Coronary angiography after thrombolytic therapy for acute myocardial infarction

PURPOSE: To review the status of emergency, urgent, routine, and selective angiography after intravenous thrombolytic therapy. DATA SOURCES: Relevant English-language articles published from January 1985 to July 1990 were identified through MEDLINE. STUDY SELECTION: For emergency angiography, four major randomized studies were reviewed and data from nine studies that incorporated rescue coronary angioplasty were pooled for meta-analysis. For urgent angiography, two controlled trials were reviewed. Comparisons of routine and selective angiography were done using data from two dedicated, large-scale, controlled trials and the ancillary findings of four other studies of reperfusion that incorporated angiography. DATA EXTRACTION: The review emphasizes the findings from multicenter, randomized, controlled trials. DATA SYNTHESIS: Emergency coronary angiography is done primarily in preparation for primary or rescue angioplasty; the value of rescue angioplasty has yet to be assessed in a randomized trial, but technical success and reocclusion improve significantly after therapy with nonspecific plasminogen activators compared with relatively specific agents (success rate, 86% compared with 75%, respectively; P = 0.03; reocclusion rate, 10.9% compared with 26.8%, respectively; P less than 0.001). Urgent coronary angiography has value for treating recurrent ischemia, but patients who develop this complication after thrombolysis are likely to have a suboptimal outcome despite aggressive care. Studies support the use of either selective or routine angiography in uncomplicated patients after thrombolytic therapy; either approach is acceptable, but the former is more practical and may prove to be cost effective. CONCLUSIONS: Optimal follow-up for patients with evolving myocardial infarction who receive thrombolysis may incorporate coronary angiography at various stages. Although our ability to noninvasively detect reperfusion, reocclusion, or viable but ischemic myocardium is limited at present, available data may assist in selecting a catheterization strategy.     

Bleeding during thrombolytic therapy for acute myocardial infarction: mechanisms and management

Hemorrhage is the major adverse effect of thrombolytic therapy, but its incidence can be reduced by careful selection of patients and avoidance of unnecessary invasive procedures. More than 70% of bleeding episodes occur at vascular puncture sites. Hypofibrinogenemia and elevation of fibrinogen degradation products have been weakly correlated with the risk of hemorrhage. Although depletion of factors V and VIII may occur, the role of such depletion in bleeding is unknown. Several in-vitro studies have shown plasmin-induced platelet dysfunction, but clinical data are limited. Nevertheless, the role of platelet inhibition should be considered because many patients are treated with antiplatelet agents. Most patients who have bleeding can be managed by interruption of thrombolytic and anticoagulant therapy, volume replacement, and manual pressure applied to an incompetent vessel. Protamine should be considered if heparin has been administered within 4 hours of the onset of bleeding. In the few patients who fail to respond to these conservative measures, judicious use of transfusion products may be indicated. Transfusion of cryoprecipitate, fresh frozen plasma, and platelets should be considered with clinical and laboratory reassessment after each administration. A target fibrinogen level of 1 g/L is desirable with cryoprecipitate infusion. Antifibrinolytic agents are available as a last alternative. We have developed an algorithm for using these products.     

Diagnosis and management of failed thrombolytic therapy for acute myocardial infarction

Thrombolytic therapy continues to remain the most frequently adopted treatment for patients of acute myocardial infarction. Despite our best efforts, thrombolytic therapy is not uniformly successful. In this review we have discussed the incidence, diagnosis and management of failed thrombolysis. The different meta-analysis of rescue angioplasty and various nuances of this treatment are presented.     

Management of patients after thrombolytic therapy for acute myocardial infarction

The coronary artery thrombus that causes acute myocardial infarction can be lysed, and reperfusion can be achieved, in the first few hours after infarction. However, the infarct vessel will reocclude in 15-30% of patients, and this event is frequently associated with pain, reinfarction, arrhythmias, or death. The risk of reocclusion is greatest in patients with high-grade residual stenosis after thrombolysis. Percutaneous coronary angioplasty may be performed safely after thrombolytic therapy. Angioplasty effectively decreases the degree of residual stenosis, and may thereby reduce the risk of reocclusion and consequent ischemic events. However, a substantial proportion of patients with acute infarction are not suitable candidates for angioplasty. Coronary artery bypass surgery has also been safely performed within several days after thrombolytic therapy. Further studies are needed to determine which patients will benefit most from this aggressive approach to acute myocardial infarction.     

Role of heparin after intravenous thrombolytic therapy for acute myocardial infarction

The optimal approach to management of patients after thrombolytic therapy for acute myocardial infarction (AMI) is unclear. The role of anticoagulation with heparin was evaluated in 75 consecutive patients who received intravenous streptokinase for AMI. Heparin therapy was titrated to keep the partial thromboplastin time (PTT) between 90 and 120 seconds. Seventeen episodes of definite myocardial ischemia (associated with reversible electrocardiographic changes) were observed in 13 patients. When episodes of probable myocardial ischemia are included (typical chest pain relieved by nitroglycerin or associated with more than a 15-mm Hg change in blood pressure but without electrocardiographic changes), 52 episodes occurred in 28 patients. Four episodes of definite and 4 of probable myocardial ischemia occurred within 24 hours of discontinuation of heparin. Analysis of the level of anticoagulation as assessed by PTT at the time of the ischemic events shows that ischemia occurred more often at lower PTTs. Nine hemorrhagic complications occurred, all within 24 hours of streptokinase infusion. In 4 patients bleeding was believed to be major and heparin administration was discontinued; 2 patients with gastrointestinal bleeding required blood transfusions. Our data suggest that after thrombolytic therapy for AMI, the level of anticoagulation is inversely related to the frequency of recurrent ischemic events; that discontinuation of heparin is frequently associated with ischemia; and that administration of heparin is associated with a low incidence of hemorrhagic complications.     

Predictors of cardiogenic shock after thrombolytic therapy for acute myocardial infarction

OBJECTIVES: This study characterized clinical factors predictive of cardiogenic shock developing after thrombolytic therapy for acute myocardial infarction (AMI). BACKGROUND: Cardiogenic shock remains a common and ominous complication of AMI. By identifying patients at risk of developing shock, preventive measures may be implemented to avert its development. METHODS: We analyzed baseline variables associated with the development of shock after thrombolytic therapy in the Global Utilization of Streptikonase and Tissue-Plasminogen Activator for Occluded Coronary Arteries (GUSTO-I) trial. Using a Cox proportional hazards model, we devised a scoring system predicting the risk of shock. This model was then validated in the Global Use of Strategies to Open Occluded Coronary Arteries (GUSTO-III) cohort. RESULTS: Shock developed in 1,889 patients a median of 11.6 h after enrollment. The major factors associated with increased adjusted risk of shock were age (chi2 = 285, hazard ratio [95% confidence interval] 1.47 [1.40, 1.53]), systolic blood pressure (chi2 = 280), heart rate (chi2 = 225) and Killip class (chi2 = 161, hazard ratio 1.70 [1.52, 1.90] and 2.95 [2.39, 3.63] for Killip II versus I and Killip III versus I, respectively) upon presentation. Together, these four variables accounted for >85% of the predictive information. These findings were transformed into an algorithm with a validated concordance index of 0.758. Applied to the GUSTO-III cohort, the four variables accounted for > 95% of the predictive information, and the validated concordance index was 0.796. CONCLUSIONS: A scoring system accurately predicts the risk of shock after thrombolytic therapy for AMI based primarily on the patient's age and physical examination on presentation.     

The assessment of contractile reserve after thrombolytic therapy for acute myocardial infarction

"Stunned" myocardium prevents the assessment of myocardial salvage after streptokinase. In order to unmask "stunning," we sought to evaluate left ventricular inotropic contractile reserve of patients after streptokinase. Radionuclide ventriculograms were obtained in 75 consecutive patients 2 weeks after myocardial infarction, at rest and during intravenous isoproterenol infusion. Resting and isoproterenol-stressed ejection fractions were compared in the patent and closed-infarct vessel groups. Although there was no difference in the resting ejection fractions between the patent group (0.48 +/- 0.02) and the closed group (0.48 +/- 0.02), isoproterenol increased the ejection fractions in the patent group (increase 0.14 +/- 0.01) significantly more than in the closed group (increase 0.06 +/- 0.01) (p less than 0.0001). Thus, despite identical resting ventricular function, the greater inotropic contractile reserve in the patent infarct vessel group suggests that restoration of blood flow in acute myocardial infarction salvages myocardium.     

Adoption of thrombolytic therapy in the management of acute myocardial infarction

A national survey of 1,065 physicians was carried out to document current use of thrombolytic therapy for acute myocardial infarction (AMI). In early 1987, thrombolytic therapy was used by 66% of respondents. Among those who used thrombolytic therapy, 92% used streptokinase, 13% used tissue-type plasminogen activator and 3% used urokinase. Most (72%) used intravenous administration exclusively and only 5% used intracoronary administration exclusively. Despite widespread acceptance of thrombolytic therapy, most physicians gave it to less than 25% of their patients. Duration of symptoms was rated as the single most important factor affecting the decision to use thrombolytic therapy; 45% had a time limit of less than 4 hours and 85% had a time limit of less than 6 hours. Complications of AMI and electrocardiographic findings were factors also considered in the decision to give this therapy. A physician's adoption of thrombolytic therapy was significantly associated with several characteristics: specialty type, number of AMI patients treated, physician age and access to cardiac catheterization. In addition, physicians using thrombolytic therapy had a significantly different use of medications and laboratory tests for all patients with AMI. This survey documents rapid acceptance of thrombolytic therapy for AMI, particularly in patients with short duration of symptoms or evidence of high risk.     

Comparison of primary angioplasty with conservative therapy in patients with acute myocardial infarction and contraindications for thrombolytic therapy

The benefit of primary angioplasty in patients with acute myocardial infarction (AMI) and contraindications for thrombolysis compared to a conservative regimen is still unclear. Out of 5,869 patients with AMI registered by the MITRA trial, 337 (5.7%) patients had at least one strong contraindication for thrombolytic therapy. Out of these 337 patients 46 (13.6%) were treated with primary angioplasty and 276 (86.4%) were treated conservatively. Patients treated conservatively were older (70 years vs. 60 years; P = 0.001), had a higher rate of a history with chronic heart failure (14.8% vs. 4.4%; P = 0.053), a higher heart rate at admission (86 beats/min vs. 74 beats/min; P = 0.001), and a higher prevalence of diabetes mellitus (27.1% vs. 12.8%; P = 0.056). Patients treated with primary angioplasty received more often aspirin (91.3% vs. 74.6%; P = 0.012), β-blockers (60.9% vs. 46.1%; P = 0.062), angiotensin converting enzyme (ACE) inhibitors (71.7% vs. 44%; P = 0.001), and the so-called optimal adjunctive medication (54.4% vs. 32.3%; P = 0.004). Hospital mortality was significantly lower in patients who received primary angioplasty (univariate: 2.2% vs. 24.7%; P = 0.001; multivariate: OR = 0.46; P = 0.0230). In patients with AMI and contraindications for thrombolytic therapy, primary angioplasty was associated with a significantly lower mortality compared to conservative treatment. Therefore, hospitals without the facilities to perform primary angioplasty should try to refer such patients to centers with the facilities for such a service, if this is possible in an acceptable time.Cathet. Cardiovasc. Intervent. 46:127–133, 1999. © 1999 Wiley-Liss, Inc.     

东菱克栓酶冠状动脉溶栓治疗急性心肌梗塞的临床研究

报告6例发病时间在4～10小时内的急性心肌梗塞患者，采用冠状动脉狭窄口堵塞近端注入东菱克栓酶（DF－521）20～30BU（Batroxobinunit简称BU，是Batroxobin的酶活性量的表示单位。37℃以下，标准人～枸椽酸血浆0．3ml中加入Batroxobin溶液0．1ml，19．0±0．2秒发生凝固时其酶活性为2BU）。进行溶栓治疗，60～90分钟后重复冠状动脉造影。结果全部有效，4例闭塞管腔再通（TIMI达Ⅲ级）2例大部分再通（TIMI达Ⅱ级），从而限制了梗塞发展且无出血及其它并发症，效果显著，值得进一步研究推广。     

Long-term effect of thrombolytic therapy on left ventricular ejection fraction after acute myocardial infarction

To assess the long-term effect of thrombolytic therapy on left ventricular (LV) systolic function, 222 patients with acute myocardial infarction treated with intravenous tissue plasminogen activator within 4 hours of symptom onset underwent assessment of LV ejection fraction (EF) by radionuclide equilibrium angiography at hospital discharge and 1 year later. Mean EF at hospital discharge (46 ± 12) was similar to that at 1 year (45 ± 13). Stepwise multivariate linear regression analysis identified EF at discharge and patency of the infarct-related artery before discharge as independent predictors of EF change at 1 year (p = 0.0002 and 0.003, respectively). Random assignments to invasive versus conservative treatment strategies or to early versus delayed β-blocker therapy did not affect EF change during follow-up. No significant deterioration of EF was observed in patients with larger infarcts. However, EF decreased from 45 ± 10 at hospital discharge to 39 ± 12 (p = 0.005) at 1-year follow-up in a subgroup of patients with history of prior infarction.

Thus, patients with acute myocardial infarction, treated with intravenous tissue plasminogen activator early after onset of symptoms, appear to have stable LV function between hospital discharge and 1 year follow-up. The change in EF between hospital discharge and 1 year can be predicted from the EF value at discharge, patency of the infarct-related artery before discharge and history of previous myocardial infarction.     

Heparin as an adjunctive treatment after thrombolytic therapy for acute myocardial infarction

The rationale for considering heparin therapy as an adjunct to thrombolytic treatment for patients with acute myocardial infarction is to prevent rethrombosis after successful thrombolysis. The risk of reocclusion is high immediately after thrombolysis because blood flowing through the newly opened coronary artery is exposed to thrombin bound to fibrin in the residual thrombus. Clinical studies of patients with venous thrombosis and acute myocardial infarction indicate that there is a relation between the anticoagulant response to heparin and clinical efficacy and that the concept of a therapeutic heparin level is valid. Subcutaneous doses of approximately 15,000 U twice a day fail to provide an adequate anticoagulant response at 24 hours in the majority of patients, whereas intravenous administration of a bolus of 5,000 U followed by continuous infusion of 30,000 U per 24 hours produces an adequate anticoagulant response at 24 hours in approximately 80% of patients. Studies of patients with myocardial infarction who received streptokinase showed a significant beneficial effect on mortality when 12,500 U of heparin was administered subcutaneously 2 times per day. In contrast, the single largest study evaluating heparin 12,500 U administered subcutaneously 2 times per day as an adjunct to recombinant tissue-type plasminogen activator (rt-PA) treatment did not show a beneficial effect on mortality. However, studies using full-dose intravenous heparin therapy demonstrated that heparin improves patency after coronary thrombolysis with rt-PA.(ABSTRACT TRUNCATED AT 250 WORDS)     

溶栓疗法在初发急性心肌梗死中的应用

目的 :调查初发急性心肌梗死 （AMI）溶栓疗法的应用现状及近期疗效。方法 :总结我院 1996 - 0 1～ 1999- 0 8期间所有确诊初发 AMI患者的临床资料 ,发病超过 2 4h入院、外院转来、心内膜下心梗、再梗患者除外。结果 :2 0 2例初发 AMI患者中 ,148例 （73.3% ）符合溶栓适应证 ,132例 （6 5 .3% ）应用溶栓疗法 ,36例 （2 4.3% ）未溶栓 （16例 ）或溶栓药物剂量不足 （2 0例 ）。 70例未溶栓患者中 ,发病—入院 >12 h、符合适应证而未予溶栓、溶栓禁忌、入院心电图不能确诊 AMI的比例分别为 6 0 .0 % ,2 2 .8% ,8.6 %和 8.6 %。溶栓组住院期间病死率显著低于未溶栓组（6 .1% vs15 .7% ,P<0 .0 5 ） ,其中再通组病死率显著低于未通组 （2 .3% vs2 0 .8% ,P<0 .0 1）。结论 :尽管溶栓疗法改善了 AMI的近期预后 ,但合理应用溶栓疗法的比例仍有待提高 ,患者入院过迟、溶栓治疗不积极是溶栓疗法应用偏低的主要原因。     

Thrombolytic therapy followed by early revascularization for acute myocardial infarction

During a 24-month period, 192 patients with acute myocardial infarction were treated with intracoronary or intravenous streptokinase (SK). In 147 patients (77%) an open infarct artery was demonstrated by coronary angiography; 117 of these 147 patients were judged to have viable myocardium supplied by a critically narrowed coronary artery and underwent revascularization 3 +/- 2 days after SK therapy. In-hospital mortality was 6% (12 of 192). The mortality rate over the subsequent 20 +/- 7 months of follow-up was lower for those in whom SK therapy was successful (1 of 137, 0.7%) than in those in whom it was not (6 of 43, 14%) (p less than 0.001), and tended to be lower for those treated with intravenous (2 of 111, 2%) rather than intracoronary SK (5 of 69, 7%, p = 0.11). Reinfarction occurred in 3% of the 180 survivors of hospitalization, angina pectoris in 11% and congestive heart failure in 7%. Clinical outcome was similar for patients treated with intravenous and intracoronary SK and for patients treated in community hospitals and the referral center.     

急性心肌梗死静脉溶栓治疗的疗效分析

目的 探讨分析静脉溶栓治疗早期急性心肌梗死的安全性及临床疗效.方法 在心电监测下应用尿激酶静脉溶栓治疗93例急性心肌梗死患者,并对其临床资料进行回顾分析.结果 93例患者中冠脉达到再通标准69例,再通率为74.19%;24例未达再通标准,其中3例死亡,病死率为3.23%.发病<6 h溶栓治疗的成功率明显高于6～12 h的再通成功率,差异有统计学意义(P＜0.05).结论 急性心肌梗死患者应尽早行静脉溶栓治疗,以减少并发症、降低病死率、提高再通的成功率.     

Spontaneous hemarthrosis following thrombolytic therapy for acute myocardial infarction

We describe a 45-year-old man who developed a spontaneous hemarthrosis of his right knee following thrombolytic therapy with streptokinase and rtPA for acute myocardial infarction. Surprisingly, despite the wide use of thrombolytic therapy, only four cases of spontaneous hemarthrosis following thrombolysis have been previously reported. Prompt aspiration of the joint, after stopping anticoagulant therapy, and splinting will provide early diagnosis and may prevent further damage to the joint.     

Systemic embolization following thrombolytic therapy for acute myocardial infarction

We describe a patient with acute inferior myocardial infarction who developed a "saddle" aortic embolus during streptokinase infusion. Three months previously, this patient had sustained an anterior infarction, and an apical aneurysm was found. This patient's embolus had most probably originated from a left ventricular mural thrombus that had been dislodged by streptokinase. As fibrinolytic treatment is gaining wide acceptance, physicians should be aware of this rare, but possible, complication.     

急性心肌梗死的药物溶栓治疗进展

早期溶栓治疗 (ｔｈｒｏｍｂｏｌｙｔｉｃｔｈｅｒａｐｙ ,ＴＴ)可获得梗塞相关动脉 (ＩＲＡ)早期开放 ,有效缩小心肌梗死面积 ,保护左室功能 ,降低病死率 ,因而成为急性心肌梗死(ＡＭＩ)的常规疗法之一。然而 ,目前最佳的溶栓方案仅能使 5 4%的ＡＭＩ获得充分再灌注 ,溶栓后血管再闭塞率为 8 0 %～13 5 % ,出血并发症仍存在 ,尤其颅内出血为 0 3 %～ 1%。如何提高溶栓疗效、降低副反应仍是当前倍受关注的课题。现将这方面的一些进展综述如下。1　溶栓适应证在扩大　　溶栓病例选择在 1996年中华心血管病杂志编委会制定的参考方案基础上有…