Use of initial ST-segment deviation for prediction of final electrocardiographic size of acute myocardial infarcts

The decision to administer thrombolytic therapy for limitation of acute myocardial infarction (AMI) size must occur when only the history, physical examination and 12-lead electrocardiogram of a patient are available. A method that could quickly assess the amount of jeopardized myocardium would greatly aid the physician. This study developed formulas from 68 anterior and 80 inferior AMI patients using the extent of initial ST-segment deviation (ST delta) to predict the final AMI size estimated by the Selvester QRS score in a population not receiving reperfusion therapy. Inclusion required: initial anterior or inferior AMI; admission electrocardiogram less than or equal to 8 hours after the onset of symptoms with evidence of epicardial injury; elevated creatine kinase-MB; a predischarge electrocardiogram taken greater than or equal to 72 hours after admission; and no AMI extension before the predischarge electrocardiogram. The extent of epicardial injury was quantified by counting the number of leads with greater than or equal to 0.1 mm ST delta, by the sum (sigma) of ST delta in all leads and by the sigma ST delta in the lead groups associated with each AMI location. These results were compared to the AMI size estimated from the predischarge electrocardiogram. Univariable and multivariable analyses generated these formulas for AMI size: anterior = 3[1.5 (number leads ST increases) - 0.4]; inferior = 3[0.6 (sigma ST increases II, III, aVF) + 2.0]. Thus, formulas based on quantitative measurements of ST delta on the admission electrocardiogram are predictive of final QRS-estimated AMI size, and may be useful in determining the efficacy of acute reperfusion therapy.     

High dose intravenous streptokinase in acute myocardial infarction

Early recanalization of infarct-related coronary arteries has been attempted in 40 patients with acute myocardial infarction (AMI) and angiographically proven total occlusion by brief high dose intravenous streptokinase infusion (IVSK). In 24 patients (60%) recanalization was achieved after 48 +/- 14 min of IVSK at an infusion rate of 30,000 to 40,000 IU/min (group A), in 16 patients there was a late (greater than 2 h) or no recanalization (group B). The total dose of SK was 1.7 +/- 0.48 Mio IU in group A and 1.74 +/- 0.41 Mio IU in group B, the time from the onset of symptoms to peak myocardial enzyme of creatine phosphokinase (CKMB) 11 +/- 3 h in group A and 22 +/- 6 h in group B (p less than 0.001). Biplane left ventricular ejection fraction increased from 55 +/- 9% at the time of acute angiography to 58 +/- 10% after 14 to 24 days in group A (p less than 0.1) and decreased from 49 +/- 11 to 41 +/- 11% in group B (p less than 0.005). There were four reocclusions in group A, two could be reopened by i.v. urokinase (1 Mio IU over 30 min). During a follow-up period of 18 +/- 8 months one patient in group A died from an early ventricular rupture 2 hours after recanalization, and one patient in group B from heart failure 7 months after IVSK. There was no serious bleeding or other complication related to IVSK. We conclude that IVSK is an effective and safe means of early recanalization of coronary thrombosis in AMI, and feasible in the majority of patients with AMI.     

Influence of infarct artery patency on the relation between initial ST segment elevation and final infarct size

Thirty seven patients with acute myocardial infarction were studied to determine the effect of perfusion of the infarct artery on the relation between the extent of initial ST segment elevation and final electrocardiographic infarct size. The sum of the initial peak ST elevations in all leads correlated with electrocardiographic infarct size in patients with anterior infarction and total occlusion of the infarct artery without collaterals. In patients with anterior infarction and subtotal occlusion of the infarct artery and in all patients with inferior infarction, infarct size was smaller than predicted from the extent of initial ST segment elevation. Collaterals to the infarct artery were present in eight of the 10 patients with inferior infarction and total occlusion. In patients with a persistently occluded infarct artery without collaterals the final infarct size correlated with the extent of initial peak ST segment elevation. This study provides further evidence that spontaneous reperfusion by anterograde flow or via collaterals may salvage jeopardized myocardium.     

Immunoglobulin response to intravenous streptokinase in acute myocardial infarction

OBJECTIVE--To devise assays to assess and follow the specific antibody response in patients treated with streptokinase for acute myocardial infarction. DESIGN--Venous blood samples were collected before treatment with streptokinase started and subsequently at regular intervals over one year. Specific IgG and subclass IgG1 were assessed by an enzyme linked immunosorbent assay. SETTING--Coronary care unit in a general hospital. PATIENTS--48 patients with acute myocardial infarction: 22 patients had venous blood samples taken at presentation only; serial blood samples were taken from 20 patients who then received thrombolytic therapy with streptokinase and six patients who were unsuitable for thrombolytic therapy. RESULTS--Titres of antibodies to streptokinase were low at presentation in 36 (75%) of the 48 patients. Serial measurements made in 20 patients showed the virtual disappearance of antibody within the first 24 hours. This was followed by a steady increase in the specific IgG1 titre, which peaked at day 14 before gradually declining. Values at one year remained significantly higher than baseline values. There was no evidence of an IgM response in the patients studied. CONCLUSION--Low titres of antibodies to streptokinase were widespread in the population. Antibody was consumed after treatment and the subsequent immunoglobulin rise suggested a secondary immune responses; the recently described neutralising capacity to streptokinase is probably related to this antibody.     

Pulmonary hemorrhage following intravenous streptokinase for acute myocardial infarction

A 50-year-old man was given 1.2 million units of intravenous streptokinase 3 hours after the onset of a hyperacute inferior myocardial infarction. He had been treated for pneumonia 4 weeks previously. Five days after thrombolytic therapy, he developed a massive hemoptysis. The implications of this side effect are discussed.     

Comparison of intravenous anisoylated plasminogen streptokinase activator complex and intracoronary streptokinase in acute myocardial infarction

Coronary angiography was used to compare the efficacy of anisoylated plasminogen streptokinase activator complex (APSAC) administered intravenously and streptokinase given by intracoronary infusion in inducing reperfusion in patients with a proven acute myocardial infarction. Forty-two patients received 30 U of APSAC intravenously over 5 minutes and 43 patients received 250,000 IU of streptokinase given via intracoronary infusion over 90 minutes, after occlusion of the infarct-related vessel was demonstrated by angiography. Reperfusion was achieved in 23 (64%) of 36 patients (mean time to reperfusion 46 minutes) treated with APSAC and 25 (67%) of 37 patients (mean time to reperfusion 45 minutes) treated with intracoronary streptokinase, who were angiographically evaluated 90 minutes after the start of treatment. Twenty-four hours after treatment, reocclusion had occurred in 1 (5%) of 22 patients in the APSAC group and in 3 (13%) of 23 patients in the streptokinase group. No major bleeding was observed in either treatment group despite a similar systemic lytic state that lasted for up to 48 hours. Two patients treated with APSAC died after severe left ventricular failure unrelated to therapy. The results indicate that APSAC given intravenously is as effective as streptokinase given intracoronary in producing thrombolysis in acute myocardial infarction. The major advantages of APSAC are its rapid and convenient administration by a single intravenous injection, the low rate of arterial reocclusion and good patient tolerance.     

Randomized double-blind trial of intravenous streptokinase for acute myocardial infarction

To determine the efficacy of intravenously administered streptokinase (SK) on infarct artery patency, global left ventricular (LV) function and clinical course in transmural acute myocardial infarction (AMI), 38 patients were studied using a randomized, double-blind, placebo-controlled scheme. Nineteen patients received 1.0 million units of SK followed by 72 hours of heparin infusion and 19 received placebo followed by heparin infusion, all within 5 hours (mean 3.3 hours) after AMI onset. Patients ineligible for inclusion in the randomized trial were followed as a second, "historical control" group. Compared with placebo, SK caused a higher frequency of enzymatic evidence of reperfusion (6% vs 79%, p less than 0.001) and of patent infarct-related arteries at predischarge coronary arteriography (64% vs 88%, difference not significant). (Patients in the control group had a relatively low frequency of spontaneous thrombolysis--28%.) In the SK group LV ejection fraction increased from early (average 7.3 hours after AMI) to late (predischarge) study (from 40% early to 47% late, p less than 0.05); in the placebo group LV ejection fraction did not change significantly (from 41% to 42%). Predischarge exercise radionuclide ventriculography showed mild and similar degrees of inducible ischemia in both groups. After a mean of 12.8 months of follow-up, 1 SK patient and 4 placebo patients had died (difference not significant). In conclusion, intravenous SK is efficacious for thrombolysis in patients with AMI. It improves global LV function without augmenting exercise-inducible ischemia.     

Influence of infarct artery patency on the relation between initial ST segment elevation and final infarct size.

Thirty seven patients with acute myocardial infarction were studied to determine the effect of perfusion of the infarct artery on the relation between the extent of initial ST segment elevation and final electrocardiographic infarct size. The sum of the initial peak ST elevations in all leads correlated with electrocardiographic infarct size in patients with anterior infarction and total occlusion of the infarct artery without collaterals. In patients with anterior infarction and subtotal occlusion of the infarct artery and in all patients with inferior infarction, infarct size was smaller than predicted from the extent of initial ST segment elevation. Collaterals to the infarct artery were present in eight of the 10 patients with inferior infarction and total occlusion. In patients with a persistently occluded infarct artery without collaterals the final infarct size correlated with the extent of initial peak ST segment elevation. This study provides further evidence that spontaneous reperfusion by anterograde flow or via collaterals may salvage jeopardized myocardium.     

Hypersensitivity vasculitis complicating intravenous streptokinase therapy in acute myocardial infarction

A 52-year-old man developed a hypersensitivity vasculitic rash on his legs nine days after receiving intravenous streptokinase therapy for acute myocardial infarction. The histological and immunological features and the differential diagnosis of this unusual complication of streptokinase therapy are reviewed.     

Importance of the early intravenous administration of streptokinase in acute myocardial infarct

To evaluate the importance of early initiation of fibrinolytic therapy with intravenous streptokinase (IVSK), we studied 34 consecutive patients, within less than six hours of the onset of acute myocardial infarction, who were treated with 1.5 million units of intravenous streptokinase. All the patients had coronary angiograms in the first seventy two hours. We correlated the angiograms with the time of onset of the IVSK. The patients were divided into 3 groups: Group num. 1: From zero to two hours (twelve patients); Group num. 2: From two to four hours (13 patients); and Group num. 3: From four to six hours (nine patients). We had angiographic reperfusion in twenty-four patients (70.2%) P less than 0.05. We observed reopening in the patients of group num. 1 (83.3%); in group 2, nine patients (69%) and in group num. 3, five patients, (55.5%), with statistical significance only in group num. 1 (p less than 0.05). We also demonstrated the utility of the electrocardiographic and enzymatic criteria to predict reperfusion. No mortality was related to the procedure. We concluded that a higher percentage of reperfusion is obtained the sooner intravenous streptokinase therapy is initiated.     

Effectiveness of intravenous streptokinase on infarct size and left ventricular function in acute myocardial infarction. Prospective and randomized study

Within 3 h after the onset of symptoms of myocardial infarction, 64 patients were randomly assigned to receive either a 1-h intravenous infusion of 1,500,000 IU of streptokinase (SK) or a conventional therapy. Infarct size was estimated in CK gram equivalent (CKg) by measurement of CK-MB every 3 hours during a 48-h period. Enzymatic study revealed that myocardial infarction of the SK group was significantly smaller (61.4 +/- 45 vs. 89.4 +/- 56 CKg, p less than .05). Angiograms were performed at early stage and five weeks after myocardial infarction. At first coronary angiogram, the infarct-related vessel was open in 82% in the SK group versus 12% in controls. The SK group had higher global ejection fraction at second angiogram (57 +/- 11% vs. 49 +/- 11%, p less than .02), but differences in regional wall motion were not significant. By analysis according to patency or occlusion of infarct-related vessel, global and regional ejection fractions were significantly better at first and at second angiograms in all patients and in anterior infarctions with a patent infarct-related coronary artery. There was no significant difference for inferior infarction. We conclude that intravenous streptokinase infusion early after the onset of myocardial infarction reduces infarct size and improves left ventricular function, chiefly in anterior infarction. This benefit appears to be closely correlated to patency of infarct-related vessels.     

Echocardiographic evaluation of intravenous streptokinase in myocardial infarction in the acute phase

The effects of intravenous fibrinolysis on left ventricular function in acute myocardial infarction were investigated by two-dimensional echocardiography in patients aged less than 70 for whom fibrinolysis was not contra-indicated and who were admitted less than 6 hours after the onset of a first myocardial infarction without heart failure. The 12 patients thus recruited were male; their mean age was 55 years and the infarct was anterior in 6 cases and posterior in 6 cases. Streptokinase was administered first by bolus intravenous injection (250,000 IU over 20 min), then by intravenous infusion (100,000 IU over 12 hours); this was followed by heparin. No other medication was given, except for intravenous lidocaine and oral nifedipine. Two-dimensional echocardiography was performed after 24 hours and on the 21st day, using the apical, two-cavities projection. The ejection fraction and the percentage of shortening in 16 ventricular segments (8 in the anterior and 8 in the inferior territories) were evaluated from systolic and diastolic ventricular contours. Ventricular angiography and coronary arteriography were performed concomitantly with echocardiography. No significant improvement in ejection fraction was observed. On both day 1 and day 21, the kinetics of the lower segments was improved and that of the anterior segments was distinctly reduced in inferior infarcts. The kinetics of all segments, irrespective of their territory, was significantly improved in anterior infarcts.     

Thrombolysis in acute myocardial infarction: effect of intravenous followed by intracoronary streptokinase application on estimates of infarct size

The effect of pretreatment with intravenous infusion of streptokinase (SK) (16,700 U/min for 90 minutes), started after diagnosis and followed by intracoronary application (2000 U/min) (protocol 1), was assessed retrospectively in 55 consecutive patients with acute transmural myocardial infarction (MI). Another 46 patients with acute MI treated previously by intracoronary thrombolysis served as control subjects (protocol 2). Reperfusion at first coronary injection was observed after pretreatment in 25 patients (45%), but in no control patient (p less than 0.001). Fifteen patients with successful pretreatment (group A), 20 patients with successful treatment according to protocol 2 (group B) and 9 patients with unsuccessful thrombolysis (group C) were restudied after 4 weeks. Data from patients with reinfarction, coronary bypass surgery or percutaneous transluminal coronary angioplasty before restudy were excluded. Thallium-201 scintigraphy was performed before and 24 hours after treatment, serum creatine kinase activity was measured every 8 hours for 3 days and regional ejection fraction (EF) of acute MI was determined before and 4 weeks after treatment. The scintigraphic, enzymatic and hemodynamic data before treatment indicated severe and comparable ischemia among the 3 groups. The thallium-201 perfusion defect decreased in group A (from 41 to 21%, p less than 0.01) and in group B (from 38 to 26%, p less than 0.01), but did not change in group C (from 37 to 31%, difference not significant). Peak serum creatine kinase levels normalized by the perfusion area of acute MI was 20, 33 and 58 U/liter unit in groups A, B and C. The mean values of groups A and C were significantly different (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Prospective randomized trial of intravenous and intracoronary streptokinase in acute myocardial infarction

To evaluate the relative thrombolytic efficacy and complications of intracoronary vs high-dose, short-term intravenous streptokinase infusion in patients with acute myocardial infarction, we performed baseline coronary arteriography and then randomly allocated 51 patients with acute myocardial infarction to receive either intracoronary (n = 25) or intravenous (n = 26) streptokinase. Patients getting the drug by the intracoronary route received 240,000 IU of streptokinase into the infarct-related artery over 1 hr, whereas those getting the drug by the intravenous route received either 500,000 IU of streptokinase over 15 min (n = 10) or 1 million IU of streptokinase over 45 min (n = 16). Angiographically observed thrombolysis occurred in 76% (19/25) of the patients receiving intracoronary streptokinase, in 10% (1/10) of the patients receiving 500,000 IU of streptokinase intravenously, and in 44% (7/16) of the patients receiving 1 million IU of streptokinase intravenously. Among patients in whom thrombolysis was observed, mean elapsed time from onset of streptokinase infusion until lysis was 31 +/- 18 min in patients receiving intracoronary streptokinase and 38 +/- 20 min in those receiving intravenous streptokinase (p = NS). Among patients in whom intravenous streptokinase "failed," intracoronary streptokinase in combination with intracoronary guidewire manipulation recanalized only 7% (1/15). Fibrinogen levels within 6 hr after streptokinase were significantly lower in the patients receiving intravenous streptokinase (39 +/- 17 mg/dl) than the levels in those receiving intracoronary streptokinase (88 +/- 70 mg/dl) (p less than .05) but were similar 24 hr after streptokinase in the two groups. Bleeding requiring transfusion occurred in one patient in each group. Thus, in this prospective randomized trial of intracoronary vs intravenous streptokinase, hemorrhagic complications were few, although both regimens produced a systemic lytic state. Although the thrombolytic efficacy of intracoronary streptokinase was superior to that of high-dose, short-term intravenous streptokinase, the higher-dose intravenous regimen (1 million IU over 45 min) achieved thrombolysis in a significant minority (44%) of patients and might be useful therapy for patients not having access to emergency catheterization.     

Value of immediate angioplasty after intravenous streptokinase in acute myocardial infarction

To improve reperfusion, immediate percutaneous transluminal coronary angioplasty (PTCA) was considered after intravenous streptokinase (0.75 to 1.5 million U) was administered to 98 patients with acute myocardial infarction less than 4 hours after the onset of chest pain. Thirty-four culprit arteries were occluded (group A); 42 arteries were patent with residual stenosis of more than 70% (group B). Twenty-two patients had residual stenosis of less than 70% (group C); eight of these had severe disease of the remaining vessels. Group C patients were either treated conservatively or underwent bypass surgery. Immediate PTCA was attempted in 74 patients (32 in group A, 42 in group B) and was successful in 68 (92%). Emergency bypass surgery for acute occlusion after PTCA was required in two patients. Follow-up averaged 23 months (range, 16 to 47 months). Asymptomatic occlusion recurred in three patients. Restenosis occurred in five patients: four had early restenosis (one in group A, three in group B) and one had late restenosis (group B). These arteries were successfully redilated. Late reinfarction occurred in two patients. They were treated with intravenous urokinase and repeat PTCA. Elective bypass surgery was performed in three patients because of recurrent angina. They had severe three-vessel disease as revealed by control angiography. The mortality rate was 2.7% (two patients; one in group B had early reinfarction, and one patient in group A died suddenly after 17 months). Eighty-five percent of patients treated with PTCA alone remain free of symptoms. This approach has a high success rate and low morbidity and mortality rates. Long-term results are superior to thrombolysis alone.     

High dose intravenous streptokinase in acute myocardial infarction--short and long term prognosis

Streptokinase (1 million international units) was given intravenously over 30 or 60 minutes to 50 patients four hours or less after the onset of acute myocardial infarction. All were aged less than or equal to 70 years and had 4 mm or greater ST segment elevation in anterior or inferior leads. Rapid (mean 95 min) ST segment resolution, which was taken to indicate reperfusion of the myocardium, occurred in 36 (72%) patients. In these 36 the average time from onset of symptoms to peak creatine kinase, creatine kinase MB, and myoglobin was 9.45 hours, whereas it was 17 hours in the 14 patients in whom indirect criteria did not indicate reperfusion. Reperfusion arrhythmias were invariably present and ventricular tachycardia developed in five patients and ventricular fibrillation in two. The infarct related artery was seen to be open in 28 (70%) of the 40 patients who had delayed coronary arteriography. The frequency of patency in the infarct related artery was no different in patients given streptokinase less than 2 hours or between 2-4 hours from onset of symptoms nor did it differ when streptokinase was infused over 30 or 60 minutes. Mean left ventricular ejection fraction was 57% in those with a patient infarct related artery and 48% in those with an occluded vessel. Eight patients subsequently underwent elective percutaneous transluminal coronary angioplasty after successful thrombolysis and six had coronary artery bypass grafting. There were nine in-hospital reocclusions of the infarct related coronary arteries. Two bleeding episodes occurred; one required transfusion. Five of the 50 patients died in hospital. All of them had had an anterior myocardial infarction; four had bifascicular block and one had right bundle branch block. During follow up, four patients died, two suddenly and two from reinfarction. During follow up (mean 15 months) the frequency of reinfarction, dyspnoea, and angina was low and there was no difference in the proportions of patients returning to work between those with an open infarct related artery and those with a closed infarct related artery. Intravenous administration of high dose streptokinase to selected patients during the acute phase of myocardial infarction is a safe, effective, and practical method of thrombolysis. It must, however, be followed by coronary arteriography to select those patients in whom percutaneous transluminal coronary angioplasty or coronary artery bypass grafting will be helpful.