RCA)53例,占35.8%,左主干1例,占0.7%.犯罪血管狭窄程度及危险程度分层中,狭窄在50%～74%者35例,占23.6%,狭窄在75%～99%者82例,占55.4%,完全闭塞者24例(其中AMI 20例,UAP 4例),占16.2%,狭窄<50%者7例,占4.7%.犯罪血管危险程度分层中,低危者27例,占18.2%,中危者54例,占36.5%,高危者53例,占35.8%,极高危者7例,占4.7%;中、高危病变共计107例,占总数的72.3%.结论 ACS患者冠脉造影显示大部分有严重的冠脉病变,部分完全闭塞,应积极考虑急诊PTCA及支架术等介入治疗或外科手术,血运重建,改善预后.     

Immediate effect of intensive atorvastatin therapy on lipid parameters in patients with acute coronary syndrome

Background  

Intensive statin therapy decreases mortality and incidence of coronary events in patients after acute coronary syndrome (ACS). Recently it has been reported that spontaneous lipid levels remain clinically stable during ACS. The immediate influence of lipid levels by high-dose statin therapy initiated at admission in ACS patients is, however, not clear.