Administration Of Streptokinase Research Articles

Thrombolytic Therapy in Acute Myocardial Infarction

Early thrombolytic therapy has been shown to reduce hospital mortality after myocardial infarction by 20-50%. This is achieved through reperfusion of the ischemic myocardium, which leads to limitation of infarct size by 15-30% and preservation of regional and global left ventricular function. Thrombolysis and reperfusion can be achieved by intravenous administration of streptokinase, urokinase, APSAC, or rt-PA, or by intracoronary administration of streptokinase or urokinase. Thrombolytic therapy is most effective in patients with extensive myocardial ischemia (large infarction) treated early after the onset of symptoms, but also patients with smaller infarcts may benefit from the therapy. It is uncertain whether treatment later than six hours after the onset of symptoms is beneficial, and if so, in which patients. Thrombolytic therapy leads to bleeding complications in a minority of patients. The risk of intracranial bleeding is approximately 0.5%. However, in several large trials the rate of cerebrovascular accidents (bleeding plus embolism) was not higher after thrombolytic therapy with streptokinase or rt-PA than after placebo. In order to prevent rethrombosis, additional treatment with acetyl salicylic acid and heparin is recommended. Nitrates and antiarrhythmic drugs are not recommended as routine practice. Immediate PTCA does not improve patient outcome. At present angiography and subsequent angioplasty or bypass surgery is recommended in patients with recurrent ischemia (spontaneous or upon exercise) after the infarct.

Late results after intracoronary thrombolysis and early bypass grafting for acute myocardial infarction

Successful thrombolysis for acute myocardial infarction reduces early mortality. For definite correction of the underlying arteriosclerotic lesion, invasive treatment is mandatory. Early bypass grafting has been performed in 70 patients with an ischemic interval of less than 4 hours before reperfusion by thrombolysis. Surgery was undertaken an average of 4.5 days after the streptokinase administration. The hospital mortality rate was 1.4%. At 8 years the actuarial survival rate was 88% and the complication-free survival rate, 84%. At the latest follow-up study, 90% of the patients were in functional class I or II. Because of advanced age, 37% of the survivors have retired and 29% are working. Thirty-four percent did not return to work after the operation. In 24 patients a transmural needle biopsy specimen was taken at operation to study the extent of ischemic damage. Surprisingly, the extent of necrosis did not correlate with the ischemic interval (r = 0.17), whereas enzyme activity and extent of necrosis did correlate (r = 0.76). Late angiography was done in 44 patients (56%). The correlation between ischemic interval and regional wall motion score was weak when the whole group was considered (r = 0.35), but 70% of the patients with an ischemic interval of less than 3 hours had normal or near normal regional wall motion. In patients with prolonged ischemia, distribution between normal function and severe damage was uniform. In patients with ultrastructural and wall motion studies, early necrosis and late left ventricular function correlated fairly well (r = 0.69). We conclude that additional early bypass grafting after successful thrombolysis yields excellent long-term clinical results, especially in patients with an ischemic interval of less than 3 hours.

Streptokinase binds to lactate dehydrogenase subunit-M, which shares an epitope with plasminogen.

The bacterial thrombolytic agent streptokinase binds to human, porcine, and chicken lactate dehydrogenase (EC 1.1.1.27; LD) isoenzyme subunit M, but not to the H or C subunits. There is amino acid sequence homology between LD and the streptokinase binding site on plasminogen to account for this interaction that results in the formation of high-molecular-mass complexes in serum that contain LD activity. Binding of highly immunogenic streptokinase with LD may lead to induction of anti-LD autoantibodies, known to occur in some patients after therapeutic administration of streptokinase for treatment of acute myocardial infarction. This interaction may also be a general mechanism for inducing autoimmunity against other proteins that share the streptokinase binding epitope.

Treatment of pain in acute myocardial infarction.

The treatment of pain in acute myocardial infarction varies with local practice. Narcotic analgesics are still the usual treatment in many hospitals. Knowledge of optimal doses, duration of pain relief, and time between drug administration and pain relief is inadequate. Many studies indicate that the relief of pain is often incomplete after treatment with narcotic analgesics. There is often a need for alternative treatments. Large randomised studies consistently show that beta blockade, initially given intravenously and then orally, relieves pain and reduces the need for analgesics. Studies also indicate that early administration of streptokinase and glyceryl trinitrate relieves pain. There is evidence that drugs that limit ischaemic damage also relieve pain.

Do different doses of intravenous streptokinase alter the frequency of coronary reperfusion in acute myocardial infarction?

This study assessed the relative efficacy of 3 doses of intravenous streptokinase in causing hypofibrinogenemia and coronary reperfusion in patients with acute myocardial infarction. Accordingly, 56 patients (50 men and 6 women, ages 58 ± 10 years [mean ± standard deviation]) with evolving acute myocardial infarction and chest pain ≤5 hours in duration were assigned to receive varying doses of streptokinase. Twenty were administered 500,000 units during 145 minutes, 18 were given 750,000 units during 30 minutes and 18 received 1.5 million units in 60 minutes of streptokinase. Serum creatine kinase was measured on admission and 6, 12, 18 and 24 hours after the initiation of streptokinase. The time intervals from onset of pain to peak creatine kinase and from streptokinase administration to peak creatine kinase were used to determine the occurrence of reperfusion. The plasma fibrinogen concentration was measured 30, 60, 90 and 120 minutes after the initiation of streptokinase. For the 3 groups, the time from onset of pain to peak creatine kinase was <17 hours and the time from streptokinase to peak creatine kinase was 6 or 12 hours in 15 (75%), 16 (89%) and 12 patients (67%), respectively (differences not significant). The plasma fibrinogen concentration decreased to 45 ± 34 mg/dl, 19 ± 14 mg/dl and 29 ± 43 mg/dl, respectively, during the 2 hours after streptokinase was begun (p < 0.05 for the first versus the second and third values). Thus, if sufficient streptokinase is given to produce a systemic fibrinolytic state, smaller doses (500,000 and 750,000 units) are as effective as larger ones (1.5 million units) in inducing coronary reperfusion. In addition, 750,000 and 1.5 million units produce a similar degree of hypofibrinogenemia, so that the administration of >750,000 units of intravenous streptokinase to patients with acute myocardial infarction appears to offer no demonstrable advantage.

Relation of peak creatine kinase levels during acute myocardial infarction to presence or absence of previous manifestations of myocardial ischemia (angina pectoris or healed myocardial infarction)

The hypothesis that acute myocardial infarction (Ml) is more extensive in patients without previous angina or healed MI was evaluated in 177 patients with documented recent acute MI. Ninety-nine patients (56%) had no previous angina or healed MI (negative history group), and the remaining 78 patients (44%) had a previous history of angina or healed MI (positive history group). The mean peak creatine kinase (CK) level in the negative history group was 784 compared with 419 IU in the positive history group (p < 0.0001). The mean peak CK-MB level in the negative history group was 128 compared with 76 IU in the positive history group (p < 0.001). The mean peak CK-MB level was higher in the negative history group after controlling for age, streptokinase administration, previous coronary artery bypass grafting or treatment with β-blocking agents. Despite the high frequency of healed MI in the positive history group (73%), the rates of in-hospital complications were similar for the 2 groups. Patients with acute MI without previous angina or healed MI have substantially higher peak CK and CK-MB levels; this implies a larger MI than in patients with previous angina or healed MI.

Experimental thromboembolic stroke studied by positron emission tomography: immediate versus delayed reperfusion by fibrinolysis.

Acute obstruction of the middle cerebral artery (MCA) was obtained by injecting a single autologous blood clot into the internal carotid artery of dogs. The technique induced very reproducible unilateral ischemic lesions in the MCA territory; hemorrhagic transformation of the lesions was often seen. The hemodynamic and metabolic effects of blood clot embolism were studied in 35 dogs with positron emission tomography (PET) and the 15O steady-state technique, and compared with a control group of seven intact animals. In the acute phase, the involved brain tissue still had a nearly normal oxygen consumption (-11%) despite the lowered tissue perfusion (-20%) caused by the vascular obstruction. The lowered oxygen availability was compensated by an increased oxygen extraction ratio (+11%). Twenty-four hours after the insult, the hemodynamic situation had barely changed, and the ischemic event had evolved into a brain infarct in which oxygen consumption was clearly lowered (-25%) and accompanied by a significant lowering (-22%) of the oxygen extraction ratio compared with the acute situation. Therapeutic thrombolysis by local administration of streptokinase (500,000 IU), starting 30 min after the insult, was not able to salvage any brain tissue or to ameliorate tissue perfusion despite angiographically confirmed clot lysis. However, when fibrinolytic therapy was started within the first 5 min after the insult, hemispheric blood flow was normalized, and most of the threatened brain tissue was salvaged, as was indicated by its normalized oxygen consumption and oxygen extraction ratio. Early fibrinolysis was accompanied by definite clinical improvement and substantial reduction in the severity of the morphological lesions that were never hemorrhagic.

Urokinase Efficacy for Deep Vein Thrombosis Developing During Streptokinase Therapy—A Case Report

A patient with embolic occlusion of the right femoral artery and the left tibial arteries received streptokinase as treatment to lyse the emboli. Blood flow in both lower extremities improved with streptokinase administration. On the fourth day of therapy, however, the patient developed pain and swelling of the right calf. A venogram confirmed the presence of a clot obstructing the right popliteal vein. Streptokinase infusion was stopped, and urokinase infusion was started. Pain and swelling in the right calf disappeared and venous blood flow was greatly improved during urokinase therapy. Urokinase infusion was stopped after sixty hours, and heparin therapy was started. The patient was discharged from the hospital one month after admission. Patients should be closely monitored during thrombolytic therapy to detect any signs of complica tions, including new thrombotic episodes.

Streptokinase-induced, antibody-mediated platelet aggregation: A potential cause of clot propagation in vivo

The administration of intracoronary streptokinase to a patient with a prior history of rheumatic fever was associated with the retrograde propagation of thrombus from the left anterior descending coronary artery into the left main coronary artery with near catastrophic consequences. The addition of streptokinase to platelet-rich plasma from the patient initiated platelet aggregation and secretion in vitro. Platelet aggregation was also seen in 1 of 15 control subjects after the addition of streptokinase, and the addition of plasma or immunoglobulin G (IgG) from the index patient supported platelet aggregation in the presence of streptokinase in all of the previously nonreactive control subjects.This in vitro platelet aggregation was specific for streptokinase and not initiated by either urokinase or tissue plasminogen activator. Streptokinase-induced platelet aggregation was not inhibited by aprotinin, but was completely attenuated by the addition of an excess of antihuman IgG Fab. These findings suggest that streptokinase can initiate specific antibody-mediated platelet aggregation in vitro and may be more than coincidentally related to clot propagation or thromboembolism in vivo.

Differential effects of activation of prothrombin by streptokinase compared with urokinase and tissue-type plasminogen activator (t-PA)

We have previously reported paradoxical prothrombotic effects manifest by elevations of fibrinopeptide A (FPA) after administration of streptokinase to patients with acute myocardial infarction. To characterize mechanisms responsible and their dependence on streptokinase (SK) as opposed to other activators of the fibrinolytic system, the present study was performed to compare effects of streptokinase, tissue-type plasminogen activator (t-PA), and urokinase on plasma and on purified prothrombin in concentrations similar to those achieved pharmacologically. The effects of plasmin were assessed to determine the extent to which the elevations of FPA seen could be attributed to activation of plasminogen. Elevations of FPA were observed after incubation of each of the activators with citrated plasma at 37°C for 60 minutes. However, they were most marked with streptokinase (64.5 ± 4.6 pmol FPA/ml (mean ± SE) with 100 IU SK/ml, and 77.6 ± 5.0 pmol/ml with 500 IU SK/ml). Elevations of FPA induced by streptokinase were attenuated by 100 IU/ml heparin [15.2 ± 1.9 pmol/ml after 100 IU of SK (p < 0.001 compared with results with streptokinase without heparin)). Human plasmin, 2.5 CTA/ml, caused changes similar to those induced by streptokinase. The minimal elevations of FPA induced by t-PA or urokinase (< 10 pmol/ml without heparin) were not significantly attenuated by heparin. Incubation of barium citrate adsorbed plasma (vitamin K factor depleted) with streptokinase markedly attenuated elevation of FPA. Addition of prothrombin (1.5 μM) and streptokinase (100 IU/ml) to the barium citrate adsorbed plasma elicited elevations of FPA similar to those induced by streptokinase in citrated plasma. Amidolytic activity with the “thrombin” substrate H-D-phenylalanyl-Lpipecolyl-L-arginine-p-nitroanilide dihydrochloride (S-2238) was evident when streptokinase, plasminogen (0.24 μM), and prothrombin (1.5 μM) were incubated in buffer. Thus, concentrations of streptokinase that are low in terms of therapeutic blood levels activate prothrombin in plasma, likely due to activation of plasminogen. Neither tissue-type plasminogen activator nor urokinase in pharmacologically comparable concentrations increase thrombin activity appreciably perhaps because of less intense activation of plasminogen. Consideration of the prothrombotic effects observed maybe relevant to selection of specific agents for therapeutic thrombolysis, to appropriate titration of dose, and to the need for the use of heparin conjointly with particular activators of the fibrinolytic system such as streptokinase.

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 < 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.

Immediate versus delayed coronary grafting after streptokinase treatment: Postoperative blood loss and clinical results

Of all patients with acute evolving myocardial infarction treated surgically at Duke University Medical Center between 1984 and 1986, 27 patients given high doses (greater than 1.5 million units) of streptokinase preoperatively were studied. Eleven patients who received streptokinase had coronary bypass grafting 12 hours after thrombolytic therapy (early hours), eight patients between 12 and 72 hours (delayed), and eight patients beyond 72 hours (late hours). Seventeen patients who underwent coronary bypass grafting within 6 hours of the onset of symptoms, without preoperative streptokinase, were included as control patients. Only the patients having early operation had significantly greater postoperative blood loss; postoperative use of red blood cells; fresh-frozen plasma; cryoprecipitate; prolonged postoperative prothrombin time; and prolonged partial thromboplastin time. Patients having delayed or late operations did not differ significantly from patients not receiving streptokinase. Only the interval between time of streptokinase administration and operation could account for the coagulopathy and the postoperative bleeding complications in the early group. Patients in the early group had a higher in-hospital mortality (27% versus 6% for the non-streptokinase group) and major noncardiac morbidity (36% versus 12% for the non-streptokinase group). Patients in the delayed and late groups had minimal postoperative complications and no mortality. Observations were not explained by differences in total ischemic time, number of angioplasty failures, or number of patients with cardiogenic shock between the early group and the non-streptokinase group. Postoperative bleeding and massive use of blood products seemed to be contributory factors: Two of three deaths in the patients having early operations were associated with clinical suspicion of tamponade. Patients undergoing coronary bypass grafting within 12 hours of streptokinase therapy appear to be a high-risk group in a more emergent, uncontrolled clinical setting and require aggressive monitoring and correction of coagulopathy.

Role of nitrates in acute myocardial infarction.

Management of patients after myocardial infarction includes several therapeutic options. Lysis of the coronary thrombosis with intravenous or intracoronary administration of streptokinase or intravenous administration of one of the newer, currently experimental agents, such as tissue plasminogen activation or prourokinase, can directly restore oxygen and substrate delivery to potentially salvageable myocardium. Percutaneous transluminal coronary angioplasty can likewise restore vessel patency with potential salvage of ischemic myocardium, if perfused sufficiently early after symptom onset. Another strategy is to administer intravenous thrombolytic therapy and then perform early angioplasty on patients with acute myocardial infarction who reach the hospital within 4 hours of symptom onset. These patients should have intravenous nitroglycerin begun before or simultaneously with beginning thrombolytic therapy. The infusion is titrated to lower systolic arterial pressure by 10% to 15%, and then maintained at a constant rate for up to 48 hours. Patients seen more than 4 hours after symptom onset, with evidence of viable myocardium (e.g., persistent R waves in those electrocardiographic leads demonstrating ST-segment elevation) may also receive intravenous nitroglycerin and thrombolytic or percutaneous transluminal coronary angioplasty therapy. The combined results of the several clinical trials of intravenous nitroglycerin in acute myocardial infarction would support its use in patients seen 4 to 12 hours after onset of symptoms or in patients seen earlier, in whom thrombolytic or percutaneous transluminal coronary angioplasty therapy cannot be utilized.

Early prediction of left ventricular function in streptokinase-treated acute myocardial infarction.

We administered 750,000 units of intravenous streptokinase to 121 consecutive patients experiencing their first acute myocardial infarction within 4 h of pain onset. The following information was collected: hours between pain onset and streptokinase administration (TS), hours of pain after streptokinase administration (DP), initial and peak creatine phosphokinase levels (ICK and PCK), time to peak creatine phosphokinase, time to electrocardiographic ST segment resolution. Six days after the infarction, catheterization was performed to calculate ejection fraction, infarct-related regional ejection fraction, and dysfunction index. Data was analyzed using stepwise multiple regression. In patients experiencing anterior infarctions, the following equation was obtained predicting the ejection fraction (EF) with a correlation coefficient of 0.86: EF = 69 - 0.0050(PCK) - 3.7(TS) - 1.8(DP). In anterior infarctions the infarct-related ejection fraction and dysfunction index were similarly predictable. We were slightly less accurate in forecasting the outcome of inferior infarctions. The outcome of intravenous streptokinase therapy can be predicted early in the evolution of acute myocardial infarction using routinely available information.

Coronary perfusion during acute myocardial infarction with a combined therapy of coronary angioplasty and high-dose intravenous streptokinase.

Two hundred and sixteen patients with acute myocardial infarction were treated with immediate infusion of high-dose (1.5 million units) intravenous streptokinase followed by emergency coronary angioplasty. The infarct lesion was crossed and dilated in 99% and persistent coronary perfusion after the procedure was achieved in 90% (including 3% with significant residual stenosis). Total in-hospital mortality was 12%. Multivariable analysis showed a higher hospital mortality with cardiogenic shock (41% vs 5% without shock), older age, lower left ventricular ejection fraction, and female sex. Final patency of the infarct-related vessel was determined by follow-up in-hospital cardiac catheterization. Coronary reocclusion occurred in 11% (symptomatic in 7%, treated with emergency angioplasty or bypass surgery; silent in 4%, treated medically). Of the surviving patients with successful initial establishment of infarct vessel patency, 94% were discharged from the hospital with an open infarct artery or a bypass graft to the infarct vessel. There was significant improvement in both ejection fraction (44% to 49%; p less than .0001) and regional wall motion in the infarct zone (-3.0 SD to -2.4 SD; p less than .0001) among patients with persistent coronary perfusion and insignificant residual stenosis at the time of the follow-up cardiac catheterization. Thus, a treatment strategy for acute myocardial infarction that includes immediate administration of streptokinase followed by emergency coronary angioplasty, and coronary bypass surgery when necessary, results in a high rate of early and sustained patency of the infarct-related vessel.

Intravenous streptokinase-mediated thrombolysis of acute occlusion of the left main coronary artery

In the absence of collaterals, acute occlusion of the left main (LM) coronary artery causes extensive myocardial necrosis and cardiogenic shock. 1 We report on 2 patients in whom thrombolysis, with administration of intravenous streptokinase, of an occluded LM coronary artery resulted in reversal of clinically diagnosed shock. Both patients survived with excellent preservation of the left ventricular function.

Role of nitrates in acute myocardial infarction

Management of patients after myocardial infarction includes several therapeutic options. Lysis of the coronary thrombosis with intravenous or intracoronary administration of streptokinase or intravenous administration of one of the newer, currently experimental agents, such as tissue plasminogen activation or prourokinase, can directly restore oxygen and substrate delivery to potentially salvageable myocardium. Percutaneous transluminal coronary angioplasty can likewise restore vessel patency with potential salvage of ischemic myocardium, if perfused sufficiently early after symptom onset. Another strategy is to administer intravenous thrombolytic therapy and then perform early angioplasty on patients with acute myocardial infarction who reach the hospital within 4 hours of symptom onset. These patients should have intravenous nitroglycerin begun before or simultaneously with beginning thrombolytic therapy. The infusion is titrated to lower systolic arterial pressure by 10% to 15%, and then maintained at a constant rate for up to 48 hours. Patients seen more than 4 hours after symptom onset, with evidence of viable myocardium (e.g., persistent R waves in those electrocardiographic leads demonstrating ST-segment elevation) may also receive intravenous nitroglycerin and thrombolytic or percutaneous transluminal coronary angioplasty therapy. The combined results of the several clinical trials of intravenous nitroglycerin in acute myocardial infarction would support its use in patients seen 4 to 12 hours after onset of symptoms or in patients seen earlier, in whom thrombolytic or percutaneous transluminal coronary angioplasty therapy cannot be utilized.

Paradoxic elevation of fibrinopeptide A after streptokinase: Evidence for continued thrombosis despite intense fibrinolysis

Elevated levels of fibrinopeptide A, a marker of thrombin activity associated with acute myocardial infarction, have been found to decrease after administration of streptokinase when reperfusion occurs. In contrast, in patients without reperfusion and those with reocclusion after streptokinase therapy, fibrinopeptide A remains elevated. In the present study early serial measurements of fibrinopeptide A were used to further characterize this paradoxic increase in thrombin activity after streptokinase and to characterize its response to heparin. In 19 patients with acute myocardial infarction fibrinopeptide A was elevated to 82.3 +/- 43.5 ng/ml (mean +/- SE) before therapy. Thirty minutes after the initiation of streptokinase, fibrinopeptide A increased to 300.1 +/- 117.4 ng/ml (p less than 0.01), consistent with extensive thrombin activity. Fibrinopeptide A remained elevated until 15 minutes after a heparin bolus injection when levels decreased to 15% of the poststreptokinase value (49.2 +/- 13.3 ng/ml) (p less than 0.001). These data document a prompt paradoxic increase in thrombin activity after administration of streptokinase that may be responsible for failure of therapy in some patients.

Effects of early high-dose streptokinase intravenously on left ventricular function in acute myocardial infarction

One hundred seven patients who recently had acute myocardial infarction were randomly assigned either to standard heparin therapy or to intravenous streptokinase within 5 hours after the onset of symptoms in 7 hospitals without catheterization facilities. In the third week, the patients were referred to a university hospital, where the patency rate of the infarctrelated artery was studied by selective coronary arteriography and left ventricular function by radionuclide angiography. Fifty-five patients received heparin and 52 streptokinase within a mean period of 190 minutes after the onset of symptoms. Seven patients in the heparin group and 4 in the streptokinase group died in hospital. The patency rate of the infarct-related artery was identical in both groups (69% in the heparin group vs 68% in the streptokinase group). Left ventricular ejection fraction was not statistically different (0.44 ± 0.13 in the heparin group vs 0.45 ± 0.12 in the streptokinase group). Left ventricular ejection fraction was significantly higher in patients with a patent infarct-related artery than in patients with an obstructed infarct-related artery (0.49 ± 0.12 vs 0.41 ± 0.15, p < 0.01). In patients with inferior wall infarction, left ventricular ejection fraction was identical (0.50 ± 0.10 in the heparin group vs 0.52 ± 0.09, in the streptokinase group). In patients with anterior wall infarction, left ventricular ejection fraction was significantly higher in the streptokinase group than in heparin group (0.40 ± 0.10 vs 0.33 ± 0.09, p < 0.05). Analysis of regional wall motion revealed that improvement occurred in the lateral wall of the left ventricle. After a mean follow-up of 23 months, 3 patients in the heparin group and 1 patient in the streptokinase group died, yielding the mortality rate at the end of the follow-up period to 18.1 % in the heparin group on 9.6% in the streptokinase group. Thus, early intravenous administration of streptokinase may lead to significant preservation of left ventricular function in patients with anterior wall infarction. One may question the suitability and utility of intravenous thrombolysis in inferior wall infarction.

Prehospital Coronary Thrombolysis: A New Strategy in Acute Myocardial Infarction

Thirty-four patients with acute myocardial infarction were treated prospectively using a new strategy of prehospital intravenous streptokinase given by a physician-operated mobile intensive care unit. The 29 prehospital-treated patients who had experienced no previous myocardial infarction were compared to a similar group treated with streptokinase inhospital. Patients receiving streptokinase in the prehospital phase of acute myocardial infarction had smaller infarcts and better residual myocardial function than the group given streptokinase inhospital in terms of peak creatinine phosphokinase, ejection fraction, computer-derived dysfunction index, and electrocardiographic QRS score. The only difference between these groups at baseline was the duration of pain prior to initiation of streptokinase therapy. There were no major complications related to prehospital administration of streptokinase.