Prevention of myocardial damage in acute myocardial ischemia by early treatment with intravenous streptokinase

We evaluated the effectiveness of early intravenous administration of 750,000 units of streptokinase in 53 patients with acute myocardial ischemia treated by a mobile-care unit at home (9 patients) or in the hospital (44 patients). Treatment was begun an average (+/- S.D.) of 1.7 +/- 0.8 hours from the onset of pain. Non-Q-wave infarctions developed subsequently in eight patients, whereas all the others had typical Q-wave infarct patterns. In 81 per cent of the patients the infarct-related artery was patent at angiography performed four to nine days after admission. Vessel patency was independent of the time of treatment, but residual left ventricular function was time dependent. Patients treated less than 1.5 hours after the onset of pain had a significantly higher ejection fraction (56 +/- 15 vs. 47 +/- 14 per cent; P less than 0.05) and infarct-related regional ejection fraction (51 +/- 19 vs. 34 +/- 20 per cent; P less than 0.01) and a lower QRS score (5.6 +/- 4.9 vs. 8.6 +/- 5.5; P less than 0.01) than patients receiving treatment between 1.5 and 4 hours after the onset of pain. Patients treated earlier by the mobile-care unit also had better-preserved left ventricular function than patients treated in the hospital. We conclude that thrombolytic therapy with streptokinase is most effective if given within the first 1.5 hours after the onset of symptoms of acute myocardial infarction.     

Effect of intravenous streptokinase on left ventricular function and early survival after acute myocardial infarction

In a double-blind trial of streptokinase for acute myocardial infarction, 219 consecutive patients presenting with infarction within four hours (mean, 3.0 +/- 0.8) of the onset of chest pain were randomly assigned to treatment with streptokinase (1.5 million units) or placebo, given intravenously over 30 minutes. The primary end point of the study was left ventricular function in patients with first infarctions. Patients who could undergo beta-blockade also received intravenous propranolol. Heparin (for 48 hours) and a combination of low-dose aspirin and dipyridamole were administered to both groups until cineangiography was performed at three weeks. In the patients with first infarctions treated with streptokinase, the left ventricular ejection fraction was 6 percentage points higher (streptokinase vs. placebo, 59 +/- 10.5 vs. 53 +/- 13.5 percent; P less than 0.005), with benefit to patients with either anterior infarction (57 +/- 11.9 vs. 49 +/- 15.9 percent; P less than 0.05) or inferior infarction (60 +/- 9.1 vs. 55 +/- 11.3 percent; P less than 0.05). Left ventricular function was improved regardless of whether concomitant propranolol was given. Survival (at 30 days) was improved with streptokinase: 2 deaths occurred among 79 patients who received this drug, as compared with 12 deaths among 93 patients who received placebo (2.5 vs. 12.9 percent, P = 0.012). Rates of reinfarction (streptokinase vs. placebo, 3 vs. 1 percent) and requirements for surgery or angioplasty (7 vs. 5 percent) were similar in the two groups. We conclude that administration of intravenous streptokinase (1.5 million units) to patients with a first myocardial infarction results in improved left ventricular function and short-term survival.     

Intravenous thrombolytic treatment for acute myocardial infarction. Effects of early intervention and early examination

Intravenous thrombolytic treatment (streptokinase or anisoylated plasminogen streptokinase activator complex (APSAC) was given to 50 consecutive patients within 3 hours after onset of symptoms of acute myocardial infarction. Left heart catheterisation with coronary angiography and simultaneous double view left ventriculography were performed approximately 4 hours after start of thrombolytic treatment. This examination showed that the acute infarct-related coronary artery was open in 36 patients (72%) and closed in 14 patients (28%). A higher left ventricular ejection fraction was found among patients with open, than among patients with closed infarct-related artery (58.8% vs. 48.4%, p = 0.05). The group with open artery also had a lower score of regional left ventricular dysfunction (1.7 vs. 2.4, p less than 0.05, on a scale from 0-3). Single, double and triple vessel coronary heart disease was found in 22, 14 and 13 patients respectively. Mean age was lower in the group with single vessel disease as compared to double and triple vessel disease (48.4 years vs. 53.4 and 55.4 years, p less than 0.05 and p less than 0.005). Independently of whether the infarct-related artery was open or closed, there tended to be an inverse correlation between number of diseased vessels and preservation of left ventricular function (statistical significance only for single vessel versus triple vessel disease with respect to score of regional left ventricular dysfunction, 1.8 vs. 2.4, p less than 0.05). These findings suggest that early thrombolytic treatment within 3 hours of onset of symptoms may preserve myocardial tissue during the evolution of acute infarction. Furthermore, a presumably better collateralisation from adjacent coronary arteries without stenoses may be important for myocardial preservation. Finally, early angiographic examination can be performed safely and is a good support for determination of further treatment, which in the actual patients was coronary bypass surgery in 8 cases, transluminal angioplasty, PTCA, in 20 cases, and medical treatment alone in 22 cases.     

Endothelin-1 in patients with complicated and uncomplicated myocardial infarction

Summary Endothelin-1 concentrations were measured in peripheral venous blood samples from 42 patients with acute myocardial infarction. In patients with ischemic or hemodynamic complications (n = l1), endothelin-1 concentrations were significantly higher already on admission (P = 0.008) and remained significantly higher until day 6 after admission compared to patients with uncomplicated infarctions (n = 31; P = 0.035). There were no close correlations between peak concentrations of endothelin-1 and creatine kinase or creatine kinase isoenzyme MB mass in either group. Only in complicated patients did left ventricular ejection fraction correlate closely and inversely with peak endothelin-1 concentrations (r = –0.71; P = 0.03). Therefore, plasma endothelin-1 concentrations in patients with acute myocardial infarction patients may reflect states of markedly depressed cardiac performance and recurrent myocardial ischemia.Abbreviations AMI acute myocardial infarction - CK creatine kinase - CKMB mass CK isoenzyme MB mass - LVEF left ventricular ejection fraction - ET-1 endothelin-1     

Effects of coronary-artery bypass on global and regional left ventricular function during exercise.

To determine the effect of coronary revascularization on exercise-induced abnormalities of left ventricular-ejection fraction and regional contraction, we obtained electrocardiograph-gated 99mTc radionuclide cineangiograms before and after operation in 23 consecutive patients. At rest, their average ejection fraction remained unchanged: 51 +/- 3 versus 54 +/- 4 per cent (+/- S.E.M.). However, 17 of the patients showed improvement of ejection fraction during postoperative exercise (increase of 51 per cent). The remaining six patients had no change or a decreased ejection fraction during exercise. All patients with improved ejection fractions during exercise were symptomatically improved. No improvement of regional function occurred at rest, but improvement did occur in regions of exercise-induced dysfunction. Although coronary revascularization has little effect on left ventricular function at rest, the ejection fraction during exercise and exercise-induced wall-motion abnormalities improve in most patients who experience symptomatic improvement.     

Protective effects of aspirin against acute myocardial infarction and death in men with unstable angina. Results of a Veterans Administration Cooperative Study

We conducted a multicenter, double-blind, placebo-controlled randomized trial of aspirin treatment (324 mg in buffered solution daily) for 12 weeks in 1266 men with unstable angina (625 taking aspirin and 641 placebo). The principal end points were death and acute myocardial infarction diagnosed by the presence of creatine kinase MB or pathologic Q-wave changes on electrocardiograms. The incidence of death or acute myocardial infarction was 51 per cent lower in the aspirin group than in the placebo group: 31 patients (5.0 per cent) as compared with 65 (10.1 per cent); P = 0.0005. Nonfatal acute myocardial infarction was 51 per cent lower in the aspirin group: 21 patients (3.4 per cent) as compared with 44 (6.9 per cent); P = 0.005. The reduction in mortality in the aspirin group was also 51 per cent--10 patients (1.6 per cent) as compared with 21 (3.3 per cent)--although it was not statistically significant; P = 0.054. There was no difference in gastrointestinal symptoms or evidence of blood loss between the treatment and control groups. Our data show that aspirin has a protective effect against acute myocardial infarction in men with unstable angina, and they suggest a similar effect on mortality.     

The western Washington randomized trial of intracoronary streptokinase in acute myocardial infarction. A 12-month follow-up report

After cardiac catheterization and coronary arteriography, 134 patients who had had an acute myocardial infarction were randomly assigned to treatment with intracoronary streptokinase (4000 U per minute, begun approximately 4 1/2 hours after the onset of symptoms, for a total of 286,000 +/- 77,800 U over 72 +/- 24 minutes); 116 control patients received standard care after they returned to the coronary care unit, immediately after angiography. Preliminary results of this trial have been published in the Journal (1983; 309:1477-81). During the first 30 days, 5 deaths occurred in the streptokinase group and 13 occurred in the control group (3.7 vs 11.2 per cent, P = 0.02); during the first year, the corresponding figures were 11 and 17 deaths (8.2 vs. 14.7 per cent, P = 0.10). However, when a minor imbalance in the ejection fraction and infarct location between the two groups was adjusted by logistic regression, the difference in one-year mortality became significant (P = 0.03). In the streptokinase group, 2 of the 80 patients in whom perfusion was reestablished (2.5 per cent) had died by one year, whereas 3 of the 13 with partial reperfusion (23.1 per cent) and 6 of the 41 with no reperfusion (14.6 per cent) had died (P = 0.008). Mortality among patients with partial reperfusion was not significantly different from that among those without reperfusion (P greater than 0.90). No base-line clinical, angiographic, or hemodynamic variable was predictive of successful reperfusion, according to univariate and multivariate analyses. We conclude that intracoronary streptokinase reduces one-year mortality among patients with acute myocardial infarction, but this improvement occurs only among those in whom thrombolysis results in coronary artery reperfusion.     

Exercise-induced ischemia in mildly symptomatic patients with coronary-artery disease and preserved left ventricular function. Identification of subgroups at risk of death during medical therapy

To determine prospectively whether the severity of reversible left ventricular ischemia provides prognostic information in mildly symptomatic patients with coronary-artery disease and preserved left ventricular function at rest (ejection fraction greater than 40 per cent), we studied 117 patients by means of exercise electrocardiography and radionuclide angiography. No patient had stenosis of the left main coronary artery. Mortality during subsequent medical therapy was significantly associated (by univariate life-table analysis) with three-vessel coronary-artery disease and the magnitude of the ejection fraction during exercise. In patients with three-vessel disease who had both ST-segment depression of 1 mm or more and a decrease in ejection fraction during exercise, in association with an exercise tolerance of 120 W or less, the probability of survival at four years was only 71 +/- 11 per cent (S.E.). All deaths occurred in this subgroup. Thus, objective evidence of left ventricular ischemia during exercise and exercise capacity identify one subgroup of minimally symptomatic patients with three-vessel disease with an excellent prognosis and another subgroup at relatively high risk of dying during subsequent medical therapy.     

The creatine kinase system in normal and diseased human myocardium

We measured creatine kinase activity, isozyme composition, and total creatine content in biopsy samples of left ventricular myocardium from 34 adults in four groups: subjects with normal left ventricles, patients with left ventricular hypertrophy due to aortic stenosis, patients with coronary artery disease without left ventricular hypertrophy, and patients with coronary artery disease and left ventricular hypertrophy due to aortic stenosis. As compared with specimens of normal left ventricles, those from all patients with left ventricular hypertrophy had lower creatine kinase activity, higher MB creatine kinase isozyme content and activity, and lower creatine content. Specimens from the patients without left ventricular hypertrophy had normal creatine kinase activity, increased MB creatine kinase isozyme content and activity, and decreased total creatine content. The normal ventricles showed almost no MB isozyme content or activity. These data suggest that changes in the creatine kinase system occur in both pressure-overload hypertrophy and coronary artery disease. Patients with myocardial infarction who have mild or no preexisting fixed coronary artery disease or pressure-overload hypertrophy would not be expected to have elevation of serum MB creatine kinase.     

非体外循环下冠状动脉旁路移植围术期血浆脑钠肽释放及其相关性研究

背景：B型脑钠肽已成为心血管疾病诊断重要的血清标志物,作为心血管疾病危险因素分层的重要因子。 目的：分析冠状动脉旁路移植前后B型脑钠肽与各项血流动力学参数的关系。 方法：选择30例冠心病行冠脉旁路移植患者,分为左室射血分数≥ 50%心功能正常患者13例;左室射血分数< 50%心功能不全患者17例。观察患者移植前1 d、移植后7 h、移植后1,3,5,7 d血浆B型脑钠肽水平变化趋势,分析移植前后B型脑钠肽与心功能各项指标的相关关系。 结果与结论：左室射血分数≥ 50%组患者冠脉旁路移植前后血浆B型脑钠肽水平显著低于左室射血分数< 50%组;组内比较移植后血浆B型脑钠肽水平均显著高于移植前(P < 0.05或P < 0.001)。患者冠脉旁路移植前B型脑钠肽水平与纽约心脏病协会心功能分级、左房内径、左室内径呈正相关(r=0.61;r=0．34;r=0．67);与左室射血分数、心排血量呈负相关(r=-0.75;r=-0.70)。患者移植后B型脑钠肽峰值浓度与出院前纽约心脏病协会心功能分级、超声心动图左室舒张末期内径、肺动脉压力呈正相关(r=0.72;r=0.70;r=0.45)。结果说明冠心病患者冠脉旁路移植前血浆B型脑钠肽质量浓度与左心室射血分数及左心室舒张末期内径有很好的相关性,能准确反映冠脉旁路移植前后的心功能状态。 中国组织工程研究杂志出版内容重点：组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程全文链接：     

Mechanical model for the simulation of ischaemia and infarction of the left ventricle

Several ischaemic states, including immediate infarction, occurring in a canine left ventricle at the onset of the ejection phase and affecting regions of varying sizes are simulated, employing a recently developed comprehensive finite-element model. The analysis assumes an instantaneous partial or complete loss of contractility in the damaged region, whereas the passive mechanical properties of the tissue are yet unaltered. The results indicate a progressive deterioration of the cardiac performance, as well as considerable geometrical changes in the kinematics of the whole ventricle, directly related to both ischaemia level and the ischaemic region size. Owing to the reduction in the stroke volume, the simulation predicts a degradation of up to 33 per cent in the ejection fraction for an infarct affecting 43 per cent of the ventricular wall volume. A quantitative relationship between the ejection fraction, the level of ischaemia and the size of the ischaemic zone is derived and presented.     

糖尿病合并冠状动脉狭窄患者左室造影前后左室舒张末压差值比较研究

目的 探讨糖尿病对合并冠状动脉狭窄患者左室造影前后舒张末压差值和左室功能的影响。方法 选择行冠状动脉造影及左室造影的患者834例，其中无冠脉病变的患者172例，冠状动脉狭窄的患者662例。根据其有无糖尿病，将之分为糖尿病合并冠状动脉狭窄组(DM组)110人，及单纯冠状动脉狭窄组(非DM组)552人，所有病人都进行左室造影，测定左室射血分数(EF)，造影前后左室舒张末压(D1、D2)。结果 DM组患者造影前后左室舒张末压的差值(D3)明显高于非DM组的患者，两组间的射血分数无明显差异，年龄增加、糖尿病、EF的降低，与造影前后左室舒张末压的差值呈负相关。结论 糖尿病合并冠状动脉狭窄患者可以在心脏的收缩功能发生异常之前，表现出对心脏舒张功能的损害，而造影前后，左室舒张末压的差值可以更为敏感地反映左室舒张功能的改变。     

Effects of the early administration of enalapril on mortality in patients with acute myocardial infarction. Results of the Cooperative New Scandinavian Enalapril Survival Study II (CONSENSUS II)

BACKGROUND. Long-term administration of angiotensin-converting--enzyme (ACE) inhibitors has been shown to improve survival in patients with symptomatic left ventricular failure and to attenuate left ventricular dilatation in patients with myocardial infarction. We studied whether mortality could be reduced during the 6 months after an acute myocardial infarction with use of the ACE inhibitor enalapril. METHODS. At 103 Scandinavian centers patients with acute myocardial infarctions and blood pressure above 100/60 mm Hg were randomly assigned to treatment with either enalapril or placebo, in addition to conventional therapy. Therapy was initiated with an intravenous infusion of enalapril (enalaprilat) within 24 hours after the onset of chest pain, followed by administration of oral enalapril. RESULTS. Of the 6090 patients enrolled, 3046 were assigned to placebo and 3044 to enalapril. The life-table mortality rates in the two groups at one and six months were not significantly different (6.3 and 10.2 percent in the placebo group vs. 7.2 and 11.0 percent in the enalapril group, P = 0.26). The relative risk of death in the enalapril group was 1.10 (95 percent confidence interval, 0.93 to 1.29). Death due to progressive heart failure occurred in 104 patients (3.4 percent) in the placebo group and 132 (4.3 percent) in the enalapril group (P = 0.06). Therapy had to be changed because of worsening heart failure in 30 percent of the placebo group and 27 percent of the enalapril group (P less than 0.006). Early hypotension (systolic pressure less than 90 mm Hg or diastolic pressure less than 50 mm Hg) occurred in 12 percent of the enalapril group and 3 percent of the placebo group (P less than 0.001). CONCLUSIONS. Enalapril therapy started within 24 hours of the onset of acute myocardial infarction does not improve survival during the 180 days after infarction.     

急性心肌梗死患者外周血CD34+细胞与肌酸激酶同工酶、N末端B型利钠肽原、左室射血分数的相关性

背景：急性心肌梗死后具有动员骨髓和外周血中的CD34⁺干细胞的潜能,参与坏死心肌的自身修复,但外周血CD34⁺细胞与其他相关指标的关系尚不明确, 目的：观察急性心肌梗死患者外周血单个核CD34⁺细胞的动态变化规律,并进一步分析其与肌酸激酶同工酶、N末端B型利钠肽原、左室射血分数的相关性。 方法：采集急性心肌梗死患者(实验组)发病第2,3,4,5,7,30,90,120天的外周静脉血及入院后相应时间点非冠状动脉粥样硬化性心脏病患者(对照组)外周静脉血,采用流式细胞仪测定外周血单个核细胞CD34⁺的百分率。同时对心肌梗死患者进行肌酸激酶同工酶、N末端B型利钠肽原及心脏超声检测。 结果与结论：①实验组单个核细胞CD34⁺细胞百分率于心肌梗死后第3天开始升高,第4天达到高峰,第90天回降至基线水平。对照组单个核细胞CD34⁺细胞百分率无明显变化。②实验组外周血单个核CD34⁺细胞与左室射血分数呈正相关关系,与N末端B型利钠肽原呈负相关关系;与肌酸激酶同工酶无相关性。提示急性心肌梗死后4~8 d内给予干细胞治疗可适度改善心脏收缩功能,并且较高的CD34⁺干细胞表达有益于急性心肌梗死后心肌功能的恢复。     

Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. The Heart Outcomes Prevention Evaluation Study Investigators

BACKGROUND: Angiotensin-converting-enzyme inhibitors improve the outcome among patients with left ventricular dysfunction, whether or not they have heart failure. We assessed the role of an angiotensin-converting-enzyme inhibitor, ramipril, in patients who were at high risk for cardiovascular events but who did not have left ventricular dysfunction or heart failure. METHODS: A total of 9297 high-risk patients (55 years of age or older) who had evidence of vascular disease or diabetes plus one other cardiovascular risk factor and who were not known to have a low ejection fraction or heart failure were randomly assigned to receive ramipril (10 mg once per day orally) or matching placebo for a mean of five years. The primary outcome was a composite of myocardial infarction, stroke, or death from cardiovascular causes. The trial was a two-by-two factorial study evaluating both ramipril and vitamin E. The effects of vitamin E are reported in a companion paper. RESULTS: A total of 651 patients who were assigned to receive ramipril (14.0 percent) reached the primary end point, as compared with 826 patients who were assigned to receive placebo (17.8 percent) (relative risk, 0.78; 95 percent confidence interval, 0.70 to 0.86; P<0.001). Treatment with ramipril reduced the rates of death from cardiovascular causes (6.1 percent, as compared with 8.1 percent in the placebo group; relative risk, 0.74; P<0.001), myocardial infarction (9.9 percent vs. 12.3 percent; relative risk, 0.80; P<0.001), stroke (3.4 percent vs. 4.9 percent; relative risk, 0.68; P<0.001), death from any cause (10.4 percent vs. 12.2 percent; relative risk, 0.84; P=0.005), revascularization procedures (16.3 percent vs. 18.8 percent; relative risk, 0.85; P<0.001), cardiac arrest (0.8 percent vs. 1.3 percent; relative risk, 0.62; P=0.02), [corrected] heart failure (9.1 percent vs. 11.6 percent; relative risk, 0.77; P<0.001), and complications related to diabetes (6.4 percent vs. 7.6 percent; relative risk, 0.84; P=0.03). CONCLUSIONS: Ramipril significantly reduces the rates of death, myocardial infarction, and stroke in a broad range of high-risk patients who are not known to have a low ejection fraction or heart failure.     

Detection of early cardiac dysfunction in patients with severe beta-thalassemia and chronic iron overload.

To detect early left ventricular dysfunction, we used radionuclide cineangiography to determine left ventricular ejection fraction during exercise in 24 patients with transfusion-dependent, congenital anemias, 21 of whom had severe beta thalassemia. Ejection fraction at rest was normal in 21 patients (greater than 45 per cent) and in all patients was 53 +/- 2 per cent (mean +/- S.E.M.)--not significantly different from the value in normal subjects. However, ejection fraction during exercise was normal in only 11 patients (53 +/- 3 per cent in all patients, P less than 0.001 as compared with the normal value). All eight patients who had received fewer than 100 transfusions but only three of 16 (19 per cent, P less than 0.001) who had received 100 or more transfusions had normal responses during exercise. Whereas echocardiographic fractional shortening at rest was normal in 16 of 19 patients studied, eight patients with normal fractional shortening had abnormal ejection-fraction responses to exercise. Thus, radionuclide cineangiography during exercise is a highly sensitive technique for detecting preclinical myocardial dysfunction in patients with systemic iron overload.     

Platelet glycoprotein IIb/IIIa inhibition with coronary stenting for acute myocardial infarction.

BACKGROUND: When administered in conjunction with primary coronary stenting for the treatment of acute myocardial infarction, a platelet glycoprotein IIb/IIIa inhibitor may provide additional clinical benefit, but data on this combination therapy are limited. METHODS: We randomly assigned 300 patients with acute myocardial infarction in a double-blind fashion either to abciximab plus stenting (149 patients) or placebo plus stenting (151 patients) before they underwent coronary angiography. Clinical outcomes were evaluated 30 days and 6 months after the procedure. The angiographic patency of the infarct-related vessel and the left ventricular ejection fraction were evaluated at 24 hours and 6 months. RESULTS: At 30 days, the primary end point--a composite of death, reinfarction, or urgent revascularization of the target vessel--had occurred in 6.0 percent of the patients in the abciximab group, as compared with 14.6 percent of those in the placebo group (P=0.01); at 6 months, the corresponding figures were 7.4 percent and 15.9 percent (P=0.02). The better clinical outcomes in the abciximab group were related to the greater frequency of grade 3 coronary flow (according to the classification of the Thrombolysis in Myocardial Infarction trial) in this group than in the placebo group before the procedure (16.8 percent vs. 5.4 percent, P=0.01), immediately afterward (95.1 percent vs. 86.7 percent, P=0.04), and six months afterward (94.3 percent vs. 82.8 percent, P=0.04). One major bleeding event occurred in the abciximab group (0.7 percent); none occurred in the placebo group. CONCLUSIONS: As compared with placebo, early administration of abciximab in patients with acute myocardial infarction improves coronary patency before stenting, the success rate of the stenting procedure, the rate of coronary patency at six months, left ventricular function, and clinical outcomes.     

A randomized trial of intracoronary streptokinase in the treatment of acute myocardial infarction

Fifty patients with acute myocardial infarction were randomly assigned to receive either intracoronary streptokinase or standard (control) therapy within about three hours after the onset of pain. Coronary perfusion was reestablished in 19 of 24 patients receiving streptokinase. Streptokinase alleviated pain (as indicated by differences in subsequent morphine use). The Killip class was significantly improved after therapy with streptokinase, as were changes in radionuclide ejection fraction between Days 1 and 10 in surviving patients (+3.9 vs. -3.0 per cent, P less than 0.01). The echocardiographic wall-motion index also showed greater improvement after streptokinase treatment (P less than 0.01). Streptokinase therapy was associated with rapid evolution of electrocardiographic changes, which were essentially complete within three hours after therapy, but loss of R waves, ST elevation, and development of Q waves in the convalescent period were greater in the control group (P less than 0.01). The time required to reach peak plasma enzyme concentrations was significantly shorter after streptokinase. The incidence of early and late ventricular arrhythmias was not affected by treatment. We conclude that intracoronary streptokinase appears to have a beneficial effect on the early course of acute myocardial infarction.     

Surgical Myocardial Revascularization of Patients with Ischemic Cardiomyopathy and Severe Left Ventricular Disfunction

OBJECTIVE:

To determine long-term survival, identify preoperative factors predictive of a favorable outcome, and assess functional improvement after coronary artery bypass grafting in patients with advanced left ventricular dysfunction.

METHODS:

Between 1995 and 2001, 244 patients who underwent coronary artery bypass grafting and had a preoperative left ventricular ejection fraction less than or equal to 35% were included. left ventricular ejection fraction was determined by uniplanar or biplanar ventriculography during left heart catheterization. Indication for surgery was predominance of tissue viability. Functional improvement was evaluated through echocardiography and gated scintigraphy at exercise/rest. Survival was determined by Kaplan-Meier analysis.

RESULTS:

Mean left ventricular ejection fraction was 29±4% (ranged from 9% to 35%). An average of 3.01 coronary bypass grafts per patient were performed. In-hospital mortality was 3.7% (9 patients). The 4-year survival rate was 89.7%. Multivariate correlates of favorable short- and long-term outcome were preoperative New York Heart Association Funcional classification for congestive heart failure class I/II, lower PAsP, higher left ventricular ejection fraction and gated left ventricular ejection fraction Ex/Rest ratio >5%. Left ventricular ejection fraction rise from 32±5% to 39±5%, p <0.001. Gated left ventricular ejection fraction at exercise/rest increased markedly after surgery: from 27±8%/23±7% to 37±5%/31±6%, p <0.001.

CONCLUSIONS:

In selected patients with severe ischemic left ventricular dysfunction and predominance of tissue viability, coronary artery bypass grafting may be capable of implement preoperative clinical/functional parameters in predicting outcome as left ventricular ejection fraction and gated left ventricular ejection fraction at exercise/rest.     

A randomized trial of intravenous tissue plasminogen activator for acute myocardial infarction with subsequent randomization to elective coronary angioplasty

Patients presenting within four hours of the onset of acute myocardial infarction were randomly assigned to receive 80 to 100 mg of recombinant human-tissue plasminogen activator (t-PA) intravenously over a period of three hours (n = 72) or placebo (n = 66). Administration of the study drug was followed by coronary arteriography, and candidates for percutaneous transluminal coronary angioplasty were randomly assigned either to undergo angioplasty on the third hospital day (n = 42) or not to undergo angioplasty during the 10-day study period (n = 43). The patency rates of the infarct-related arteries were 66 percent in the t-PA group and 24 percent in the placebo group. No fatal or intracerebral hemorrhages occurred, and episodes of bleeding requiring transfusion were observed in 7.6 percent of the placebo group and 9.8 percent of the t-PA group. As compared with the use of placebo, administration of t-PA was associated with a higher mean (+/- SEM) ejection fraction on the 10th hospital day (53.2 +/- 2.0 vs. 46.4 +/- 2.0 percent, P less than 0.02), an improved ejection fraction during the study period (+3.6 +/- 1.3 vs. -4.7 +/- 1.3 percentage points, P less than 0.0001), and a reduction in the prevalence of congestive heart failure from 33 to 14 percent (P less than 0.01). Angioplasty improved the response of the ejection fraction to exercise (+8.1 +/- 1.4 vs. +1.2 +/- 2.2 percentage points, P less than 0.02) and reduced the incidence of postinfarction angina from 19 to 5 percent (P less than 0.05), but did not influence the ejection fraction at rest. These data support an approach to the treatment of acute myocardial infarction that includes early intravenous administration of t-PA and deferred cardiac catheterization and coronary angioplasty.