重视心电图在评价心肌灌注中的作用

急性心肌梗死（acute myocardial infarction,AMI）时早期再灌注治疗可挽救濒临坏死的缺血心肌,改善AMI患的预后,是AMI治疗史上的里程碑。然而,在实践中逐渐发现,约有20％～25％的AMI患梗死相关冠状动脉（IRA）的前向血流恢复到了TIMI3级,但其供血区心肌微循环却得不到充分灌注,表现为无血流（no-reflow）或低血流（low-flow）现象,心电图表现为抬高的ST段在IRA再通后无明显下降,     

急性心肌梗死的再灌注治疗进展

急性心肌梗死（AMI）是由于冠状动脉内粥样斑块破裂，急性闭塞导致前向血流中断，心肌因严重持久缺血而坏死。近20多年来，心血管临床工作者一直对急性心肌梗死的各种治疗方法进行客观的评价。大量的研究结果表明，只有迅速恢复梗死相关血管的有效前向血流，挽救濒死心肌，才能从根本上防止心肌重构和改善近远期预后。     

急性心肌梗死再灌注治疗后心肌组织灌注评价

急性心肌梗死（AMI）的再灌注治疗，包括急诊经皮冠状动脉（冠脉）介入治疗（PCI）和溶栓治疗，能使血栓性闭塞的冠脉迅速再通，恢复心肌再灌注，已成为治疗AMI的首选方法。然而，有研究发现冠脉再通后心肌再灌注可能并不完全、甚至无再灌注，称为心肌组织无再流（myocardial no-reflow），其发生率高达37％～43％。心肌无再流是发生于再灌注后逐渐发展的动态过程，其结果是心肌彻底坏死、梗死范围扩大，心室扩张和重构，心力衰竭和恶性心律失常的发生率增高，住院病死率增加5～10倍，严重影响AMI患者的预后。因此，实现心肌组织完全再灌注是现代AMI再灌注治疗的最重要目标和再灌注治疗后时代的研究重点，准确、有效地评价心肌组织灌注也已成为当今临床工作的重要任务，目前的评价方法包括以下几个方面。     

不同介入治疗方案选择对急性心肌梗死患者心功能及心肌组织灌注的影响

目的对接受急诊、易化、延迟介入治疗(PCI)的急诊心肌梗死(AMI)患者心功能及心肌组织血液灌注进行评价。探讨AMI患者行PCI最佳时机和方法。方法69例AMI患者分急诊PCI(A)、易化PCI(B)、延迟PCI(C)三组。术后7d、30d行超声心动图及99 mTc-甲氧基异丁基异晴(MIBI)心肌灌注断层显像(SPECT)评价近期心功能及心肌组织灌注,观察1年期间心血管事件的发生情况。结果(1)三组患者扩张后即刻造影结果管腔残余狭窄率<10%,手术成功率100%。(2)超声心动图30d时A、B两组左心室收缩、舒张末容积指数(LVESVI、LVEDVI)、左心室射血分数(LVEF)均优于C组(。3)SPECT显像放射性缺损面积(MIA),A、B两组低于C组,A、B两组心肌组织血流灌注均优于C组。结论(1)直接PCI、易化PCI可显著提高AMI患者的近期心肌组织血流灌注,缩小心肌梗死面积,保护心功能;(2)延迟PCI宜早期进行。     

急性心肌梗死再灌注后心肌无再流的评价和防治

急性心肌梗死（AMI）再灌注治疗包括溶栓、急诊经皮冠状动脉腔内介入术（PCI），其主要目标是：1．尽快开通梗死相关血管，缩短发病至开通时间；2．恢复心肌有效再灌注。然而，AMI冠状动脉再通恢复血供后，心肌组织再灌注并不完全、甚至无再灌注，称为心肌无再流现象（myocardial no-reflow phenomenon），发生率高达37％。     

心肌组织水平再灌注心电图的演变及机制研究进展

急性心肌梗死（AMI）是在冠状动脉病变的基础上发生的冠状动脉血供急剧减少或中断,使相应心肌严重而持久的急性缺血引起的任何面积大小的心肌细胞的坏死,是常见的心血管急危重症.既往WHO定义的急性心肌梗死的诊断标准包括缺血症状、心电图动态改变和血清心肌坏死标志物变化.目前,根据心电图有无ST段抬高将心肌梗死分为ST段抬高型心肌梗死和非ST段抬高型心肌梗死.诊断心肌梗死时,心肌坏死标志物通常于发病2～4小时后出现,而对于ST段抬高型心肌梗死,发病早期即可出现心电图的改变.心电图作为临床常规检查对急性心肌梗死的诊断及再灌注的判断具有简单、快捷、方便、直观的优点,对于ST段抬高型心肌梗死的诊断及再灌注的评价有着极其重要的作用.本文就ST段抬高型心肌梗死心肌组织水平再灌注心电图的演变及其可能的机制加以阐述.     

急性心肌梗死再灌注治疗中的心肌保护

早期再灌注治疗是治疗急性心肌梗死(AMI)最为重要的手段,可以明显减少心脏事件并降低死亡率.但是再灌注却是一把双刃剑,一方面使缺血心肌重获血供,挽救了缺血心肌,但另一方面又产生再灌注损伤,加重了对心肌和内皮细胞损伤,继而可造成无再流、心律失常、心肌顿抑或死亡,使再灌注治疗的效果大打折扣.     

从急性心肌梗死治疗指南看再灌注治疗策略的选择

急性ST段抬高心肌梗死（STEMI）发病是由于斑块破裂，继之血栓形成，血管急性闭塞而引起的，而血管闭塞以后心肌坏死有一个从心外膜向心内膜进展的过程，通常需6h以上方发生全层透壁性坏死。动物试验及临床研究均已证明，如果在该时间窗口内使闭塞冠状动脉再通，可明显缩小心肌梗死面积，并改善心功能。20世纪80代以来，急性心肌梗死（AMI）治疗进入了再灌注治疗的年代。     

急性心肌梗死心肌再灌注评价技术的临床应用

急性心肌梗死(acute myocardial infarction,AMI)再灌注治疗的目标是实现梗死相关血管的心外膜下血流再通,并达到心肌组织水平的充分再灌注[1,2]。心肌组织水平再灌注不良会影响AMI患者的心脏功能恢复及预后。相当一部分AMI患者     

急性心肌梗死心肌组织再灌注评价方法

急性心肌梗死后心肌组织再灌注程度与左心室功能和临床预后密切相关,因此,及时、准确的评估心肌梗死后心肌组织灌注水平对患者有着重要的意义.现就评价心肌组织再灌注的方法及应用做一综述.     

Usefulness of real-time myocardial perfusion imaging to evaluate tissue level reperfusion in patients with non-ST-elevation myocardial infarction

Microvascular integrity is a prequisite for functional recovery in patients who have myocardial infarction after recanalization of the infarct-related coronary artery. In this study, we investigated whether impaired myocardial perfusion is present in patients who have non-ST-elevation myocardial infarction and whether the extent and time course of myocardial tissue reperfusion as assessed by myocardial contrast echocardiography (MCE) are related to functional recovery. Consecutive patients (n = 32) who presented with a first non-ST-elevation myocardial infarction were included in our study. MCE was performed on admission, 1 to 4 hours after angioplasty, and at 24 hours, 4 days, and 4 weeks of follow-up. Contrast images were analyzed visually and quantitatively. Myocardial blood flow was estimated by calculating the product of peak signal intensity and the slope of signal intensity increase. Improvement of wall motion on follow-up echocardiograms after 4 weeks served as a reference for functional recovery of impaired left ventricular function. Of 496 segments available for analysis, 128 (26%) were initially dysfunctional and 96 (75%) recovered at 4 weeks of follow-up. Myocardial tissue reperfusion occurred gradually, expanding over the first 24 hours after percutaneous coronary intervention (myocardial blood flow of 0.4 +/- 0.3 initially, 0.6 +/- 0.4 at 24 hours, and 1.6 +/- 0.7 dB/s at 4 weeks of follow-up, p <0.001). Extent of tissue reperfusion was closely related to grade of improvement of global ejection fraction (r2 = 0.76, p <0.001). MCE predicted functional recovery with a sensitivity of 81%, a specificity of 88%, and accuracy of 83% on a segmental level. Thus, impaired microvascular integrity is suggested by MCE in patients who present with non-ST-elevation myocardial infarction. Improvement of regional tissue perfusion after revascularization is closely related to functional recovery. This information may aid risk stratification and allow monitoring of the effectiveness of reperfusion therapy in these patients.     

心肌缺血/再灌损伤时TXNIP表达水平升高并增加心肌自噬

目的 探讨心肌缺血/再灌注（MI/R）时硫氧还蛋白相互结合蛋白（TXNIP）表达及对心肌细胞自噬水平的影响。 方法 构建TXNIP敲除鼠及TXNIP过表达小鼠,制作上述小鼠MI/R模型,观察MI/R后心肌TXNIP表达水平是否与心肌损伤及自噬有关。 结果 与假手术组（Sham）小鼠相比,小鼠心肌TXNIP表达水平在缺血及再灌注损伤过程中持续升高（P<0.01）。在小鼠MI/R后,心脏超声证实与野生型（WT）小鼠相比,TXNIP过表达小鼠LVEF（%）值更低（P<0.05）;伊文氏蓝/TTC染色同样证实TXNIP过表达小鼠心肌梗死面积更大（P<0.05）。而TXNIP敲除鼠MI/R后心脏LVEF（%）值（P<0.05）及心肌梗死面积（P<0.05）均较WT小鼠显著减轻。通过免疫印迹（LC3Ⅱ/LC3I及P62表达）及电子显微镜观察自噬小体检测发现,相比WT小鼠,TXNIP敲除小鼠心肌自噬程度更轻（P<0.05）,TXNIP过表达小鼠则心肌自噬程度更重（P<0.05）。 结论 上述结果证实了在MI/R后TXNIP升高导致心脏功能的降低,心肌梗死面积的增加及心肌细胞自噬的增多。     

Effect of reactive hyperemia after coronary recanalization on myocardial tissue reperfusion by thrombolysis in myocardial infarction flow grade in acute myocardial infarction

Thrombolysis In Myocardial Infarction (TIMI) flow grade is widely used to evaluate myocardial tissue reperfusion in acute myocardial infarction (AMI), but the current grading system is incomplete. Therefore, we clarified the regulation of epicardial coronary flow velocity with the progression of microvascular dysfunction in AMI. We studied 36 patients with first anterior AMI. After intervention, we assessed TIMI flow grade and measured average peak velocity (APV) at baseline and after infusion of adenosine triphosphate (48 microg; baseline and hyperemic APVs, respectively) with a Doppler guidewire. We performed myocardial contrast echocardiography after 2 weeks to assess microvascular integrity (good reflow vs no reflow) and left ventriculography at admission and discharge (24 +/- 2 days) to measure regional wall motion (SD/chord). Patients were classified into 3 groups based on TIMI flow grade and microvascular integrity: TIMI grade 3 flow/good reflow (n = 16), TIMI grade 3 flow/no reflow (n = 12), and TIMI grade 2 flow (n = 8). Baseline APV was comparable in the patients with TIMI grade 3 flow but hyperemic APV was higher in patients with TIMI grade 3 flow/good reflow than in those with TIMI grade 3 flow/no reflow (hyperemic APV 59.3 +/- 25.8 vs 32.8 +/- 8.9 cm/s, p <0.01). All patients with TIMI grade 2 flow showed no reflow and the lowest values of baseline and hyperemic APVs. Regional wall motion at discharge was higher in patients with TIMI grade 3 flow/good reflow than in those with TIMI grade 3 flow/no reflow and TIMI grade 2 flow (-1.44 +/- 0.70, -2.69 +/- 0.31, and -2.88 +/- 0.48 SD/chord, respectively, p <0.01). In conclusion, compensatory reactive hyperemia preserves epicardial coronary flow velocity even in patients with microvascular damage, and with the progression of damage, this compensatory hyperemia can no longer preserve epicardial coronary flow velocity, and baseline APV is decreased in TIMI grade 2 flow.     

老年急性ST段抬高心肌梗死急诊介入治疗后心肌组织水平再灌注不良的发生率及其对临床预后的影响

目的探讨老年急性心肌梗死（acute myocardial infarction,AMI）-急诊经皮冠状动脉介入（percutaneous coronary intervention,PCI）治疗后心肌组织水平再灌注状态不良的发生率及其对近、远期临床预后的影响。方法回顾性收集398例老年急性ST段抬高心肌梗死（ST-elevationmyocardi-alinfarction,STEMI）行急诊PCI治疗患者的临床资料、冠状动脉造影资料与心电图,以ST段回落程度与TIMI心肌灌注（TIMIMyocardialPerfusion,TMP）分级等指标评估心肌组织水平再灌注状态,患者分为4组,A组为ST段回落率〉50%并且术后TMP分级为Ⅲ级;B组为ST段回落率〈50%而术后TMP分级=Ⅲ级;C组为术后TMP分级≤Ⅱ级而ST段回落率〉50%;D组为ST段回落率〈50%并且术后TMP分级≤Ⅱ级。分析心肌组织水平再灌注不良患者的发生率及其对近远期预后的影响。结果 STEMI急诊PCI术后梗死相关血管（infarctionrelatedartery,IRA）前向血流达到TIMIⅢ级而TMP分级为Ⅱ级以下者占37.2%,心电图ST段回落小于50%者占37.2%,均接近1/3。12.5%的患者具有远端栓塞。术后ST段回落率〉50%并且TMP分级为Ⅲ级者占总人数的39.8%,ST段回落率〈50%,并且术后TMP分级≤Ⅱ级占总人数的14.3%。心肌组织灌注状态不良者与心肌组织灌注状态良好者相比平均住院日更长,左室EF值更低,梗死后心绞痛发生率更高,远端栓塞发生率更高,IABP辅助应用比率更大,心功能恶化、心脏性死亡更高。与D组相比,随访期间MACE的发生风险在C组为43%（P=0.11）,在B组为24%（P〈0.01）,在A组为2.7%（P〈0.01）。结论老年急性心肌梗死行急诊PCI治疗后IRA再通者仅有不到40%的患者其心肌组织水平得到了良好的再灌注,其近、远期预后较好,而剩余约60%的患者其心肌组织水平存在不同程度的再灌注障碍,其中有大概约超过10%的患者其心肌组织水平存在较差的再灌注状态,这些患者在住院期间以及远期随访期间有着极高的MACE发生风险。     

The case for early direct myocardial reperfusion

The treatment of choice, in Des Moines, Iowa for evolving myocardial infarction, is emergency reperfusion by medical or surgical means that are appropriate to the individual patient. If the patient exhibits clinical evidence of continuing evolution at any time distance from the onset of chest pain, cardiac catheterization is done immediately. With single vessel disease, streptokinase lysis is attempted and augmented when necessary by percutaneous transluminal coronary angioplasty. If multiple vessel disease is present, surgical intervention is carried out immediately. As mentioned above, time is not a predictor as to the final outcome whereas the endocardial ventricular architecture correlates well with wall motion recovery. This therapeutic protocol has resulted in an overall mortality rate of 3.5% in patients with evolving myocardial infarction. As mentioned above, all deaths occurred in the patients who were in cardiogenic shock before therapy, and all other 303 patients with evolving myocardial infarction recovered. We certainly do not discourage controlled clinical trials, utilizing these and other techniques, but do encourage you to adopt reperfusion as the primary therapy for evolving myocardial infarction for your patients.     

Effects of electroacupuncture at different time during reperfusion on the expression of Bcl-2and Beclin1 in myocardial tissue in rats with myocardial ischemia reperfusion injury

<正>Objective To compare the effects of electroacupuncture (EA) at different time during reperfusion on the expression of autophagy-related protein Bcl-2 and Beclin1in myocardial tissue in rats with myocardial ischemia reperfusion injury (MIRI),and to explore the autophagy-related mechanism of EA on protecting MIRI. Methods A total of 72 SD rats were randomly divided into a     

Pathophysiology of myocardial reperfusion

The feasibility of myocardial reperfusion is established. However, restoring patency to epicardial coronary arteries does not necessarily signify restoration of tissue perfusion or restoration of biochemical or mechanical function to the heart muscle previously supplied by the occluded vessel. This review examines the biochemical, functional, and histopathologic changes associated with myocardial reperfusion in an attempt to define the constraints within which reperfusion may lead to optimal recovery of myocardium, and to explore future possibilities for maximizing benefits of reperfusion while minimizing potential reperfusion injury.