Magnesium, acute myocardial infarction and reperfusion injury

Coronary artery disease (CAD) ranks top with respect to morbidity and mortality in humans. Development of high-tech diagnostic and therapeutic strategies has greatly improved the prognosis of CAD and acute myocardial infarction (AMI) over the past decade. Data from experimental and clinical research have provided important information on the role of magnesium in CAD and AMI. In relation to duration and severity of CAD, an adrenaline induced systemic stress arises, which provokes enhanced magnesium requirements, because magnesium is the co-factor in ATP dependent myocardial metabolism. The success of pharmacological or mechanical intervention in AMI can be compromised by reperfusion injury, which is probably caused by myocardial calcium accumulation. Since magnesium blocks myocardial calcium influx, reperfusion injury might be diminished or even prevented by magnesium application. Thus, the common procedure of invasive cardiac intervention and intravenous magnesium administration before reperfusion could become the gold standard in treatment of AMI.     

Mechanical complications of acute myocardial infarction

Rupture of the left ventricular myocardium during the course of an acute myocardial infarction may affect the free wall, the interventricular septum, or the papillary muscles. When a rupture occurs, it is referred to as a mechanical complication of acute myocardial infarction. All mechanical complications may lead to cardiogenic shock. However, the location of the rupture can often be suspected clinically. To confirm the diagnosis, echocardiography must be performed. Since the advent of thrombolytic therapy and percutaneous coronary intervention, the incidence of mechanical complications has declined. Even though mortality remains high, their recognition is important since survivors may have an excellent long-term prognosis. The cases convey two main messages: 1) Mechanical complications must be carefully searched for in any patient with an acute coronary syndrome and signs of cardiogenic shock and/or a systolic murmur. 2) Aggressive and timely medical and surgical treatment should be provided even though in a substantial proportion of these patients prognosis may be dismal.     

The endogenous cardioprotection during reperfusion in acute myocardial infarction

A prompt primary percutaneous coronary intervention with aspiration thrombectomy and subsequent stent implantation at the culprit lesion combined with optimal anti-platelet and anti-thrombotic pharmacotherapy is the safest and most effective reperfusion strategy. Unfortunately, this therapy does not guarantee always a good, long-term clinical outcome and left ventricular function recovery. Despite the unquestionable benefit of reperfusion, we have evidence that its initial phase leads to additional damage at the area at risk, so the final effect is the compromise between benefits and destruction, which come with the reperfusion wavefront. Experimental studies suggest that postconditioning with several very brief cycles of ischaemia alternating with reperfusion applied immediately after relief of a prolonged epicardial occlusion is associated with the infarct size limitation. The cellular protective effect of postconditioning seems to be related to prevention of mitochondrial permeability transition pore activation. We have still to wait for confirmation of the clinical effectiveness of both postconditionig as well as pharmacotherapy that mimics postconditioning effects (e.g. with cyclosporine) in a randomised, multicenter clinical trial with properly designed endpoint. To date, most clinically tested agents that induced endogenous cardioprotection such as adenosine, erythropoietin, protein kinase C-δ inhibitor, atrial natriuretic peptide, atorvastatin and nicorandil were failed to reduce infarct size. Time will tell whether postconditioning and therapy that it mimics meet expectation and find place in the recommendations concerning management of acute myocardial infarction. Kardiol Pol 2011; 69, supl. III: 67-74.     

通心络对急性心肌梗死患者再灌注后心肌和微血管的保护性研究

目的观察通心络胶囊对急性心肌梗死(AMI)接受经皮冠状动脉介入治疗(PCI)或溶栓治疗后患者心肌和微血管保护作用和可能产生的机制。方法对我院收治的ST段抬高的AMI患者,成功实施PCI或溶栓治疗的患者,随机分为常规药物治疗作为对照组(52例)和同时加服用通心络胶囊的治疗组(60例)。于发病后不同时间连续观察多普勒二维超声心动图(2DE)的室壁异常节段恢复状态、左室舒张末容积(LVEDV)、左室射血分数(LVEF)改变,并于6个月时与同位素心肌显像结果进行对照分析。结果冠状动脉血管重建后(1)在通心络组中,1周、2周和1个月时异常室壁运动节段恢复率(分别为11.7%,18.1%和18.8%)较对照组明显高(分别为4.1%,8.3%和11.1%)(均P<0.05);6个月时通心络组的总恢复率高达70.0%,也明显高于对照组的51.7%。(2)1周、2周和1个月时通心络组LVEDV与对照组容积增加比率相当(均P>0.05);3个月和6个月时通心络组LVEDV增加比率较对照组明显降低(均P<0.01)。(3)治疗初,通心络组LVEF与对照组相当(P>0.05);治疗后1周、2周和1个月时两组间差异无统计学意义(均P>0.05);3个月时和6个月时,通心络组恢复明显高于对照组(P<0.01和0.05)。(4)2DE的左心室室壁节段运动评分指数(WMSI)治疗初通心络组与对照组间差异无统计学意义(P>0.05);6个月时,通心     

Multimodality reperfusion therapy for acute myocardial infarction

With the strong and direct relation between early reperfusion in acute myocardial infarction (AMI) and improved clinical outcomes, attention has focused on new means of improving rates of reperfusion and accelerating every stage of AMI evaluation and management, from the onset of symptoms of myocardial infarction to the achievement of reperfusion. Critical pathways to streamline the evaluation and management of AMI have cut minutes and even hours off in-hospital treatment times for patients with AMI; public health initiatives focus on educational efforts to shorten time to hospital arrival. The latest advance in fibrinolytic therapy is the availability of bolus fibrinolytic agents with safety and efficacy in large phase III trials comparable to accelerated intravenous infusion regimens. Faster and simpler fibrinolytic regimens may shorten door-to-needle time, reduce medication errors, and facilitate prehospital thrombolysis. Bolus fibrinolytic agents are being evaluated for use in combination with other interventions to open occluded coronary arteries, including acute percutaneous coronary intervention, the glycoprotein IIb/IIIa platelet inhibitors, or both. The goal of this "multimodality" approach to AMI management is to minimize time to reperfusion and maximize the percentage of patients who achieve complete arterial patency and myocardial perfusion without bleeding complications.     

Reperfusion and reperfusion injury in acute myocardial infarction

Recognition of the clinical markers of reperfusion and comprehension of the effects of reperfusion injury in acute myocardial infarction provide a unique challenge for today's critical care nurse. In this article we will explore the processes of reperfusion injury. A review of relevant literature and presentation of a clinical case study and care plan will enable the critical care nurse to construct a larger knowledge base and assist in the nursing management of patients with acute myocardial infarction. Evaluation and treatment of reperfusion and reperfusion injury remains under investigation, but through the skills of assessment, planning, and intervention the critical care nurse can coordinate prompt and appropriate care to the patient with an acute myocardial infarction.     

The surgical complications of acute myocardial infarction: Color Doppler evaluation

Summary Two-dimensional echocardiography in combination with Doppler and color Doppler flow mapping is now considered the technique of choice for the early diagnosis and assessment of the surgical complications of acute myocardial infarction. It has the advantage of being a rapid, safe technique with ease of portability and repeatability, at relatively low cost. Transesophageal echocardiography may provide an alternative window for imaging cardiac structure and function, but as yet its value in the diagnosis of the complications of myocardial function is not proven.In the acute phase, color Doppler flow mapping can diagnose the cause of hemodynamic deterioration by distinguishing primary pump failure from the mechanical complications such as ventricular septal rupture or papillary muscle rupture. In the subacute phase, complications including left ventricular true and false aneurysms may be detected and this information allows optimal management decisions to be made. Thus, color Doppler flow mapping has become an indispensable technique in the coronary care unit. It provides a complete picture of cardiac structure and function making it superior to other methods in the clinical situation of an acute myocardial infarction which has such a volatile and unpredictable course.     

Early definition of treatment outcomes after reperfusion therapy for myocardial infarction

AIMS: Early definition of treatment outcomes, including coronary patency and infarct size, after reperfusion therapy for myocardial infarction (MI) is desirable to identify patients requiring further intervention. METHODS AND RESULTS: Patients receiving reperfusion therapy for a first MI had continuous 12-lead ST segment monitoring to document reperfusion and ischaemia time. Infarct size was measured by 12-lead QRS score and radionuclide scintigraphy ((201)Tl single-photon emission computed tomography, SPECT) at 1 week, and left ventricular function by echocardiography at 1 week and 1 month. Resolution of ST elevation accurately detected TIMI 2 or 3 reperfusion (predictive accuracy 93%) in 55 patients undergoing immediate angioplasty, but ST recovery was delayed (17+/-14min) after angiographic reperfusion. A multivariate model, including risk region and ischaemia time, accurately predicted MI size (R(2)=0.80, P<0.00001) in these patients. The same model, prospectively applied on Day 1 to 154 patients receiving thrombolytic therapy, accurately predicted MI size, measured by QRS score (R(2)=0.88, P<0.0000001) and (201)Tl SPECT (R(2)=0.75, P<0.000001) at 1 week for individual patients. Regional myocardial wall motion at 1 month was directly correlated with MI size predicted by the model on Day 1 (r=0.73, P<0.0001). CONCLUSIONS: Use of ST segment monitoring during reperfusion therapy facilitates early prediction of treatment outcomes, including coronary reperfusion, infarct size and ventricular function.     

Renin and the complications of acute myocardial infarction

To determine whether plasma renin activity in addition to catecholamines could be used as risk indicators, these parameters were measured in 19 patients with acute myocardial infarction. During the course of hospitalization, five patients developed ventricular fibrillation and three, cardiogenic shock. On admission, heart rate, plasma norepinephrine, epinephrine, and renin levels of these eight patients were significantly higher than those of the other patients with uncomplicated course. Peak creatine kinase MB activity was positively related to initial plasma renin activity (r = 0.62, p less than 0.01). Thus, the patients with the highest sympathetic activity following an acute myocardial infarction also had the highest plasma renin levels. They seem particularly prone to develop large infarcts and life-threatening complications.     

Gender and myocardial salvage after reperfusion treatment in acute myocardial infarction

OBJECTIVES: The aim of this study was to investigate whether there are gender-associated differences in the amount of myocardial salvage after primary percutaneous coronary intervention (PCI) in patients with acute myocardial infarction (AMI). BACKGROUND: Despite having a more adverse cardiovascular risk profile, women with AMI have similar or even better outcomes after primary PCI compared with men. The reasons for these findings are unclear. METHODS: In this study we included 202 women and 561 men with AMI who underwent primary PCI in the setting of three randomized trials. The primary end point of the study was myocardial salvage index (proportion of initial perfusion defect salvaged by reperfusion therapy), obtained by paired scintigraphic studies performed 7 to 10 days apart. RESULTS: The amount of myocardium at risk or initial perfusion defect (median [25th, 75th percentiles]) did not differ significantly between women and men (22.0% [12.0, 40.0] vs. 24.0% [14.0, 39.0] of the left ventricle [LV], p = 0.26). Final infarct size, measured in the follow-up scintigraphy, was significantly smaller in women than in men (6.0% [0.71, 18.7] vs. 10.0% [3.9, 21.8] of the LV, p = 0.001). Myocardial salvage index was 0.64 (0.35, 0.95) in women versus 0.50 (0.26, 0.77) in men (p < 0.001). After adjustment for baseline characteristics, female gender was an independent predictor of greater myocardial salvage after PCI (p = 0.002). CONCLUSIONS: The efficacy of primary PCI in patients with AMI appears to be gender-dependent. Myocardial salvage achieved by primary PCI is greater in women than in men.     

腺苷对猪急性心肌梗死再灌注后无再流的影响

目的评价腺苷防治猪急性心肌梗死(AMI)再灌注后无再流的作用。方法中华小型猪24只随机分成对照组、腺苷组(100μg·kg-1·min-1持续静点)和假手术组,每组8只。前2组行冠状动脉结扎3h,松解1h建立AMI再灌注模型。AMI前、后和再灌注后均行血流动力学测定和心肌声学造影检查,最终行病理学分析。结果(1)与AMI前相比,对照组AMI后3h主动脉收缩和舒张压、左室收缩压、心排量和左室内压最大收缩和舒张变化速率(±dp/dtmax)均显著下降(P<0.05～0.01),肺毛细血管楔压和左室舒张末压均显著升高(P<0.01);再灌注后1h仅左室舒张末压显著恢复(P<0.05)然而±dp/dtmax继续显著下降(P<0.05);而腺苷组AMI后3h各项指标变化与对照组相同;但再灌注后1h左室收缩压、左室舒张末压、±dp/dtmax和心排量均显著恢复(P均<0.05),且比对照组更显著(P均<0.05)。(2)对照组心肌声学造影和病理染色所测的冠状动脉结扎区心肌范围高度一致,再灌注后无再流面积分别为67.5%和69.3%,心肌坏死面积(NA)占结扎区心肌面积(LA)的98.5%;而腺苷组LA均与对照组相当,但两方法所测无再流面积仅分别为21.5%和20.8%,NA仅为75.2%,均显著小于对照组(P<0.05～0.01)。(3)对照组再灌注即刻和再灌注后1h冠状动脉血流量仅占AMI前的45.8%和50.6%(P均<0.01),而腺苷组冠     

福辛普利对猪急性心肌梗死再灌注后无再流的影响

目的评价福辛普利防治猪急性心肌梗死再灌注后无再流的作用。方法中华小型猪24只随机分成对照组、福辛普利组(1mg·kg-1·d-1)和假手术组,每组8只。冠状动脉结扎3h,松解1h制备急性心肌梗死再灌注模型。梗死前、后和再灌注后均行血液动力学测定和心肌声学造影检查,最终行病理学分析。结果心肌声学造影和病理染色所测的冠状动脉结扎区心肌范围(LA)差异无统计学意义。与对照组相比,福辛普利可促进急性心肌梗死后心功能的恢复,增加再灌注后1h冠状动脉血流量(对照组50·6%,福辛普利组72·1%,P<0·01),减少无再流面积(对照组心肌声学造影和病理:78·5%和82·3%LA;福辛普利组心肌声学造影和病理:24·5%和25·2%LA,P均<0·01),减少心肌坏死面积(对照组98·5%,福辛普利组88·9%LA,P<0·05)。结论福辛普利能有效地防治心肌梗死再灌注后无再流。     

急性心肌梗死溶栓、介入和再灌注治疗评价

急性心肌梗死(acute myocardial infarction, AMI)是在冠状动脉病变的基础上,发生冠状动脉供血急剧减少或中断,使相应的心肌因严重而持久的急性缺血而发生的心肌缺血性坏死.……