急性心肌梗死合并心原性休克患者的血运重建治疗

心源性休克是急性心肌梗死患者最严重的并发症。虽然已经有了多种药物治疗、综合的监护管理以及先进的器械辅助，但急性心肌梗死合并心源性休克患者依旧保持着较高的死亡率。多项研究表明，尽早进行血运重建治疗是目前唯一可以明显改善急性心肌梗死合并心源性休克患者预后的治疗措施。因此尽早进行血运重建治疗是急性心肌梗死合并心源性休克患者治疗中最重要的一环。该文综述了其研究进展。     

直接经皮冠脉介入治疗在抢救急性心肌梗死合并心源性休克中的应用

目的探讨急性心肌梗死合并心源性休克的抢救方法。方法用急诊直接经皮冠脉介入治疗(PCI)治疗意大利波洛尼亚大学附属医院2001—2002年收治的15例急性心肌梗死合并心源性休克患者。结果15例患者中,共有13例抢救成功。结论急诊PCI是治疗急性心肌梗死合并心源性休克的有效方法。     

心源性休克的机制与治疗进展

近年来随着经皮冠状动脉介入治疗的发展,急性心肌梗死患者预后明显改善,然而心源性休克的发生及其预后却无很大的改变。不可逆的泵衰竭引起循环衰竭和重要器官灌注减少是患者死亡的重要原因,尽管治疗方法不断改进,急性心肌梗死并发心源性休克仍然有较高的病死率。急性心肌梗死后早期血运重建可防止心源性休克的发生,发生心源性休克后早期血运重建可改善患者的预后。     

心源性休克的机制与治疗进展

近年来随着经皮冠状动脉介入治疗的发展,急性心肌梗死患者预后明显改善,然而心源性休克的发生及其预后却无很大的改变.不可逆的泵衰竭引起循环衰竭和重要器官灌注减少是患者死亡的重要原因,尽管治疗方法不断改进,急性心肌梗死并发心源性休克仍然有较高的病死率.急性心肌梗死后早期血运重建可防止心源性休克的发生,发生心源性休克后早期血运重建可改善患者的预后.     

急性心肌梗死合并心源性休克的临床诊断及治疗进展

在当今经皮冠状动脉介入术治疗时代,心源性休克是急性心肌梗死患者的主要并发症和首要死亡原因。随着经皮冠状动脉介入术治疗的快速发展和广泛应用,ST段抬高型心肌梗死患者住院病死率已经显著下降到大约5%,然而急性心肌梗死合并心源性休克患者住院期间病死率仍超过50%。此外,机械辅助循环装置的不断更新出现虽然可以改善血流动力学状态,但未能降低心源性休克患者的远期病死率。如何抢救治疗心源性休克是心血管介入医生面临的一大挑战。现主要就急性心肌梗死合并心源性休克的病因、诊断及治疗进展做一归纳综述。     

急性心肌梗死合并心源性休克的急救处理

目的分析急性心肌梗死合并心源性休克的急救处理。方法选取2014年6月—2016年6月乐山市人民医院收治的急性心肌梗死合并心源性休克患者40例,均给予急救处理。结果 40例患者抢救成功36例,抢救成功率为90.0%。结论急性心肌梗死合并心源性休克患者抢救能否成功关键是早期诊断,并且给予不同原因的患者进行相应的抢救。     

急性心肌梗死并发心源性休克的治疗进展

心源性休克是急性心肌梗死的严重并发症,是急性心肌梗死患者早期死亡的最主要原因。再灌注治疗,结合药物及辅助装置可显著改善患者预后。现总结了近年国内外的相关研究,对急性心肌梗死并发心源性休克的诊断及治疗进展做一综述。     

主动脉内气囊反搏支持治疗急性心肌梗死合并心源性休克的护理

目的探讨急性心肌梗死合并心源性休克患者行主动脉内气囊反搏(intra-aortic balloon pump,IABP)支持治疗的术后护理程序和注意事项。方法回顾性分析2007年1月至2008年12月间20例急性心肌梗死合并心源性休克患者行IABP支持治疗的术后护理资料。结果通过精心、系统的护理,急性心肌梗死合并心源性休克患者行IABP支持治疗后均恢复良好,顺利出院。结论落实系统的护理程序,是保证急性心肌梗死合并心源性休克患者行IABP支持治疗后恢复的关键措施和重要手段。     

老年急性ST段抬高心肌梗死合并心源性休克患者主动脉内球囊反搏辅助下经皮冠状动脉介入治疗的护理体会

心源性休克是急性心肌梗死的严重并发症之一，老年急性ST段抬高心肌梗死（ST—elevatedmyocardialinfarction，STEMI）合并心源性休克是临床上的高危人群，内科药物治疗效果差，病死率通常在90％以上。     

急重症诊治(1)--心源性休克的诊治经验

心源性休克是指因心脏功能严重受损而引起的休克综合征。它可以是严重的心律失常及任何心脏病的末期表现 ,但急性心肌梗死是引起心源性休克最常见的病因。1　心源性休克常见病因引起心源性休克的“心泵功能不全” ,其原因大致分为心输出不全型和心室充盈不全型。主要病因是心肌梗死、心肌炎 ;还可继发于心包填塞、心肌病及原发性肺动脉高压等。因急性心肌梗死 (AMI)致 4 0 %以上心室肌失去功能 (包括梗死及严重缺血的濒危心肌 )时则发生休克 ,AMI所致的心源性休克占全部心源性休克 80 %以上。心源性休克相当于Kil lip分类的 4型 ,病死率…     

Cardiogenic shock complicating acute myocardial infarction--a review

Cardiogenic shock is characterized by inadequate tissue perfusion due to cardiac dysfunction and is the leading cause of death in patients hospitalized with acute myocardial infarction. Mortality from cardiogenic shock still remains high. The development of cardiogenic shock is rarely unexpected; most patients who develop cardiogenic shock do so within 48 hrs of admission, with only 10% shocked on arrival. Mortality rate is exceedingly high and reaches 70-80% in those treated conservatively. Early revascularization is the cornerstone treatment of acute myocardial infarction complicated by cardiogenic shock. According to the guidelines, revascularization is effective up to 36 hours after the onset of cardiogenic shock and performed within 18 hours after the diagnosis of cardiogenic shock. Primary percutaneous coronary intervention is the most efficient therapy to restore coronary flow in the infarct-related artery. However, invasive strategy in a developing country like ours is not only costly but also technically demanding. We present a case of acute myocardial infarction complicated with cardiogenic shock that underwent primary percutaneous coronary intervention and also review the incidence, pathophysiology, management and outcome of cardiogenic shock complicating acute myocardial infarction.     

Cardiogenic shock complicating acute coronary syndromes

Cardiogenic shock remains the major cause of death among patients with all types of acute coronary syndromes. Thus, there is a growing interest in the identification of patients who are at risk for developing cardiogenic shock, in the exploration of different therapeutic approaches to preventing its development, and in the improvement of outcome when it occurs. This article reviews the aetiology and pathophysiology of cardiogenic shock, its epidemiology, its treatment (including pharmaceutical agents, counterpulsation, and revascularisation), and its outcome. Algorithms are presented that predict its occurrence in both ST-segment-elevation myocardial infarction and unstable angina or non-ST-elevation myocardial infarction, and that predict its mortality in patients with ST-segment-elevation acute myocardial infarction. Such new areas as metabolic therapy and glycoprotein IIb/IIIa inhibitors are discussed, as are the economic implications of shock.     

Thrombolysis in acute myocardial infarction complicated by cardiogenic shock

The adverse impact of the development of cardiogenic shock in the setting of acute myocardial infarction was first described by Killip and Kimball in 1967. While the inhospital mortality rate in patients with myocardial infarction and no evidence of heart failure was only 6%, the mortality rate in those patients who developed cardiogenic shock was 81%. Despite advances in cardiovascular care and therapy since that initial report, including universal institution of cardiac care units, advances in hemodynamic monitoring, new inotropic and vasodilating agents, and even increasing utilization of thrornbolytic therapy, the mortality from acute myocardial infarction, when complicated by cardiogenic shock, remains disturbingly high, and cardiogenic shock remains the leading cause of death of hospitalized patients following acute myocardial infarction.The grave prognosis associated with this condition has resulted in increased interest in potential therapeutic interventions, particularly in the area of reperfusion therapy. Several studies suggest that, in contrast to the beneficial effects of thrombolytic therapy in most patient populations suffering acute myocardial infarction, mortality rates are not decreased in those patients with cardiogenic shock at the time of lytic administration. Thrombolytic administration does, however, appear to lead to a modest reduction in the percent of patients with myocardial infarction who will subsequently develop cardiogenic shock during hospitalization.Reperfusion rates with lytic therapy in patients with cardiogenic shock are disappointingly low, in the range of 42–48%, significantly lower than those achieved in patients without cardiogenic shock. These low perfusion rates may, in part, be explained by decreased coronary blood flow and perfusion pressure in patients with left ventricular pump failure.Although promising as adjunctive therapy, it is unclear whether institution of balloon counterpulsation has any long-term benefit in patients with cardiogenic shock treated with thrombolytic therapy. Whether other or additional interventions, such as coronary angioplasty and coronary artery bypass graft (CABG), decrease mortality rates in patients with cardiogenic shock remains to be determined.     

Experiences with laser therapy in acute myocardial infarct

Our clinical and instrumental investigations showed that invasive laser therapy has a multiple therapeutic effect. Acting favourably on principal pathogenetic mechanisms of acute myocardial infarction, it decreases the pain syndrome, normalize electrical instability of the heart, limits myocardial ischemic damage area and accelerates scarring process. It leads to a decrease in mortality and in the incidence of severe complications of myocardial infarction such as ventricular fibrillation, cardiogenic shock, cardiac insufficiency. Thus, the new method of treating acute myocardial infarction with He-Ne laser irradiation significantly enhances treatment efficacy, improves the course and prognosis of myocardial infarction.     

Acute left main coronary artery occlusion. Survival following emergent coronary bypass

Emergent aortocoronary bypass surgery for acute myocardial infarction is controversial. We describe a patient with total occlusion of the left main coronary artery associated with acute anterior wall infarction and refractory cardiogenic shock. The patient underwent successful emergent coronary bypass surgery to manage refractory cardiogenic shock. He has subsequently experienced a prolonged survival (60 months postsurgery). This report suggests that emergent aortocoronary bypass surgery should be considered in patients with acute myocardial infarction with refractory cardiogenic shock in whom other forms of reperfusion are unsuccessful.     

Outcomes of Acute Myocardial Infarction in Patients with Influenza and Other Viral Respiratory Infections

BackgroundAcute influenza infection can trigger acute myocardial infarction, however, outcome of patients with acute myocardial infarction during influenza infection is largely unknown.MethodsPatients ≥ 18 years old with ST-elevation and non-ST-elevation myocardial infarction during January 2013-December 2014 were identified using the National Inpatient Sample. The clinical outcomes were compared among patients who had no respiratory infection to the ones with influenza and other viral respiratory infections using propensity score-matched analysis.ResultsOf 1,884,985 admissions for acute myocardial infarction, acute influenza and other viral infections were diagnosed in 9,885 and 11,485 patients, respectively, accounting for 1.1% of patients. Acute myocardial infarction patients with concomitant influenza infection had a worse outcome than those with acute myocardial infarction alone, in terms of in-hospital case fatality rate, development of shock, acute respiratory failure, acute kidney injury, and higher rate of blood transfusion after propensity scores. The length of stay is also significantly longer in influenza patients with acute myocardial infarction, compared with patients with acute myocardial infarction alone. However, patients who developed acute myocardial infarction during other viral respiratory infection have a higher rate of acute respiratory failure but overall lower mortality rate, and are less likely to develop shock or require blood transfusion after propensity match. Despite presenting with acute myocardial infarction, less than one-fourth of patients with concomitant influenza infection underwent coronary angiography, but more than half (51.4%) required revascularization.ConclusionInfluenza infection is associated with worse outcomes in acute myocardial infarction patients, and patients were less likely to receive further evaluation with invasive coronary angiography.     

Cardiogenic shock due to dynamic left ventricular outflow tract obstruction as a mechanical complication of acute myocardial infarction

We report the clinical case of a 77-years-old woman with cardiogenic shock caused by dynamic left ventricular outflow tract (LVOT) obstruction that appeared after anterior acute myocardial infarction. Dynamic LVOT obstruction has been reported in various circumstances aside from hypertrophic obstructive cardiomyopathy, such as acute myocardial infarction. In a patient with cardiogenic shock and a heart murmur after acute myocardial infarction, an acute mechanical complication, ventricular septal defect, and acute mitral regurgitation must be ruled out because the treatment of these conditions differs completely. We describe the diagnostic and therapeutic measures used in the diagnosis and treatment of this complication.     

血清热休克蛋白70与急性心肌梗死后心力衰竭的相关性

血清热休克蛋白70是一种高度保守的分子蛋白,其在应激时总被高度诱导。研究发现在动脉粥样硬化斑块中有热休克蛋白70的表达,且抗原递呈细胞也高度激活。热休克蛋白70与冠心病密切相关,且与冠状动脉病变程度有关,新近国外研究报道,热休克蛋白70在急性心肌梗死后心力衰竭患者中高度表达。现综述热休克蛋白70与急性心肌梗死后心力衰竭的相关性,热休克蛋白70有望成为急性心肌梗死后心力衰竭的新诊断标记物及判断病情的重要指标。     

Free-radical lipid peroxidation in acute myocardial infarction complicated by cardiogenic shock

The pattern of variation in primary and end products of erythrocyte lipid peroxidation (LPO) was examined in 131 patients with acute myocardial infarction. The levels of LPO products were found to be increased dramatically, the magnitude and duration of the increase being dependent on the severity of cardiogenic shock complicating myocardial infarction. The changes were particularly marked in true cardiogenic shock. The level of LPO products fell significantly on day 2-3 of myocardial infarction where it stabilized until the end of the study in patients with uncomplicated infarction treated with alpha-tocopherol acetate in addition to a symptomatic therapy. This pattern is attributed to an inhibitory effect this antioxidant may have on LPO.