Management of cardiogenic shock attributable to acute myocardial infarction in the reperfusion era

Cardiogenic shock is the leading cause of death among patients hospitalized with acute myocardial infarction. It is defined as tissue hypoperfusion resulting from ventricular pump failure in the presence of adequate intravascular volume. Rapid assessment and triage of patients presenting in cardiogenic shock followed by appropriate institution of supportive therapies including vasopressor and inotropic agents, mechanical ventilatory support, and intra-aortic balloon pump counterpulsation are critical for effective management of these patients. However, emergency percutaneous coronary intervention or coronary artery bypass graft surgery is required to decrease mortality rates. Novel approaches, including inhibition of nitric oxide synthase and new mechanical support devices, may further decrease mortality rates, which remain high despite reperfusion therapy.     

Update on the management of cardiogenic shock

PURPOSE OF REVIEW: Cardiogenic shock is a life-threatening emergency that occurs frequently with acute coronary syndromes. If rapid myocardial reperfusion following acute myocardial infarction is not obtained, either with thrombolytics or by revascularization, cardiogenic shock frequently develops and the mortality rate is high. This review summarizes recent advances in the pathophysiology, incidence and treatment of cardiogenic shock. Particular attention is given to pharmacologic advances. RECENT FINDINGS: Cardiogenic shock continues to occur in 5-10% of patients who suffer a myocardial infarction and the mortality remains over 50% in most studies. Treatment preference is referral to a cardiac center capable of reperfusion using multiple therapies. While no delay in reperfusion is acceptable, emphasis on implementing supportive treatment such as vasopressors, inotropes, and fluids remains critical. There is a wide variance in treatment standards despite established guidelines. Overall mortality from cardiogenic shock has decreased but the incidence remains unchanged. SUMMARY: Emerging pharmacological interventions designed to counteract the underlying proinflammatory pathophysiologic mechanisms may, in combination with early revascularization, result in improved patient outcomes, but there is no magic bullet on the horizon. Attention to the timeliness of transport and treatment of patients with a focus on revascularization is required for cardiogenic shock patients.     

Current clinical management of acute myocardial infarction complicated by cardiogenic shock

ABSTRACT

Introduction

Cardiogenic shock (CS) remains the leading cause of death among patients admitted with acute myocardial infarction (AMI). Early restoration of blood flow of the infarct-related artery is of paramount importance, either with percutaneous coronary intervention (PCI) or with coronary artery bypass grafting (CABG). In addition, early risk stratification is a critical task and required to guide complex decisions on management and therapy of CS after AMI. The use of short-term mechanical circulatory support (MCS) is increasing, although evidence for their effectiveness is limited.     

Pathophysiology of cardiogenic shock complicating acute myocardial infarction

Cardiogenic shock is a rapidly progressive, often fatal complication of acute myocardial infarction. A vicious circle of ischemia, decreased cardiac output and reinfarction progress to left ventricular failure and death. The fundamental pathophysiology of this cascade and other mechanisms beyond the classic paradigm of ischemia and dysfunction are discussed in detail.     

Delayed cardiac tamponade after pacemaker insertion

Cardiogenic shock is one of the most dramatic presentations in Emergency Medicine and requires rapid and accurate assessment, evaluation, and treatment. The cardiovascular disasters that present with shock include acute myocardial infarction with pump failure, aortic dissection, massive pulmonary emboli, and cardiac tamponade. We report a patient who presented to our Emergency Department (ED) in cardiogenic shock 10 days after insertion of a permanent cardiac pacemaker. The patient had developed pericardial tamponade secondary to the insertion. In reviewing the literature, we found many reports relating to complications of pacemakers and even more information regarding the various etiologies of cardiac tamponade, but cardiac tamponade as a consequence of pacemaker insertion rarely has been reported. Cardiac tamponade can occur secondary to perforation of the right ventricle during pacemaker electrode insertion and manipulation. Perforation is generally believed to be benign and self-limiting and only rarely causes tamponade and hemodynamic compromise; however, that was not the case for our patient.     

Prise en charge du choc cardiogénique d’origine ischémique : mise au point

Cardiogenic shock complicating myocardial infarction still remains a clinical challenge. Early revascularization represented the last major improvement aiming at the mortality reduction; however, despite optimal pharmacological treatments, mortality still exceeds 40%. Treatment with catecholamines is limited by arrhythmia, increases myocardial oxygen consumption, and is associated with worsened prognosis. Due to multiple beneficial hemodynamic and systemic effects, therapeutic hypothermia seems a promising tool. At least, life support aims to ensure adequate coronary and systemic circulation to limit multi-organ failure while preserving the myocardium and reducing the risk of ischemia. While intra-aortic balloon pump has been questioned recently in a large randomized controlled trial, other circulatory support devices have proved their effectiveness on early hemodynamic parameters without improving mortality, except for refractory shock. Large randomized trials are required to define the exact role of these devices according to patient’s hemodynamic status. Early diagnosis, coupled with the intensive management of shock based on effective reperfusion and adequate circulatory support, is the only way to limit or even better prevent multi-organ failure occurrence and thus improve outcome.     

Measures to reduce infarct size (author's transl)]

Reduction of infarct size is a concept limited in clinical practice by the long period elapsing before hospital admission. Most patients are admitted only after the critical period of 6 to 8 hours following infarction when it might be possible to save the ischaemic, but not yet necrotic myocardium. Nevertheless, patients with altered haemodynamics and, therefore, a disturbed myocardial balance between oxygen requirement and oxygen supply may benefit from optimum management of the haemodynamic situation. This is achieved primarily by manipulation of preload and afterload and by enhancement of the collateral circulation to the ischaemic myocardium. However, the effects of cardiac surgery are limited by the negative sequelae of late reperfusion 6 hours after coronary ligation. Intra-aortic balloon pumping can be used only in large cardiosurgical centres because most of the so-treated patients remain pump dependent. The described measures have improved the hospitalisation period in patients with acute myocardial infarction, but the further prognosis is dictated by the nature and extent of underlying coronary heart disease.     

Cardiogenic shock complicating myocardial infarction

Cardiogenic shock is the primary cause of death among patients hospitalized with acute myocardial infarction. It is defined as tissue hypoperfusion resulting from ventricular pump failure in the presence of adequate intravascular volume. These patients need rapid assessment and appropriate institution of supportive therapies including vasopressor and inotropic agents, ventilatory support, and intra-aortic balloon pump counterpulsation. Emergency coronary artery revascularization is the only therapy that reduces mortality, and this should be provided early to patients to achieve maximal benefit, unless further care is deemed futile. Whereas newer support devices can provide better hemodynamic augmentation, their impact on mortality is limited. Novel therapies are needed to further decrease mortality rates, which remain high despite reperfusion therapy.     

急诊体外膜肺氧合辅助下重症心肌梗死的介入治疗

目的 探讨体外膜肺氧合辅助下对急性重症心肌梗死(AMI)患者中的行急诊经皮冠状动脉介入治疗(PCI)的疗效. 方法 回顾分析2003年1月至2007年12月期间中山大学附属中山医院住院的25例诊断急性心肌梗死合并心脏骤停、严重心律失常或心功能衰竭的患者,在体外膜肺氧合(ECMO)支持下行急诊PCI治疗的临床疗效观察. 结果 25例患者均在ECMO支持下血流动力学稳定,并成功行PCI,梗死相关动脉全部开通,20例患者血流达到TIMI 3级,5例患者发生慢血流或无复流(血流TIMI 0～2级).急诊介入手术中无一例死亡,介入治疗术后住院期内死亡7例,住院期间总的死亡率为28%(7/25). 结论 ECMO支持下,能促进重症AMI患者血流动力学恢复稳定,为重症患者进行PCI提供了必备的前提条件;为冠状动脉血运重建赢得了时间,从而提高了重症AMI患者的存活率.     

A multidisciplinary overview of cardiogenic shock

Cardiogenic shock complicating acute myocardial infarction (AMI) is reviewed from multidisciplinary viewpoints encompassing both basic and clinical aspects. Insights into the absolute obligate aerobic nature of the heart which possesses neither facultative capability nor functional collateral channels, together with O2 diffusion gradients, mitochondrial O2 sensing and anaerobic ATP deficiencies, are described in some detail. Myocardial adaptive responses against energy crisis, termed the Pasteur Effect, and hypoxia inducible factor (HIF)-1 alpha are implicated for cardiomyocyte viability. Oncosis and/or lysosomal autophagy cause such overwhelming numbers (several billions) of cardiomyocyte death, virtually simultaneously following coronary thrombotic occlusion. Apoptosis is briefly described and cardiogenic shock is discussed in terms of the diagnostic criteria by MIRU, unique hemodynamic manifestations, infarct sizes and border zone extension, and potentially jeopardized myocardium in the remote areas. Reperfusion injury, i.e., reactive oxygen species (ROS), is noted as a double-edged sword. The importance of early revascularization by means of PCI, CABG, and IABP support is emphasized according to current guidelines. For innovative promise in the future, de novo development of collateral channels by growth factors and trials of stem cell implantation aimed at myocardial regeneration are introduced.     

急性心肌梗死后猪血清内皮型一氧化氮合酶的表达:体外低能震波物理能量的影响途径

背景:体外心脏震波治疗通过体外导入心肌的低能震波物理能量,使活体内血管再生因子及其受体表达上调,促进缺血组织的血管新生和加速侧支循环建立,但其具体作用机制尚不完全明确.目的:观察体外心脏震波治疗对急性心肌梗死后猪血清内皮型一氧化氮合酶水平的影响.方法:以冠脉左前降至远端栓塞法制作猪急性心肌梗死模型.造模后以抽签法随机分为2组:实验组于术后1,3,5 d接受3次体外心脏震波治疗,200击,点,共12点,能量为0.09 mJ/mm~2.以单纯心肌梗死为对照组.于术前,术后即刻、1 d、3 d、5 d、1周、2周、3周、4周采用酶联免疫反应方法检测血清内皮型一氧化氮合酶水平.结果与结论:实验组及对照组术后即刻血清内皮型一氧化氮合酶水平均较术前明显减少.实验组术后1 d接受体外心脏震波治疗后内皮型一氧化氮合酶表达开始升高,而对照组内皮型一氧化氮合酶呈下降趋势,说明实验组导入体内的超声波能量在心肌缺血局部产生了正性作用.第3次接受体外心脏震波治疗治疗后内皮型一氧化氮合酶表达达高峰,可持续两三周,第4周下降.对照组内皮型一氧化氮合酶随时间推移逐渐减少,两组间比较差异有非常显著性意义(P＜0.01).结果说明体外心脏震波可通过效地促进内皮型一氧化氮合酶表达治疗急性心肌梗死.     

IABP在急性心肌梗死并心源性休克救治中应用现状

急性心肌梗死作为临床上常见的疾病,起病急,易引起并发症,其中,心源性休克死亡率较高。临床上常规应用补液、扩血管、升压及溶栓、血管重建等。近年来,IABP被广泛应用于临床,它作为一种辅助装置可以增加血液灌流,降低心脏后负荷,降低心脏做功,从而快速改善循环灌注不足状态。本综述研究IABP作为血流动力辅助装置,应用于急性心肌梗死并发心源性休克患者的临床现状。     

Aortic counterpulsation in cardiogenic shock during acute myocardial infarction

Intra-aortic balloon counterpulsation is the most widely used form of mechanical hemodynamic support in the setting of cardiogenic shock due to ST-segment elevation myocardial infarction (STEMI). Intra-aortic balloon pump (IABP) is also strongly recommended (class 1b) in the current European guidelines for treatment of STEMI. The evidence of a possible benefit of IABP in this setting is based mainly on registry data and a few randomized trials. Cardiogenic shock and subsequent death due to STEMI result from three factors: hemodynamic deterioration, occurrence of multiorgan dysfunction and systemic inflammatory response. IABP does not cause an immediate improvement in blood pressure, but the recent SHOCK II trial shows positive effects on multiorgan dysfunction. Some experimental and clinical studies have indicated that IABP results in hemodynamic benefits as a result of afterload reduction and diastolic augmentation with improvement of coronary perfusion. However, the effect on cardiac output is modest and may not be sufficient to reduce mortality. Furthermore we can say that the use of IABP before coronary revascularization in the setting of STEMI complicated with cardiogenic shock may make the interventional procedure safer by improving left ventricular unloading. The purpose of the present review is to clarify the state of the art on this topic.     

腺苷后适应对糖尿病急性心肌梗死再灌注的保护作用

目的:观察经皮冠状动脉介入治疗(PCI)术中腺苷后适应对糖尿病急性心肌梗死(AMI)再灌注的保护作用。方法:将84例AMI患者按入选条件分为非糖尿病再灌注组(IR),非糖尿病腺苷后处理组(POST),糖尿病再灌注组(DIR),糖尿病腺苷后处理组(DPOST),糖尿病组按入院时所测糖化血红蛋白(HbA1c)值再分为DIR1(HbA1c<7%)、DIR2(HbA1c≥7%)、DPOST1(HbA1c<7%)、DPOST2(HbA1c≥7%)。POST及DPOST组于支架植入前静滴腺苷,IR及DIR组于支架植入前静滴等量生理盐水。检测PCI术前及术后30min冠脉血浆中的MDA、SOD及PCI术后6、12、24及48h静脉血CM-MB水平。结果:6组患者术后MDA值均较术前升高(P﹤0.01),SOD值均较术前降低(P﹤0.01);POST及DPOST组MDA值比IR及DIR组升高较少(P﹤0.05),SOD值比IR及DIR降低较少(P﹤0.05)。术后POST及DPOST组CK-MB峰值较IR及DIR组降低(P﹤0.05)。结论:糖尿病急性心肌梗死PCI治疗时应用腺苷后处理可以减轻心肌缺血再灌注损伤,起到心肌保护的作用。     

主动脉气囊反搏联合急诊经皮冠状动脉介入治疗急性心肌梗死合并心源性休克

目的研究主动脉气囊反搏（IABP）联合急诊经皮冠状动脉介入治疗（PCI）对急性心肌梗死合并心源性休克的疗效。方法比较36例患者急性心肌梗死合并心源性休克治疗前后的肺毛细血管楔压（PCWP）、心脏指数（CI）、中心静脉压（CVP）、平均动脉压（MAP）和每小时尿量变化。结果接受IABP联合PCI治疗后,患者的CVP、PCWP较治疗前明显降低,分别为（4．1±4．3）mmHgVS（10．4±6．8）mmHg,（10．5±7．1）mmHgVS（23．6±8．3）mmHg（P〈O．05）,而CI、MAP和每小时尿量均较治疗前明显增加,分别为（2．2±1．3）L·min-1·m-2 VS（1．3±0．9）L·min-1·m-2,（83．4±13．6）mm HgVS（56．8±15．2）mmHg,（44．5±14．9）ml／hVS（12．6±5．4）ml／h（P〈0．05）。结论对于急性心肌梗死并发心源性休克的患者,IABP联合急诊PCI治疗,疗效确切。这对不能开展急诊冠状动脉旁路手术的医院,IABP联合急诊PCI治疗具有特殊的临床意义。     

冠状静脉逆行灌注碱性成纤维细胞生长因子的体内浓度梯度

背景：体外研究发现,碱性成纤维细胞生长因子浓度梯度能够促进干细胞的迁移和增殖。然而,采用冠状静脉逆行灌注途径能否建立在体碱性成纤维细胞生长因子浓度梯度尚不明确。目的：评价冠状静脉逆行灌注实验方法的安全性,建立并检测冠状静脉与局部缺血心肌间的碱性成纤维细胞生长因子浓度梯度,探讨逆行灌注后碱性成纤维细胞生长因子浓度梯度存在的时间窗。方法：开胸结扎法建立犬急性心肌梗死模型,1周后经冠状静脉逆行灌注碱性成纤维细胞生长因子。灌注结束后球囊充盈时间分别为0,5,10,15min。解除球囊充盈后即刻处死动物,ELISA法测量血浆和梗死区心肌、梗死边缘区心肌组织匀浆中碱性成纤维细胞生长因子的浓度,在体评价在不同时间点冠状静脉血液与梗死区心肌以及梗死边缘区心肌之间的碱性成纤维细胞生长因子浓度梯度。结果与结论：逆行灌注成功率为100％,无死亡、心脏压塞和恶性心律失常等并发症发生。灌注后5min和10min,冠状静脉血液与梗死区心肌之间碱性成纤维细胞生长因子浓度的差异有显著性意义,梗死区心肌浓度明显高于其他2种组织。球囊充盈15min后2组之间浓度差异无显著性意义。结果表明,经冠状静脉逆行灌注碱性成纤维细胞生长因子后,球囊充盈的时间为5-10min能在冠状静脉血液与梗死心肌之间建立稳定的碱性成纤维细胞生长因子浓度梯度,而且在梗死心肌区域浓度最高。此时间窗内灌注干细胞有望增强其移行活力。     

体外心脏震波对急性心肌梗死模型猪左心室重塑的影响

背景:初期实验已经证实体外心脏震波治疗可从基因和细胞水平改善缺血心肌代谢,但是否在形态学水平也可缓解梗死后心室重塑的发展?目的:观察体外心脏震波对急性心肌梗死后左心室心功能及形态学指标的影响。方法:将25只猪随机分为3组:震波治疗组于制作心肌梗死模型后第3,5,7天,给予体外震波治疗,假震波组于制作心肌梗死模型后实施与震波治疗组相同的震波治疗操作,但不施以震波及能量,假手术组除了不造成心肌梗死,其余操作假震波组。结果与结论:与假震波组比较,震波治疗可明显缓解左室收缩末容积和舒张末容积扩大及改善左心室整体心功能(P<0.001),能显著改善心肌梗死交界区心肌局部室壁运动功能和左心室各节段运动协调性。说明及早有效的进行体外心脏震波治疗可在一定程度上延缓心肌梗死后左心室重塑由可逆阶段向不可逆阶段发展。     

主动脉内球囊反搏联合溶栓治疗急性心肌梗死并心源性休克的疗效分析

目的评估主动脉内球囊反搏(IABP)联合溶栓治疗急性心肌梗死(AMI)并心源性休克的疗效。方法收集2010年1月至2011年1月因AMI合并心源性休克入住我院行溶栓治疗的患者33例为研究对象,进行回顾性研究。根据患者是否接受IABP治疗,将患者分为治疗组和对照组,比较两组患者溶栓后的冠状动脉开通率、溶栓后2 h血流动力学指标、入院后8 h死亡率及院内死亡率。结果治疗组溶栓后冠状动脉开通率较对照组高,但差异无统计学意义(P>0.05);溶栓后治疗组的血流动力学指标均较对照组有明显改善,差异有统计学意义(P<0.05);治疗组入院8h死亡率及院内死亡率均较对照组明显降低,差异有统计学意义(P<0.05)。结论当AMI合并心源性休克时,尽早选择应用IABP联合溶栓治疗,将有助改善此类高危患者的临床预后。     

心肌梗死单个核细胞移植心肌运动的组织多普勒观察

目的：观察新生犬外周血单个核细胞心肌内移植对急性心肌梗死左室心肌运动的影响。方法：新生犬外周血单个核细胞经分离纯化后直接注射进入成年犬前壁心梗区域，对照组注射无血清培养基，分别应用组织多普勒技术（2．5MHz）分别检查术前，术后2d，术后30d心脏左室各部位心运动速度的变化。常规超声心动图检测射血分数，心输出量的变化。结果：术后2d两组均出现左室缺血区心肌运动速度下降，前壁增厚度率下降，左室其余各壁（室间隔除外）代偿性运动增强，二尖瓣侧壁运动显示左室收缩舒张功能降低无明显差别，心输出量，射血分数降低，术后30d，细胞移植组左室收缩舒张功能得以较好保持，左室运动改善，两组相比差别显著。结论：单个核细胞移植可以有效改善心肌梗死后左室心肌运动，有效维持心脏收缩及舒张功能。     

主动脉球囊反搏在急性心肌梗死所致的心源性休克和心脏破裂中的应用

目的 对采用主动脉内球囊反搏（IABP）治疗的心源性休克和心脏破裂病人的住院死亡情况进行回顾性分析。方法 对心源性休克和心脏破裂的28例病人，均安装IABP，其中20例进行了冠状动脉造影。13例接受了冠状动脉成形术（PTCA），冠脉旁路移植术（CABG）或心脏外科手术。结果 1例因急诊血管成形失败而行急诊CABG成功，11例急诊血管成形（直接PTCA）开通了梗死相关动脉（IRA），12例（42.9%)存活，16例死亡（57.1%)；11例因休克死亡；4例心脏破裂因没有手术干扰的时机死亡；1例游离壁破裂因心肌坏死面积过大死于手术台上；还有1例病人在出院7d后死于室颤，在所有无心脏破裂的心源性休克病人中，与接受PTCA和CABG的病人相比，未接受PTCA和CABG的病人的死亡率较高（81.8%vs16.7%)。所有心脏破裂的病人无一存活，死亡率100%。结论 使用IABP对于急性心肌梗死（AMI）所致的心源性休克有显著的效果。但仅使用IABP结合常规治疗而不开通IRA并不能提高这些病人的生存率。心脏破裂的病人若不能及时修补缺损，使用IABP仅能延长病人的存活时间。不能改善病人的生存率。