硝酸酯类药物在急性冠脉综合征中的合理应用

急性冠状动脉综合征（ACS）是一组由冠状动脉粥样硬化斑块破裂、血栓形成或血管痉挛而致急性或亚急性心肌缺血的临床综合征,主要包括不稳定心绞痛（UA）、ST段抬高的心肌梗死（STEMI）、非ST段抬高的心肌梗死（NSTEMI）及猝死。其临床决策的正确性、实效性极大程度地影响了患者的预后,硝酸酯类药物目前仍是ACS治疗中最常用的一类药物。     

156例急性冠脉综合征患者血尿酸水平分析

急性冠脉综合征（ACS）是以冠状动脉粥样硬化斑块破裂或糜烂，继发完全或不完全闭塞性血栓形成为病理基础的一组临床综合征。包括不稳定型心绞痛（UAP）、急性ST段抬高型心肌梗死（STE-AMI）和急性非ST段抬高型心肌梗死（NSTE—AMI）。血尿酸作为心血管疾病的相关危险因子及预测因素逐渐引起人们重视。本文对156例ACS患者血尿酸值进行分析，现报道如下。     

急性冠脉综合征的抗凝治疗

急性冠脉综合征（acute coronary syndrome．ACS）是由于冠状动脉粥样斑块破裂或溃烂．进而诱发血栓形成引起冠脉血流完全中断或极度降低的病理生理改变所导致的综合衙．主要包括不稳定性心绞痛（UA）、急件非ST段抬岛心肌梗死{NSTEMI）和ST段抬高心肌梗死（STEMI）,     

急性冠状动脉综合征诊治进展

急性冠状动脉综合征（ACS）,主要包括不稳定心绞痛（UAP）、非Q波性心肌梗死（NQMI）、Q波性心肌梗死（QMI）和冠心病猝死（SCD）.目前又根据ACS中UAP、NQMI和QMI的病生理特点、临床表现和治疗原则的有所不同又将ACS分为ST段抬高型心肌梗死（STEMI）和非ST段抬高型心肌梗死（NSTEMI）.在病理改变方面均有冠状动脉粥样硬化斑块破裂、表面破损或出现裂纹,继而出血和血栓形成,引起冠状动脉（冠脉）不完全或完全阻塞所致,约占冠心病的30%.各型均有不同程度的心肌损害及不同的预后,危害甚大,已经成为发达国家和我国人群致死致残的主要原因之一,40岁后发病率开始增加,男性多于女性,且呈上升趋势.因此,如何早期诊治ACS,挽救濒死的心肌是治疗的关键.就近年对ACS的研究进展作一综述.     

急性冠脉综合征--不稳定性心绞痛/非ST段抬高型心肌梗死概述

急性冠脉综合征（acute coronary syndrome,ACS）是心血管内科常见的危重急症,及时恰当治疗是降低致死致残挽救生命的关键。     

非ST段抬高急性冠脉综合征诊治现状

急性冠脉综合征（Acute coronary syndrome，ACS）是冠状动脉内不稳定斑块破裂引起血栓形成而导致的心脏急性严重缺血综合征。本病具有发病急、病情变化快及死亡率高的特点。因此对ACS早期诊断、及时危险分层以及合理的临床干预有其重要的临床意义。按2000年美国心脏病学会（ACC）及美国心脏协会（AHA）联合发布的不稳定型心绞痛和非ST段抬高心肌梗死的治疗指南，根据患近期缺血性胸痛发作时ECG的ST段变化．ST段抬高ACS主要演变为Q波型急性心肌梗死（AMI）．非ST段抬高ACS主要演变为非Q波型心肌梗死（N-QMI）和UAP。     

急性冠状动脉综合征治疗的新机遇

急性冠状动脉综合征包括ST段抬高心肌梗死、无ST段抬高心肌梗死及不稳定心绞痛。共同的病理生理学特征为动脉粥样硬化斑块破裂、侵蚀，或者同时伴有冠状动脉内血栓形成。     

心电图在鉴别急性肺栓塞与非ST段抬高型急性冠脉综合征中的价值探讨

目的评价床旁12导联ECG在鉴别急性肺栓塞(Acute pulmonary embolism,APE)和非ST段抬高型急性冠脉综合征(acute coronary syndrome,NSTE-ACS)中的价值。方法回顾性研究我院2010年1月～2011年10月连续收治的80例APE患者和40例NSTE-ACS患者。对两组患者入院时的ECG进行组间比较。结果右束支传导阻滞(RBBB)及S1Q3T3改变在两组间发生率无显著性差异,分别是APE(8例,10%)/NSTE-ACS(5例,13%)和APE(21例,26%)/NSTE-ACS(6例,15%)。而V1～3T波倒置同时伴有Ⅱ、Ⅲ、aVF导联T波倒置在APE组明显增多,阳性预测价值和特异性分别是83%和85%。结论右束支传导阻滞(RBBB)及S1Q3T3对于鉴别APE和NSTE-ACS没有帮助,而V1～3同时伴有Ⅱ、Ⅲ、aVF导联T波倒置是APE较特异的心电图表现。     

应激性高血糖与急性冠脉综合征

急性冠脉综合征(acute coronary syndrome,ACS)是指由冠状动脉粥样硬化斑块破裂出血或冠状动脉内内出血栓形成导致的严重心肌缺血事件,是缺血性心肌脏病最常见的表现形式,包括不稳定型心绞痛、急性非ST段抬高的心肌梗死和急性ST段抬高的心肌梗死。目前,临床上经常遇到ACS合并糖     

急性冠状动脉综合征合并糖尿病临床分析

急性冠状动脉综合征(ACS)是指有冠状动脉粥样硬化斑块破裂出血或冠状动脉内血栓形成导致的严重心肌缺血事件,包括不稳定型心绞痛、急性非ST段抬高的心肌梗死和急性ST段抬高的心肌梗死。而糖尿病(DM)患者脂代谢、糖代谢、血小板功能异常及纤溶活力下降,易于出现高凝倾向和血栓形成并易合并ACS。有文献报道,ACS患者合并DM的比率为21.5%[1]。本文对我院88例ACS进行分析,其中伴糖尿病41例(46.6%),非糖尿病患者47例(53.4%)。目的在于探讨ACS患者合并糖尿病的临床与预后特点。1临床资料1.1一般资料选择我院自2002年12月～2004年12月收住…     

Angiotensin receptor blockers: RAAS blockade and renoprotection

ABSTRACT

Introduction: Chronic kidney disease (CKD) is an increasingly prevalent public health concern and is associated with a high risk of adverse cardiovascular outcomes. Renal impairment is frequently associated with hypertension and there is compelling evidence of the benefits of antihypertensive therapy for reducing progression of kidney disease. The central role of the renin-angiotensin-aldosterone system (RAAS) in hypertension and renal disease has led to interest in the ability of RAAS-blocking agents to provide benefits beyond blood pressure control.

Scope: This review explores the mechanisms involved in CKD development, assesses markers of CKD progression, explores the role of the RAAS in renal disease, and examines RAAS blockade as a therapeutic option for renoprotection. For this purpose, a non-systematic literature review was conducted using the Medline database.

Findings: Studies in patients with diabetic renal disease have shown that RAAS blockade with angiotensin converting enzyme (ACE)-inhibitors or angiotensin receptor blockers (ARBs) reduces progression of renal disease. Similarly, several studies have demonstrated the benefits of ACE inhibitors in non-diabetic renal disease, although few studies have been conducted with ARBs in this setting. At present, there is little evidence to determine the relative merits of ARBs and ACE inhibitors in terms of clinical outcomes, although ARBs appear to have advantages in terms of renal haemodynamics and measures of renal function.

Conclusions: The beneficial effects of ARBs, which result from a combination of antihypertensive, haemodynamic, antiproteinuric and pleiotropic mechanisms, provide a strong rationale for considering the use of these agents in the treatment of high-risk patients.     

RAAS抑制剂在对比剂致维吾尔族患者性肾损伤中的作用

摘要：目的 探讨对比剂致维吾尔族患者急性肾损伤（CI-AKI）发生率、危险因素及肾素-血管紧张素-醛固酮系统（RAAS）抑制剂在其中是否发挥影响作用。方法 回顾性分析新疆维吾尔自治区和田地区人民医院心脏诊疗中心成功行经皮冠状动脉介入治疗（PCI）手术,并于24～48 h后复查肾功能的218例维吾尔族患者的临床资料。按照有无CI-AKI分为CI-AKI组（n=46）及对照组（n=172）,观察2组患者一般资料,分析CI-AKI的危险因素及RAAS抑制剂在其中的作用。结果 218例患者中发生CI-AKI 46例（21.1%）。CI-AKI组中高血压患病率、对比剂用量、低密度脂蛋白胆固醇（LDL-C）水平、N末端B型脑钠肽前体（NT-proBNP）水平、高敏C反应蛋白（hs-CRP）水平高于对照组;RAAS抑制剂使用比例、左室射血分数（LVEF）水平、高密度脂蛋白胆固醇（HDL-C）水平、血红蛋白（HB）水平低于对照组（P＜0.05）。CI-AKI组及对照组术前肌酐清除率差异无统计学意义。术前CI-AKI组肌酐水平低于对照组,但术后CI-AKI组肌酐水平较术前明显增加（P＜0.05）。术前2组间尿素氮水平差异无统计学意义,但术后CI-AKI组尿素氮水平明显增加。多因素Logistic分析发现对比剂用量增加、高NT-proBNP及hs-CRP水平仍为维吾尔族患者发生CI-AKI的危险因素,使用RAAS抑制剂是保护因素。结论 对于维吾尔族拟行PCI治疗患者,术前使用RAAS抑制剂,改善术前心功能,减少术中对比剂用量能够降低CI-AKI发生风险。     

Ticagrelor for acute coronary syndrome?

Current guidelines from the National Institute for Clinical Excellence (NICE) recommend antiplatelet therapy comprising aspirin plus either clopidogrel or prasugrel for patients with acute coronary syndrome (ACS). However, such dual therapy increases the likelihood of bleeding compared to that with aspirin alone. Ticagrelor (Brilique - Astra-Zeneca) is a new oral antiplatelet drug recently licensed in the UK (since publication of the NICE guidelines) for use with aspirin in patients with ACS, including those managed medically or undergoing percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG). Here we review the place of ticagrelor in the management of people with ACS, and whether it offers advantages over standard therapy in terms of greater efficacy or lower likelihood of bleeding complications.     

Emerging antithrombotic drugs for acute coronary syndrome

Introduction: Acute coronary syndrome (ACS) encompasses acute myocardial infarction (MI) and unstable angina. Activation of platelets and coagulation cascade plays a central role in the development of ACS. Over the past decade, there have been substantial improvements in the strategies for secondary prevention of ACS, including the development of more potent oral antiplatelet agents such as prasugrel and ticagrelor. However, therapies with even better efficacy and safety profiles and more rapid onset and offset of action would be desirable.

Areas covered: This review discusses the advantages and disadvantages of the currently available antithrombotic agents and describes the findings from recent clinical trials of three novel agents; cangrelor (an intravenous P2Y12 receptor antagonist), vorapaxar (protease-activated receptor-1 inhibitor) and rivaroxaban (an oral factor Xa inhibitor).

Expert opinion: Cangrelor appears more promising than clopidogrel when a very rapid onset and reversal of antiplatelet effect is needed. Vorapaxar in addition to standard oral antiplatelet therapy was effective in patients with prior MI, but was not safe in patients with a prior stroke. Low dose rivaroxaban decreased cardiovascular events and mortality in patients post-ACS compared to placebo, although bleeding was increased.     

Clopidogrel and acute coronary syndrome

Clopidogrel (Plavix-Sanofi-Synthelabo & Bristol-Myers Squibb) blocks platelet aggregation through an action distinct from that of aspirin. In the UK, it is licensed for the secondary prevention of atherosclerotic events and for this, we concluded 3 years ago that clopidogrel "appears to offer no worthwhile advantage over aspirin". After publication of the CURE (Clopidogrel in Unstable angina to prevent Recurrent Events) trial, which assessed adjunctive use of clopidogrel with aspirin in patients with acute coronary syndrome without ST-segment elevation (unstable angina or non-Q wave infarction), clopidogrel was hailed in the lay media as "the biggest breakthrough in 20 years". Do the CURE study results warrant the use of clopidogrel in patients with acute coronary syndrome without ST elevation (currently an unlicensed indication)?     

Pharmacogenomics in acute coronary syndrome

Inheritance of cardiovascular diseases has been the subject of a large number of retrospective candidate gene studies and is now a topic of genome-wide, single-nucleotide-polymorphism investigations using chip-array techniques. The question as to whether or not genetic variants could also influence drug response is much less well investigated, although many factors involved in the etiology of coronary artery disease or acute coronary syndromes may also contribute to the clinical response to drug treatment. Moreover, inter-individual differences in the pharmacokinetics and pharmacodynamics were partly shown to affect the clinical outcome of long-term coronary artery disease treatment. However, except for the prevention of thrombosis by vitamin K antagonists, there is only weak evidence that the short-term treatment of acute coronary syndromes is dependent on any genetic trait. This review focuses on the role of polymorphic platelet aggregation, clotting factors, vascular function, and lipid metabolism and transport. The present picture is complex and many findings could not be reproduced or are often contradictory. In conclusion, statistically well-powered, prospective studies are required considering multiple genetic traits in order to estimate the impact of pharmacogenomics in acute coronary syndrome risk and individualized drug treatment. At present, no data are available that should influence a physicians decision on drug treatment in acute situations. However, for long-term treatment distinct genetic markers may be applied in the future.     

Emerging antiplatelet therapy for coronary artery disease and acute coronary syndrome

Antiplatelet therapy is used widely with proven benefit for the prevention of further ischemic cardiac complications in patients with known coronary artery disease (CAD) and a history of acute coronary syndrome (ACS). The limitations of conventional antiplatelet therapy with aspirin, clopidogrel, or prasugrel, as well as the fact that rates of recurrent ischemic events still remain high with use of these agents, underscore the need to investigate alternate agents that may further reduce event rates while limiting bleeding risk. The selection of antiplatelet therapy is further influenced by the following: ticagrelor was approved in July 2011 by the United States Food and Drug Administration (FDA), and clopidogrel is slated to become available as a generic productin 2012. We provide an overview of emerging agents for the treatment of CAD and ACS, including the reversible P2Y(12) antagonists ticagrelor, cangrelor, and elinogrel, and a new class of oral protease-activated receptor-1 (PAR-1) inhibitors, vorapaxar and atopaxar.The recently approved P2Y(12) antagonists prasugrel and ticagrelor demonstrate enhanced ability to prevent adverse cardiac outcomes. However, this comes at a cost of a potential increased risk of bleeding. New adverse effects have also emerged, including dyspnea for all of the reversible P2Y(12) antagonists (ticagrelor, cangrelor, and elinogrel) and ventricular pauses for ticagrelor. In addition, the newer P2Y(12) antagonists have a faster onset and offset. Two of these agents, cangrelor and elinogrel, are available as intravenous formulations, which may provide additional benefits in patients who undergo coronary artery bypass graft (CABG) surgery. Trials with the PAR-1 inhibitors have also shown trends toward reductions in cardiac events, but not without the possibility of increased bleeding. More than ever, as the arsenal of antiplatelet therapy expands, health care providers need to understand the pharmacologic and pharmacodynamic differences between conventional and emerging antiplatelet therapies for patients with ACS and CAD. Health care providers must also carefully assess patient-specific factors such as risk of thrombosis, concomitant disease states, age, drug adherence, and aspirin dose, and plan for those patients who will be undergoing CABG when selecting antiplatelet therapy in order to optimally balance bleeding and thrombosis risk.