Early exercise test in acute myocardial infarction treated with intravenous streptokinase

The aim of this study was to assess the value of the early exercise test (ET) in patients with acute myocardial infarction (AMI) treated with IV streptokinase (SK). The authors studied 70 patients with first AMI; 31 were treated with SK and 39 were not. Before discharge everyone was given early exercise up to 5-6 METs and catheterized within 22.9 +/- 7.2 days. There was no significant difference in the number of positive ETs between the two groups (11/31 and 14/39 respectively). There was significant difference in favor of: (1) the recanalization of the infarct-related artery in the SK group, (2) the negative ET in patients with recanalized vessels in both groups, (3) the positive ET in patients with multi-vessel coronary disease. It is concluded that the results of early ET in patients with AMI are related to the recanalization of the infarct-related artery and the coexistence of multi-vessel coronary artery disease, regardless of SK treatment. Patients with successful thrombolysis have negative ET more frequently.     

Pathological changes after intravenous streptokinase treatment in eight patients with acute myocardial infarction.

At necropsy five of eight patients (mean age 57 years) who died after intravenous streptokinase treatment for severe acute myocardial infarction (mean Peel index = 18) were found to have a patent infarct related coronary artery. Coronary artery stenoses were caused by fibrofatty atheromatous plaques; there were no residual thrombi in the lumen or acute intimal lesions. Three of these infarcts were of partial thickness (less than two thirds wall width) with sparing of the outer third of the myocardium and subendocardial zones. In the other three patients the infarct related coronary arteries remained histologically closed with residual lumen thrombi and underlying intimal lesions. Two infarcts were transmural. Six of the eight infarcts were noticeably haemorrhagic. Myocardial haemorrhage was confined to areas of necrotic myocardium and did not affect viable regions. These findings suggest that thrombus overlying a complex lesion may be more difficult to lyse than thrombus overlying a simple fibrofatty plaque. They also suggest that myocardial haemorrhage outside the infarct area, which might lead to cardiac rupture or delayed healing, does not usually occur.     

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.     

Intracoronary versus intravenous streptokinase in acute myocardial infarction

To assess the relative efficacy of coronary thrombolysis using intracoronary versus intravenous streptokinase, 32 patients with acute myocardial infarction were randomly assigned to receive intracoronary (n = 17) and intravenous streptokinase (n = 15). All patients underwent selective coronary arteriography before and after administration of streptokinase by either route within 4 hours of the onset of symptoms. Intravenous streptokinase was given as 750,000 units over 30 minutes, while a mean dose of 180,000 units was required for thrombolysis in the group having intracoronary delivery. Recanalization occurred in 71.4% (10 of 14) of patients receiving streptokinase, by the intracoronary group in contrast to only 25% of patients (3 of 12) who received the drug intravenously (P less than 0.05). Spontaneous thrombolysis was seen in 17.6% and 20% of the patients in the groups having intracoronary and intravenous delivery, respectively. Bleeding complications were few in both groups. Thus, when baseline coronary arteriography is performed, recanalization with intracoronary streptokinase is more effective in the treatment of acute myocardial infarction than intravenous streptokinase.     

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.     

Pathological changes after intravenous streptokinase treatment in eight patients with acute myocardial infarction

At necropsy five of eight patients (mean age 57 years) who died after intravenous streptokinase treatment for severe acute myocardial infarction (mean Peel index = 18) were found to have a patent infarct related coronary artery. Coronary artery stenoses were caused by fibrofatty atheromatous plaques; there were no residual thrombi in the lumen or acute intimal lesions. Three of these infarcts were of partial thickness (less than two thirds wall width) with sparing of the outer third of the myocardium and subendocardial zones. In the other three patients the infarct related coronary arteries remained histologically closed with residual lumen thrombi and underlying intimal lesions. Two infarcts were transmural. Six of the eight infarcts were noticeably haemorrhagic. Myocardial haemorrhage was confined to areas of necrotic myocardium and did not affect viable regions. These findings suggest that thrombus overlying a complex lesion may be more difficult to lyse than thrombus overlying a simple fibrofatty plaque. They also suggest that myocardial haemorrhage outside the infarct area, which might lead to cardiac rupture or delayed healing, does not usually occur.     

Vasculitis complicating treatment with intravenous anisoylated plasminogen streptokinase activator complex in acute myocardial infarction.

Vasculitis developed in six of 253 patients treated with intravenous anisoylated plasminogen streptokinase activator complex (APSAC) after acute myocardial infarction. All patients recovered spontaneously with no evidence of renal impairment and no long term sequelae. Although leucocytoclastic vasculitis and serum sickness have been reported after streptokinase treatment, such allergic reactions have not been described as a complication of other thrombolytic agents.     

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.     

Vasculitis complicating treatment with intravenous anisoylated plasminogen streptokinase activator complex in acute myocardial infarction

Vasculitis developed in six of 253 patients treated with intravenous anisoylated plasminogen streptokinase activator complex (APSAC) after acute myocardial infarction. All patients recovered spontaneously with no evidence of renal impairment and no long term sequelae. Although leucocytoclastic vasculitis and serum sickness have been reported after streptokinase treatment, such allergic reactions have not been described as a complication of other thrombolytic agents.     

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.     

A randomized controlled trial of intravenous streptokinase in evolving acute myocardial infarction

To determine the efficacy of intravenous streptokinase in acute myocardial infarction, 52 patients were randomized to intravenous streptokinase or control groups. Time from onset of infarction to randomization was similar in the streptokinase group and control group, 4.9 +/- 2.1 hours vs 5.4 +/- 2.4 hours, respectively. The 28 streptokinase patients received an intravenous infusion of 700,000 units of streptokinase followed by full-dose anticoagulation. The 24 control patients received normal saline solution followed by full-dose anticoagulation. Of 28 streptokinase patients, 12 (43%) had noninvasive evidence of reperfusion by early peaking of serum creatine kinase (peak creatine kinase less than 16 hours after onset of infarction) vs 3 of 24 control patients (13%), p less than 0.02. Two streptokinase patients (7%) had reperfusion arrhythmias during streptokinase infusion. One streptokinase patient (4%) and two control patients (8%) died during hospitalization. At angiography (16 +/- 5 days after infarction) 22 of 26 streptokinase patients (85%) had a patent infarct-related coronary artery compared to 8 of 20 control patients (40%), p less than 0.01. Comparison of radionuclide left ventricular ejection fraction assessed acutely (28 +/- 10 hours after infarction) with left ventricular ejection fraction at hospital discharge (15 +/- 3 days after infarction) showed no significant improvement in either the streptokinase or control group, 0% and +1%, respectively. At follow-up 13 +/- 7 months after infarction, total mortality rate was similar in the streptokinase group and control group, 17.8% (5 of 28 streptokinase patients) and 20.8% (5 of 24 control patients), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Successful intravenous streptokinase treatment of a child with Kawasaki disease complicated by acute myocardial infarction

A 9-year-old boy developed ischemic cardiac symptoms 1 year after he presented with Kawasaki disease. The myocardial infarction was confirmed by the typical changes of electrocardiograms, echocardiograms, cardiac enzymes, thallium myocardial scintigrams, and angiograms. With successful intravenous streptokinase therapy, he remained well during the following 4 months. © 1995 Wiley-Liss, Inc.     

A randomized trial of intravenous and intracoronary streptokinase in patients with acute myocardial infarction

The clinical effects of intravenous streptokinase in patients with acute myocardial infarction were compared with those of intracoronary streptokinase in a randomized, prospective study. Comparisons were also made with a historical control group. Fifty patients were entered into the study at 2.4 +/- 1.2 hr after onset of pain, and 27 were assigned to intravenous and 23 to intracoronary therapy. The doses of streptokinase averaged 212,000 U ic and 845,000 U iv (0.75 X 10(6) U/5 hr, n = 14 or 10(6) U/1 hr, n = 13). Results of studies of the two intravenous dosage schedules were similar and so were combined. Streptokinase was administered at 2.8 +/- 1.0 hr after onset of pain in the intravenous and at 4.3 +/- 1.4 hr in the intracoronary drug group (p less than .001). Convalescent (day 10) radionuclide ejection fractions were 54 +/- 14% for the intravenous and 50 +/- 16% for the intracoronary drug group. Change in ejection fraction from day 1 to 10 tended to be greater after intravenous drug: 5.1% (p less than .08) vs 1.2% (NS). Semiquantitative regional wall motion indexes in the infarct zone showed significant and similar modest improvement from admission to day 10 in both groups (p less than .02). Accelerated enzyme-release kinetics were noted after both therapies. Times of peak enzyme levels for patients on intravenous and intracoronary drug were, respectively, 12.5 +/- 5.0 and 11.5 +/- 4.3 hr for creatine kinase MB isoenzyme and 31.7 +/- 11.8 and 28.1 +/- 12.7 hr for lactic dehydrogenase (LDH). Peak LDH-1 level was lower in patients receiving intravenous drug than in the historical control group (p less than .05). Electrocardiographically summed ST segments diminished rapidly after therapy in both groups; Q wave development was similar and overall R wave loss was equivalent and less extensive compared with in historical control subjects. Infarct pain requiring morphine was diminished similarly in both treatment groups. Incidence of early arrhythmias and heart failure also did not differ. Posttherapy ischemic events and early surgery tended to be more common in the intracoronary group and bleeding was more common in the intravenous group. Intravenous drug did not decrease early hospital mortality (intravenous drug = 5, historical control = 4, intracoronary drug = 1); the differences in this parameter among groups were not significant. At convalescent angiographic evaluation, anterograde perfusion was present in 73% of those receiving intravenous and 76% of those receiving intracoronary drug.(ABSTRACT TRUNCATED AT 400 WORDS)     

The hypotensive effect of intravenous streptokinase in patients with acute myocardial infarction

We studied the hypotensive effect of a rapid intravenous infusion of high-dose streptokinase in 98 patients with an acute myocardial infarction. The systolic blood pressure fell from 132 +/- 20 (range 90 to 174) to 97 +/- 21 mm Hg (range 58 to 152) at 15 +/- 8 min (range 4 to 40) after the commencement of the streptokinase infusion (p less than .001). A fall in diastolic blood pressure from 80 +/- 16 (range 51 to 105) to 61 +/- 15 mm Hg (range 32 to 92) accompanied the fall in systolic pressure (p less than .001). The fall in blood pressure was associated with an increase in heart rate (73 +/- 14 to 78 +/- 17 beats/min, p less than .001), preceded the appearance of clinical signs of reperfusion by 37 +/- 38 min and was similar in magnitude and timing in patients with anterior and inferior infarction. There were direct relationships between the rate of infusion of streptokinase and both the magnitude (r = .49, p less than .001) and the rate of fall of systolic blood pressure (r = .67, p less than .001) as well as both the magnitude and rate of fall of diastolic blood pressure. In most patients, the fall in blood pressure was transient (9 +/- 6 min, range = 2 to 30) and easily managed by slowing or stopping the infusion, placing the patient in the Trendelenburg position, or by administering an infusion of low-dose norepinephrine or dopamine. However, in four patients with severe left ventricular dysfunction, severe hypotension persisted for more than 60 min.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

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.