急性冠脉综合征患者接受经皮冠状动脉介入治疗前后抗血小板策略

急性冠脉综合征(ACS)是一组由急性心肌缺血引起的临床综合征,包括不稳定型心绞痛(UA)、非ST段抬高型心肌梗死(NSTEMI)和ST段抬高型心肌梗死(STEMI).ACS主要发病机制是动脉粥样硬化斑块破裂后,血小板激活和凝血酶的形成,最终导致血栓形成.目前抗血小板治疗和抗凝治疗是ACS患者抗栓治疗的两大重要组成部分.随着经皮冠状动脉介入治疗(PCI)的广泛应用,ACS患者PCI围手术期抗栓药物的安全性及有效性备受关注.本文就ACS患者有关接受PCI前后的抗血小板治疗策略的一些大型临床试验及抗血小板药物在当今早期侵入性冠状动脉治疗时代中的应用现状作一综述.     

Role of platelet glycoprotein polymorphisms in cardiovascular diseases

Atherothrombosis is the leading cause of death in western countries. Major complications of atherothrombotic disease, which are responsible for a large burden of morbidity and mortality, are acute coronary syndromes, ischemic stroke, and peripheral occlusive disease. Plaque rupture, platelet adhesion, aggregation, and thrombosis may lead to unstable angina and may progress to myocardial infarction as well as to ischemic stroke. Platelet membrane glycoprotein receptors mediate crucial reactions in acute thrombosis and chronic processes of atherogenesis. The platelet glycoprotein GP IIb/IIIa, which is the most abundant platelet receptor, also represents the drug target of a novel class of anti-platelet drugs, which includes abciximab, tirofiban, and eptifibatide. The genes encoding the three major platelet glycoprotein receptors (GP Ib/IX/V, GP Ia/IIa, and GP IIb/IIIa) are subject to considerable genetic variability. This paper reviews how polymorphisms in the platelet glycoprotein receptors affect platelet function, susceptibility to atherothrombosis and its major complications including myocardial infarction, stroke, and complications following percutaneous coronary interventions, and individual variability of drug response. Recent data on platelet glycoprotein receptor polymorphisms as modifiers of drug action and as predictors of drug response offer the perspective of individualized drug treatment. Prospective studies will show whether this approach is useful or not. As the data reviewed here show clearly, future clinical trials should routinely take into account genetic susceptibility factors and modifiers, both for study design and for predefined patient stratification.Abbreviations ACS Acute coronary syndrome - CI Confidence interval - DCA Directional coronary atherectomy - GP Glycoprotein - MACE Major adverse cardiac event - MI Myocardial infarction - PCI Percutaneous coronary intervention - PTCA Percutaneous transluminal coronary angioplasty - RR Relative risk - SCD Sudden cardiac death - VWF Von Willebrand factor     

心脏介入术中并发急性心脏压塞的抢救与护理

目的探讨心脏介入治疗术中并发急性心脏压塞的急救治疗、病情观察及护理措施。方法回顾2010年1月至2012年12月在我院心脏介入治疗术中5例并发急性心脏压塞患者的急救、观察与护理。结果本组病例由于及时发现、正确救治和精心护理,均痊愈出院。结论护士在心脏介入治疗术前做好各项急救准备工作;术中、术后严密观察患者的生命体征、神志及病情变化,及早发现疾病的先兆症状,在成功救治急性心脏压塞患者中发挥了重要的作用。     

Brugada-like early repolarization pattern misdiagnosed as acute anterior myocardial infarction in a patient with myocardial bridging of the left anterior descending artery

The diagnosis of acute coronary syndrome in patients presenting to the emergency department with chest pain is still challenging. Since the symptoms and electrocardiographic abnormalities of patients with acute myocardial infarction can be indistinguishable from those of patients with other conditions that lead to ST-segment elevation, a high clinical index of suspicion is needed to avoid an incorrect diagnosis and subjecting the patient to unwarranted thrombolytic therapy. Our report concerns a 53-year-old male with myocardial bridging of the left anterior descending artery. He presented with the combined electrocardiographic abnormality of the Brugada-like or early repolarization pattern, which was misdiagnosed as acute anterior myocardial infarction.     

Administration of glycoprotein IIb-IIIa inhibitors in patients with ST-segment elevation myocardial infarction

Patients with ST-segment elevation acute myocardial infarction require immediate reperfusion therapy. Reperfusion therapy can be provided by either pharmacologic or mechanical means. Pharmacologic reperfusion therapy consists of administering fibrinolytics, whereas mechanical reperfusion consists of performing percutaneous intervention, usually with stent placement. Each approach has been shown to decrease mortality, but each has disadvantages in establishing flow in the infarct-related artery. Regardless of the approach, during an acute myocardial infarction, activation and externalization of glycoprotein (GP) IIb-IIIa receptors occur on the surface of platelets. The GP IIb-IIIa inhibitors block the binding of fibrinogen to these platelet receptors. These inhibitors have been investigated in combination with both reperfusion strategies. The goal of adding GP IIb-IIIa inhibitor therapy to either reperfusion approach is to obtain better early, complete, and sustained reperfusion. Subsequently, this should lead to better clinical outcomes for patients with ST-segment elevation acute myocardial infarction. Although no mortality benefit has been seen with the addition of GP IIb-IIIa inhibitor therapy, ischemic complications have been reduced significantly.     

心脏介入治疗患者并发心脏压塞的早期识别与抢救护理

目的探讨心脏介入治疗患者早期发生心脏压塞的识别及抢救体会。方法选取本院收治的10例行心脏介入治疗发生心脏压塞患者的临床资料,分析其发生心脏压塞的早期症状、急救措施及护理原则。结果在本组10例患者中有8例患者术中发生心脏压塞,另2例患者为迟发型术后5h内发生心脏压塞,经心包引流,病情得以控制,9例患者救治成功,1例患者死亡。结论严格掌握心脏介入的适应证,对于高危患者术中操作要轻柔,避免损伤冠状动脉,密切观察病情并早期识别,争取宝贵的抢救时间是救治成功的关键。     

PCI术后急性心包填塞早期识别抢救与护理

目的 探讨PCI术后急性心包填塞早期识别抢救与护理对策.方法 回顾性分析7例心脏介入术后并发急性心包填塞的临床资料,严密观察病情,及早识别,穿刺过程中严密监测生命体征、心包引流管的护理,停用抗凝药物,做好心理护理.结果 本组5例患者均经心包穿刺引流并留置引流管抢救成功;1例因病情重,家属主动放弃抢救治疗.1例因合并大片脑梗死,经抢救无效死亡.结论 立即行心包穿刺术排除心包积血,解除心脏受压是介入术后发生急性心包填塞抢救成功的关键.加强病情观察及引流管的护理,是预防术后其他并发症的重要措施.     

Platelet glycoprotein IIb/IIIa receptor antagonists

The molecular understanding of platelet function, together with an appreciation of the role of platelet thrombus in the pathogenesis of acute coronary syndromes (ACS) and abrupt vessel closure following coronary intervention, lead to the development of the class of agents now referred to as platelet glycoprotein IIb/IIIa (GP IIb/IIIa) inhibitors. Currently three parenteral GP IIb/IIIa inhibitors are licensed for use in patients undergoing coronary intervention or as empirical therapy in non-ST elevation ACS (unstable angina and non-Q wave myocardial infarction). Clinical trials using these agents in patients undergoing coronary interventions have demonstrated a consistent reduction in ischaemic end points at 30 days that is sustained during long-term follow-up. Similar benefits have been found in patients with ACS who are managed medically or who proceed to revacularization. Studies using prolonged platelet inhibition using oral GP IIb/IIIa inhibitors in patients following coronary intervention or with ACS have produced disappointing results. Further investigation with existing and newer oral agents are ongoing. The use of GP IIb/IIIa inhibitors in combination with fibrinolytic agents for optimal reperfusion in patients with acute ST-elevation myocardial infarction (MI) is an active area of interest. Angiographic outcomes with this approach have been encouraging and clinical outcome data are awaited. Beyond efficacy, GP IIb/IIIa inhibitors have proven to be safe for clinical use. Haemorrhagic complications and thrombocytopenia are the most common adverse events, though infrequent. Unresolved issues regarding drug dosing, monitoring of effect, duration of therapy, head-to-head comparisons of agents, and use of adjunctive therapies are the subject of ongoing studies.     

Platelet glycoprotein IIb/IIIa receptor antagonists

The molecular understanding of platelet function, together with an appreciation of the role of platelet thrombus in the pathogenesis of acute coronary syndromes (ACS) and abrupt vessel closure following coronary intervention, lead to the development of the class of agents now referred to as platelet glycoprotein IIb/IIIa (GP IIb/IIIa) inhibitors. Currently three parenteral GP IIb/IIIa inhibitors are licensed for use in patients undergoing coronary intervention or as empirical therapy in non-ST elevation ACS (unstable angina and non-Q wave myocardial infarction). Clinical trials using these agents in patients undergoing coronary interventions have demonstrated a consistent reduction in ischaemic end points at 30 days that is sustained during long-term follow-up. Similar benefits have been found in patients with ACS who are managed medically or who proceed to revacularisation. Studies using prolonged platelet inhibition using oral GP IIb/IIIa inhibitors in patients following coronary intervention or with ACS have produced disappointing results. Further investigation with existing and newer oral agents are ongoing. The use of GP IIb/IIIa inhibitors in combination with fibrinolytic agents for optimal reperfusion in patients with acute ST-elevation myocardial infarction (MI) is an active area of interest. Angiographic outcomes with this approach have been encouraging and clinical outcome data are awaited. Beyond efficacy, GP IIb/IIIa inhibitors have proven to be safe for clinical use. Haemorrhagic complications and thrombocytopenia are the most common adverse events, though infrequent. Unresolved issues regarding drug dosing, monitoring of effect, duration of therapy, head-to-head comparisons of agents, and use of adjunctive therapies are the subject of ongoing studies.     

Genetic and non-genetic factors affecting the response to clopidogrel therapy

INTRODUCTION: Clopidogrel (CLP) is a second-generation thienopyridine that prevents platelet aggregation by inhibiting the adenosine diphosphate receptor located on the platelet surface. The use of CLP in combination with aspirin has become standard treatment in patients with acute coronary syndromes and stent implantation. Data suggests that a significant percentage of individuals treated with CLP do not receive the expected therapeutic benefit because of a decreased platelet inhibition. The clinical consequences of an inadequate platelet response are cardiovascular complications, which can lead to acute myocardial infarction, stroke and death. The mechanism underlying CLP resistance is multifactorial and includes genetic polymorphisms and non-genetic causes (such as drug-drug interactions, co-morbidities, age). AREAS COVERED: This article reviews the so-far accumulated evidence on the role of genetic polymorphisms and non-genetic factors, as determinants of the antiplatelet response to CLP. Pharmacodynamic and clinical aspects of the CLP nonresponsiveness are also presented. Relevant papers were identified by an extensive PubMed search using appropriate keywords. EXPERT OPINION: Impaired platelet inhibition in CLP poor responders is a real problem, as it leads to serious clinical consequences. Therefore, prediction models that include pharmacogenetic knowledge and non-genetic risk factors of low response to the drug are needed in the individualization of antithrombotic therapy. Alternative antiplatelet strategies that should be considered to overcome this problem include dose modification, adjunctive antiplatelet drug usage, and use of newer agents.     

Does Magnesium Have a Role in the Treatment of Patients with Coronary Artery Disease?

Hypomagnesemia is common in hospitalized patients, especially in elderly patients with coronary artery disease (CAD) and/or those with chronic heart failure. Hypomagnesemia is associated with increased all cause mortality and mortality from CAD. Magnesium supplementation improves myocardial metabolism, inhibits calcium accumulation and myocardial cell death; it improves vascular tone, peripheral vascular resistance, afterload and cardiac output, reduces cardiac arrhythmias and improves lipid metabolism. Magnesium also reduces vulnerability to oxygen-derived free radicals, improves endothelial function and inhibits platelet function, including platelet aggregation and adhesion, which potentially confers upon magnesium physiologic and natural effects similar to adenosine-diphosphate inhibitors such as clopidogrel. However, data regarding the use of magnesium in patients with acute myocardial infarction (AMI) are conflicting. Although some previous relatively small randomized clinical trials demonstrated a remarkable reduction in mortality when intravenous magnesium was administered to relatively high risk AMI patients, two recently published large-scale randomized clinical trials (the Fourth International Study of Infarct Survival [ISIS 4] and Magnesium in Coronaries [MAGIC]) were unable to demonstrate any advantage of intravenous magnesium over placebo. Nevertheless, the theoretical benefits of magnesium supplementation as a cardio-protective agent in CAD patients, promising results from animal and human studies, its relatively low-cost and ease of handling requiring no special expertise, together with its excellent tolerability, gives magnesium a place in treating CAD patients, especially in those at high risk, such as CAD patients with heart failure, the elderly and hospitalized patients with hypomagnesemia. Furthermore, magnesium therapy is indicated in life-threatening ventricular arrhythmias such as torsades de pointes and intractable ventricular tachycardia.     

Clopidogrel and aspirin in cardiovascular medicine: responders or not--current best available evidence

Dual antiplatelet therapy represents an important advance for patients with established coronary artery disease. It is an important strategy for patients with acute coronary syndromes and those undergoing percutaneous transcatheter coronary interventions. Clopidogrel effectively inhibits ADP-induced platelet activation and aggregation by selectively and irreversibly blocking the P2Y(12) receptor on the platelet membrane. Aspirin works by irreversibly acetylating the cyclooxygenase (COX-1) enzyme, thus suppressing the production of thromboxane A(2) (TxA(2)) and inhibiting platelet activation and aggregation. Variable platelet response and potential resistance to therapy has emerged with aspirin and clopidogrel. The definitions of antiplatelet agents variability in responsiveness and nonresponsiveness are discussed. Clopidogrel and aspirin responsiveness as they are measured in the laboratory by various techniques (platelet aggregometry and point-of-care assays such as platelet function analyzer [PFA-100] and rapid platelet function assay [RPFA]) are evaluated. The mechanisms responsible for variations in responsiveness to antiplatelet agents such as clinical, cellular and genetic factors are defined. Aspirin and clopidogrel resistance are emerging clinical entities with potentially severe consequences such as myocardial infarction, stroke or death. The therapeutic interventions to deal with nonresponsiveness are reported, although specific recommendations are not clearly established. In the future, routine measurement of platelet function in patients with cardiovascular disease may become the standard of care. Personalized antithrombotic treatment strategies may be determined by ex-vivo measurements that identify critical pathways influencing thrombotic risk in the individual patient.     

急性心肌梗死介入术后早期心脏压塞四例并文献复习

目的尽早发现急性心肌梗死介入术后早期心脏压塞的征象并及时处理，以避免猝死的发生。方法回顾性分析2010年1月至2012年6月北京安贞医院急诊抢救中心收治的急性心肌梗死行经皮冠状动脉介入术后发生心脏压塞的4例患者临床资料。结果严重心脏压塞患者收缩压下降20-30mmHg（1mmHg=0．133kPa），心率增加10—20次／min，超声心动图示术后2—12h内新出现右心房液深3—5mm，并舒张期右心房或右心室塌陷。结论急性心肌梗死介入术后排除其他导致低血压的原因并存在以上临床和心脏超声的证据时，应立即停止抗凝药物，尽早行心包穿刺或开窗引流术。     

Intravenous glycoprotein IIb/IIIa inhibitors in acute coronary syndromes: lessons from recently conducted randomized clinical trials

The opportunity to completely inhibit platelet aggregation via the glycoprotein (GP)IIb/IIIa receptor represents a major innovation in antiplatelet therapy. Numerous trials conducted during the 1990s in patients undergoing percutaneous coronary intervention established GPIIb/IIIa inhibitors as a valuable component of treatment. Phase II trials in the medical management of acute coronary syndrome (ACS) patients also suggested beneficial effects, which encouraged six major phase III clinical trials to be conducted. In general, cardiac complications were reduced in those ACS patients who were not routinely scheduled for early revascularization. However, the treatment effect in the average patient is modest and overall 100 patients need to be treated in order to prevent one death or myocardial infarction. Given the current attention to healthcare costs, these agents may therefore be reserved for patients at suspected high risk of death or (re)infarction, including patients with diabetes mellitus and elevated cardiac troponins.     

Genetic and non-genetic factors affecting the response to clopidogrel therapy

Introduction: Clopidogrel (CLP) is a second-generation thienopyridine that prevents platelet aggregation by inhibiting the adenosine diphosphate receptor located on the platelet surface. The use of CLP in combination with aspirin has become standard treatment in patients with acute coronary syndromes and stent implantation. Data suggests that a significant percentage of individuals treated with CLP do not receive the expected therapeutic benefit because of a decreased platelet inhibition. The clinical consequences of an inadequate platelet response are cardiovascular complications, which can lead to acute myocardial infarction, stroke and death. The mechanism underlying CLP resistance is multifactorial and includes genetic polymorphisms and non-genetic causes (such as drug–drug interactions, co-morbidities, age).

Areas covered: This article reviews the so-far accumulated evidence on the role of genetic polymorphisms and non-genetic factors, as determinants of the antiplatelet response to CLP. Pharmacodynamic and clinical aspects of the CLP nonresponsiveness are also presented. Relevant papers were identified by an extensive PubMed search using appropriate keywords.

Expert opinion: Impaired platelet inhibition in CLP poor responders is a real problem, as it leads to serious clinical consequences. Therefore, prediction models that include pharmacogenetic knowledge and non-genetic risk factors of low response to the drug are needed in the individualization of antithrombotic therapy. Alternative antiplatelet strategies that should be considered to overcome this problem include dose modification, adjunctive antiplatelet drug usage, and use of newer agents.     

急性冠脉综合征患者血小板计数和平均血小板体积变化的临床意义

目的探讨急性冠脉综合征患者血小板计数(BPC)和平均血小板体积(MPV)变化及临床意义。方法选择深圳市孙逸仙心血管医院2009年1月—2011年9月收治的48例急性冠脉综合征患者,包括急性心肌梗死22例和不稳定心绞痛26例,采用血细胞分析仪进行BPC和MPV检测,同时以同期的50例健康体检者作为对照,进行比较研究。结果急性冠脉综合征患者与对照组比较,BPC明显减少,MPV明显增大,组间差异均有统计学意义(P<0.05);而急性心肌梗死和不稳定心绞痛患者BPC、MPV比较,差异无统计学意义(P>0.05)。结论急性冠脉综合征患者BPC和MPV变化明显,临床上可以帮助了解患者病情,为诊治该疾病提供一定的指导信息。     

A case of traumatic cardiac tamponade showing sudden spontaneous disappearance of the pericardial fluid

Traumatic cardiac tamponade must be treated by pericardial drainage as soon as possible. We recently encountered a rare case of traumatic cardiac tamponade in which the pericardial fluid disappeared spontaneously immediately before the planned drainage. This case is reported in this paper. The patient was a 22-year-old male who was transported to our hospital after he sustained injuries in a traffic accident. The patient was diagnosed to have a facial bone fracture, bilateral lung contusions, myocardial contusion (suspected), injury to the spinal cord at the L3-L4 level, injury to the left kidney and pelvic fracture. After TAE was performed to deal with the bleeding from the injured pelvis, the patient was immediately hospitalized. About 6 hours after the injury, pericardial fluid accumulation began to be noted, and about 18 hours after the injury, the patient went into shock, responding poorly to fluid resuscitation and treatment with pressor agents. At this time, a diagnosis of cardiac tamponade was made and emergency operation was arranged for. However, just before this could be executed, the patient's blood pressure showed a sharp rise, accompanied by disappearance of the pericardial fluid. He continued to show steady improvement and could eventually be discharged from the hospital.     

Bacterial Pericarditis

Bacterial pericarditis occurs by direct infection during trauma, thoracic surgery, or catheter drainage, by spread from an intrathoracic, myocardial, or subdiaphragmatic focus, and by hematogenous dissemination. The frequent causes are Staphylococcus and Streptococcus (rheumatic pancarditis), Haemophilus, and M. tuberculosis. In AIDS pericarditis, the incidence of bacterial infection is much higher than in the general population, with a high proportion of Mycobacterium avium-intracellulare infection. Purulent pericarditis is the most serious manifestation of bacterial pericarditis, characterized by gross pus in the pericardium or microscopically purulent effusion. It is an acute, fulminant illness with fever in virtually all patients. Chest pain is uncommon. Purulent pericarditis is always fatal if untreated. The mortality rate in treated patients is 40%, and death is mostly due to cardiac tamponade, systemic toxicity, cardiac decompensation, and constriction. Tuberculous infection may present as acute pericarditis, cardiac tamponade, silent (often large) relapsing pericardial effusion, effusive-constrictive pericarditis, toxic symptoms with persistent fever, and acute, subacute, or chronic constriction. The mortality in untreated patients approaches 85%. Urgent pericardial drainage, combined with intravenous antibacterial therapy (e.g. vancomycin 1g twice daily, ceftriaxone 1-2g twice daily, and ciprofloxacin 400 mg/day) is mandatory in purulent pericarditis. Irrigation with urokinase or streptokinase, using large catheters, may liquify the purulent exudate, but open surgical drainage is preferable. The initial treatment of tuberculous pericarditis should include isoniazid 300 mg/day, rifampin 600 mg/day, pyrazinamide 15-30 mg/kg/day, and ethambutol 15-25 mg/kg/day. Prednisone 1-2 mg/kg/day is given for 5-7 days and progressively reduced to discontinuation in 6-8 weeks. Drug sensitivity testing is essential. Pericardiectomy is reserved for recurrent effusions or continued elevation of central venous pressure after 4-6 weeks of antituberculous and corticosteroid therapy.     

急性左心衰竭为首发表现的急性心内膜下心肌梗死20例临床分析

目的：分析以急性左心衰竭为首发表现的急性心内膜下心肌梗死的临床特点,探讨其发生心力衰竭的特征和原因。方法：综合分析20例以急性左心衰竭为首发表现的急性心内膜下心肌梗死20例患者的病史和临床特点,粳据心电图、心肌酶的动态变化、Killip心功能分级和心脏彩超报告的心功能指标,探讨急性心内膜下心飘梗死发生急性左心衰竭的特征和原因。随访10例患者1年．3例死亡。结果：20例患者中,15例为无痛性心肌粳死．5例心肌瓣轻度升高,随访1年内死亡率为30％,均为糖尿患者;心电图特点：AVR和（或）V1导联S—T段抬高,其余导联普遍性S—T段压低〉0．1mV,尤其V3～V6S—T段压低更明显,或T波呈对称性深倒置;心脏彩超：LVEF（40±10）％。LVEF〈40%8例,LVEF〉140％12例,节段性室壁动度减弱或不协调。结论：①患者多合并有冠心病发病的主要致病因素;②以急性左心衰竭为首发表现的急性心内膜下心肌梗死多为无痛性心肌梗死;③心电图显示心肌缺血及损伤的面积广泛;④心脏彩超表现为心脏收缩、舒张功能显著减弱或不协调;⑤心力衰竭是其严重的并发症,也是主要死亡琢因之一。     

急性心肌缺血综合征患者临床特征分析

目的分析也门卡登地区急性心肌缺血综合征患者的临床特点和治疗.方法参照加拿大心血管合作协会统一设计的病例记录表(CRF),收集急性心肌缺血入院病人的资料,记录病人主要临床特征和院内事件.结果急性心肌缺血综合征(包括不稳定性心绞痛及非Q波心肌梗死)58例,平均年龄54.8岁,男性占68.2%.入院诊断不稳定性心绞痛94.8%,非Q波心肌梗死5.2%.就诊时仍有胸痛者63.7%;心电图异常者91.2%,其中56.4%为相邻导联ST段压低≥2 mm.住院期间溶栓治疗8.6%,硝酸酯剂93.1%,抗凝和抗血小板治疗分别是55.1%和96.2%,冠状动脉造影12.1%,冠脉旁路移植术(CABG)3.4%,经皮冠脉腔内成形术(PTCA)8.0%.院内发生重要并发症11.2%,其中死亡3.4%.结论也门卡登地区急性心肌缺血病人以不稳定心绞痛就诊为多.住院期间由于条件设备受限,以硝酸酯剂,抗凝及抗血小板治疗率相对较高,PTCA和CABG治疗率较低.主要死亡原因为严重心律失常或猝死.