Tissue plasminogen activator administration and nursing considerations

Intravenous thrombolytic therapy is rapidly gaining acceptance in the care of acute myocardial infarction (AMI) patients. There are several thrombolytic agents in use; however, this article will focus on tissue type plasminogen activator (t-PA). A thorough understanding of the benefits and risks associated with thrombolytic administration will be critical in the successful utilization of this form of therapy. Recent data show that infarct size is linked to mortality. In the 1980s, therapy for acute myocardial infarction patients is directed at salvaging myocardium and limiting infarct size. Prior to this, therapy consisted mainly of supportive care that resulted only in minor effects on the patients prognosis. Intracoronary thrombus has recently been recognized as the cause in most cases of acute myocardial infarction. Thrombolytic therapy represents a method of dissolving a thrombus and reestablishing blood flow to the previously occluded coronary artery. Early reperfusion of ischemic myocardial tissue can limit the amount of damage caused by evolving myocardial infarction. Intervention with thrombolytic therapy in the early hours of acute myocardial infarctions has been associated with reduction in the infarct size, improvement in left ventricular function and reduction in mortality. Nursing plays a critical role in ensuring the successful use of thrombolytic therapy by early identification of appropriate patients and accurate administration of the thrombolytic agent.     

Experiences with early fibrinolysis in coronary infarct at an acute care hospital. Second report of experiences with 200 patients 1980 to 1985

Over the past two decades patients with acute myocardial infarction have been treated with intravenous streptokinase therapy at the hospital in Geldern. Based on experiences in the first study from 1970 to 1979, the second study emphasized instruction on early thrombolytic therapy. Informations were given to general practitioners and to patients at risk for acute myocardial infarction. In the study from 1980 to 1985 the percentage of patients with acute myocardial infarction being treated with thrombolytic agents within two hours after the acute event was 69%. Patients with a duration of ischemia of less than two hours had a significantly decreased in-hospital mortality compared to patients who received therapy more than two hours after onset of symptoms. We conclude that intensified information and instruction of physicians and of patients at risk for myocardial infarction enables early thrombolytic therapy and results in reduced in-hospital mortality of acute myocardial infarction.     

Acute coronary syndrome and myocardial infarct--new definitions

Until recently a general consensus existed for the clinical entity diagnosed as myocardial infarction using the world health organisation (WHO) definition. According to the WHO definition myocardial infarction was defined by a combination of two of three typical characteristics: typical symptoms, rise of cardiac enzymes (CK, CK-MB), and a typical ECG pattern involving the development of Q waves. New insights into the development of acute myocardial infarction, the superiority of the biochemical characteristics of cardiac troponin assays over CK and CK-MB measurements in blood, and new therapeutic concepts made a new definition of myocardial infarction, e.g. of the acute myocardial infarction, necessary. Timing of the diagnosis of myocardial necrosis is of outmost importance relative to the time of observation (acute, evolving, healing, healed MI), as is the classification of the extent of myocardial damage (microscopic, small, medium or large). The term "acute coronary syndrome" (ACS) has been established as a working diagnosis for choosing the appropriate therapeutic strategy. In patients with ACS and ST elevation ischemia (STEMI ACS, true posterior ischemia inclusive) as well as in patients with presumably new LBBB, immediate reperfusion therapy should be performed (primary PTCA or thrombolytic therapy), whereas in patients with ECG changes other than ST elevation or new LBBB (NSTEMIACS) additional antiplatlet therapy on top of aspirin and heparin is indicated. In contrast to the acute phase of infarction when troponin in blood often is not detectable yet, the diagnosis of definitive myocardial infarction is based primarily on troponin elevation. Hard criteria for established infarction are the development of pathologic Q waves or healing or healed myocardial necrosis in pathology; troponin may be normal then, depending of time relapsed.     

Thrombolytic therapy and acute myocardial infarction

Coronary thrombosis and subsequent time-dependent wavefront cardiac muscle necrosis are the pathophysiological hallmarks of an acute myocardial infarction. Early treatment of the thrombus by intravenous thrombolytic therapy results in a major reduction of mortality by salvage of myocardial muscle and preservation of left ventricular function. Although the benefit of streptokinase has been best documented, second generation thrombolytics (APSAC and rt-PA) are probably superior thrombolytic agents. The data on the additive effect of inhibition of platelet aggregation with low dose acetylsalicylic acid on degree of thrombolysis and mortality after a myocardial infarction are convincing. The reduction in mortality brought about by intravenous thrombolytic therapy is highly time-dependent, so that its application in a patient presenting with an acute myocardial infarction must be considered as a race against time.     

Thrombolysis in Acute Myocardial Infarction Following Prolonged Cardiopulmonary Resuscitation

ABSTRACT
Thrombolytic therapy was administered to a 64-year-old man with an acute anterolateral myocardial infarction who had received cardiopulmonary resuscitation (CPR) for 24 minutes. At the time of thrombolytic therapy, the patient was alert and without clinical or radiographic evidence of injury. The patient developed a retroperitoneal hematoma related to femoral line placement, as well as subcutaneous bruising of the anterior chest wall; both were self-limited. No long-term morbidity developed, and the myocardial infarction was aborted. The use of thrombolytic therapy for patients with acute myocardial infarction who have received CPR is reviewed. In the absence of clinical or radiographic evidence of trauma from CPR, patients with acute myocardial infarction should not be excluded from receiving thrombolytic therapy solely because of having had CPR or the duration of CPR.     

Therapies to limit infarct size. Timing, dosage, and effectiveness

Rapid diagnosis of an evolving acute myocardial infarction and institution of thrombolytic therapy in appropriate patients can markedly decrease infarct size and thus reduce cardiovascular morbidity and mortality. Streptokinase (Kabikinase, Streptase) and recombinant tissue plasminogen activator (Activase) are both widely used, effective clot-dissolving agents. Patients who are not candidates for thrombolytic therapy can be treated with other methods, such as anticoagulant therapy, which can greatly reduce infarct size. Intravenous heparin, beta blockers, nitroglycerin, and aspirin have all been shown to limit infarct size, decrease mortality, or do both in patients with acute myocardial infarction.     

When the MAGIC stops: magnesium in acute coronary syndromes--a lesson in medical humility

There has been much debate as to whether magnesium, a well-tolerated, readily available and cheap therapy, should be used to treat patients with suspected myocardial infarction. Despite promising results from animal studies and small clinical trials conducted in the 1980s, two large recent trials have concluded that the once phenomenal treatment is ineffective. The story of magnesium for acute myocardial infarction is a lesson in medical humility.     

New Accelerated rt-PA Strategy Has Sufficient Advantage over Older Streptokinase Strategies that It should Be the Trhombolytic Strategy of Choice in Anterior and Large Infarctions

The major goal of myocardial reperfusion therapy is to restore normal coronary blood flow as quickly as possible and to maintain coronary patency in the highest number of patients with acute myocardial infarction. Recent studies support the hypothesis that more rapid and complete restoration of coronary flow through the infarct-related artery results in improved ventricular performance and lower mortality. Accelerated tissue plasminogen activator therapy appears to produce the most favorable effects compared to other lytic strategies, particularly in patients with anterior and large myocardial infarctions. However, the finding in GUSTO II trial, that even with the best strategy only 54% of patients had TIMI grade 3 flow, suggests that further improvement in the treatment of acute myocardial infarction may be possible in the future. The effectiveness of thrombolytic therapy may be enhanced by earlier identification of evolving myocardial infarction and reduced time delays in the initiation of thrombolytic therapy, bolus thrombolytic therapy, new thrombolytic agents, or more potent adjunctive antithrombotic strategies.     

Myocardial repair: from salvage to tissue reconstruction

Cardiac tissue reconstruction following myocardial infarction represents a major challenge in cardiovascular therapy, as current clinical approaches are limited in their ability to regenerate or replace damaged myocardium. Thus, different novel treatments have been introduced aimed at myocardial salvage and repair. Here, we present a review of recent advancements in cardiac cell, gene-based and tissue engineering therapies. Selected strategies in cell therapy and new tools for myocardial gene transfer are summarized. Finally, we consider novel approaches to myocardial tissue engineering as a platform for the integration of various modalities in an attempt to rejuvenate infarcted tissue in vivo.     

Intracoronary thrombolytic therapy of myocardial infarction

The results of intracoronary thrombolytic therapy with avelysine given to 21 patients with acute myocardial infarction are described. Intracoronary thrombolysis was performed on the average 5 h and 30 min after myocardial infarction onset. Recanalization of the coronary artery was attained in 16 patients, with no lethal outcomes. One patient died out of the 5, in whom attempts to recanalize the artery ended in failure. Recanalization of the coronary arteries led to improvement of left ventricle function and appreciably accelerated the time-course of the enzymatic shifts (KPK and LDH) in blood of myocardial infarction patients. After successful recanalization of the coronary artery the disease in myocardial infarction patients took a far milder course as compared to those who did receive intracoronary thrombolytic therapy.     

G-CSF- and erythropoietin-based cell therapy: a promising strategy for angiomyogenesis in myocardial infarction

Granulocyte colony-stimulating factor (G-CSF) and erythropoietin are two cytokines that have been demonstrated to improve cardiac function and perfusion in myocardial infarction. G-CSF was initially evaluated as a stem cell mobilizer and erythropoietin as a cytoprotective agent. However, both cytokines have direct cytoprotective effects and stem cell-mobilizing ability. Direct cytoprotective effects of both cytokines are commonly mediated by the Jak-STAT pathway. In preclinical study, G-CSF and erythropoietin improved cardiac function and perfusion by angiomyogenesis and protection of cardiomyocytes in myocardial infarction. However, results from recent clinical trials did not support beneficial effects of cytokine therapy with G-CSF or erythropoietin alone in patients with myocardial infarction. Further studies are required to elucidate the mechanism of action and to improve therapeutic efficacy by employing novel strategies, such as combined cytokines.     

Myocardial repair: from salvage to tissue reconstruction

Cardiac tissue reconstruction following myocardial infarction represents a major challenge in cardiovascular therapy, as current clinical approaches are limited in their ability to regenerate or replace damaged myocardium. Thus, different novel treatments have been introduced aimed at myocardial salvage and repair. Here, we present a review of recent advancements in cardiac cell, gene-based and tissue engineering therapies. Selected strategies in cell therapy and new tools for myocardial gene transfer are summarized. Finally, we consider novel approaches to myocardial tissue engineering as a platform for the integration of various modalities in an attempt to rejuvenate infarcted tissue in vivo.     

The Relative Merits of Direct Angioplasty versus Intravenous Thrombolytic Therapy for the Treatment of Acute Myocardial Infarction

There is growing interest in the use of angioplasty as the primary method to achieve coronary artery reperfusion in patients with acute myocardial infarction. The use of thrombolytic therapy has been established as effective in many large clinical trials, while only a few small studies have been completed comparing primary angioplasty with thrombolytic therapy. This paper briefly compares the use of these two treatment modalities and concludes that primary angioplasty is the preferred approach in patients with cardiogenic shock and for those patients with large myocardial infarctions who have contraindications to thrombolytic therapy. Other patients with AMI should receive thrombolytic therapy unless there are contraindications to this treatment.     

Adjunctive therapies in the treatment of acute coronary syndromes

Survival after myocardial infarction has been improving steadily in recent decades, in part because of more effective adjunctive medical therapies. However, the issue of underutilization of effective medical therapies remains. Adjunctive therapy for acute myocardial infarction should include aspirin, beta-adrenergic blocking agents, angiotensin-converting enzyme inhibitors, and lipid-lowering agents, all of which improve survival in the treatment and secondary prevention of myocardial infarction. This review presents the current knowledge supporting the use of specific adjunctive pharmacologic agents and also discusses the current status of other agents that are emerging or controversial.     

Acute myocardial infarction improved by neuroleptic analgesic therapy

Treated with orthodox therapy, a 58-year-old man with acute myocardial infarction of the anteroseptal and lateral walls continued having lethal arrhythmias, reinfarction, low blood pressure, and anuria. With modified neuroleptic analgesic therapy, which consisted only of a continuous drip injection of morphine and chlorpromazine, his condition improved dramatically. Our patient's coronary spasms, which occurred after acute myocardial infarction, might have been triggered by mental stress due to anxiety and pain, and the use of neuroleptic analgesic agent therapy prevented further coronary spasm and reinfarction.     

实时心肌声学造影评价体外心脏震波对急性心肌梗死猪的促血管生成作用

目的：用实时心肌声学造影的方法观察体外心脏震波对急性心肌梗死猪冠状动脉微循环的作用。方法：健康成年家猪10头，随机分为震波治疗A组（n=5）和对照B组（n=5），以自制球囊的方法介入堵闭冠状动脉前降支制造急性前壁心梗模型。应用GE Vivid 7彩色超声诊断仪和SonoVue超声造影剂，分别在急性心肌梗死前、梗死后1d和梗死后1月行实时心肌声学造影检查。按照美国超声心动图学会推荐的16节段划分法，将前降支供血区域锁定为间隔中段、间隔心尖段、前壁中段、前壁心尖段。应用瑞士Storz Medical公司生产的震波治疗仪，A组猪在梗死后第3d行震波治疗，每个缺血区进行9点治疗（-1～0～+1两两组合），每点释放200次脉冲，每次脉冲能量为0.09mJ/mm2，每周治疗3次，持续3周共9次。结果：10头猪急性心肌梗死模型均顺利建成。随访期间A组死亡1头，死亡率20%；B组死亡2头，死亡率40%。震波过程中无心律失常和猝死等并发症发生。A组（n=4）和B组（n=3）梗死前靶心肌血流灌注良好，A·K值差异无统计学意义。梗死后1d，4个节段血流量明显下降，2组各个节段梗死前后自身对照，A·K值差异有统计学意义（P<0.05）。梗死后1月与梗死后1d相比， A组4个节段A·K值较B组明显增高（P<0.05），其中，室壁中段的改善程度优于室壁心尖段（86.57% vs 65.54%），而B组各个节段改变甚微。结论：体外心脏震波是一项无创、安全的血管再生疗法，可促进急性心肌梗死猪缺血区域的侧支循环建立，提高局部心肌血流灌注。     

The effect of dalargin on the hemodynamics in acute myocardial infarct complicated by clinical death]

Cardiac output and myocardial contractility have been studied in dogs with experimental myocardial infarction complicated by 5 min clinical death. Control animals (16 dogs) were intravenously injected physiologic saline, while test animals (12 dogs) were administered leu-enkephalin analogue dalargin at a dose of 100 micrograms/kg, 20 min and 6-h after recovery. It has been established that dalargin improved basic hemodynamic parameters due to normalization of cardiac contractility, arrhythmia removal and reduction of the peripheral resistance. The data obtained make it possible to recommend dalargin for combined therapy of postresuscitation hemodynamic disturbances in acute myocardial infarction.     

Cell therapy for acute myocardial infarction

Evidence suggesting that bone marrow and circulating blood may harbor myocardial and vascular progenitor cells was the basis for pre-clinical studies of cell therapy for acute myocardial infarction (MI). Rapid initiation of clinical trials has since followed, with regional myocardial delivery of autologous cells being tested as adjunctive therapies for both acute and chronic left ventricular dysfunction. While clinical cell transplantation trials originally began with the explicit goal of myocardial regeneration, more recently the emphasis has shifted to attempted modulation of myocardial remodeling through other processes, such as mechanical strengthening of scar tissue and promotion of myocardial tissue survival through cellular paracrine effects. This article discusses the scientific rationale for cell therapy strategies in acute MI and provides an overview of the clinical studies that have been undertaken to date.     

Stem cells for cardiac repair in acute myocardial infarction

Despite recent advances in medical therapy, reperfusion strategies, implantable cardioverter-defibrillators and cardiac assist devices, ischemic heart disease is a frequent cause of morbidity and mortality worldwide. Cell therapy has been introduced as a new treatment modality to regenerate lost cardiomyocytes. At present, several cell types seem to improve left ventricular function in animal models as well as in humans, but evidence for true generation of new myocardium is confined to the experimental models. In the clinical perspective, myocardial regeneration has been replaced by myocardial repair, as other mechanisms seem to be involved. Clinical studies on adult stem cells suggest, at best, moderate beneficial effects on surrogate end points, but some applications may qualify for evaluation in larger trials. Complete regeneration of the myocardium by cell therapy after a large myocardial infarction is still visionary, but pluripotent stem cells and tissue engineering are important tools to solve the puzzle.