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.     

Hematocrit as an indicator for coronary intervention in patients with acute myocardial infarction

OBJECTIVES: Primary coronary intervention in patients with acute myocardial infarction complicated by persistent massive intracoronary thrombus is frequently difficult. Higher incidence of thrombus formation is associated with high hematocrit score. This study investigated the relationship between high hematocrit score and primary coronary intervention in patients with acute myocardial infarction. METHODS: Forty-five patients with acute myocardial infarction were divided into two groups according to hematocrit score on admission, the high hematocrit group (hematocrit > or = 48%, n = 8) and the low hematocrit group (hematocrit < 48%, n = 37). Time period required for coronary intervention (intervention time), number of balloon inflations, presence of persistent massive intracoronary thrombus, need for adjunctive intracoronary thrombolysis, need for intraaortic balloon pumping and achieved rate of Thrombolysis in Myocardial Infarction (TIMI) 3 were compared between the two groups. The relationships between hematocrit and intervention time or number of balloon inflations were also investigated. RESULTS: Intervention time (2.7 +/- 1.4 vs 1.4 +/- 0.7 hr, p = 0.0003), number of balloon inflations (12 +/- 9 vs 3 +/- 2 times, p = 0.0001), presence of persistent massive intracoronary thrombus (100% vs 5%, p < 0.0001), intracoronary thrombolysis (63% vs 3%, p = 0.0003), and intraaortic balloon pumping (63% vs 14%, p = 0.0092) were significantly higher in the high hematocrit group. However, the rate of TIMI 3 (25% vs 95%, p < 0.0001) was significantly lower in the high hematocrit group. The relationships between hematocrit and intervention time (r2 = 0.16, p = 0.0033), and hematocrit and number of balloon inflations (r2 = 0.19, p = 0.0015) showed positive correlations. CONCLUSIONS: Primary coronary intervention for patients with acute myocardial infarction showing high hematocrit score on admission is likely to be difficult due to the presence of persistent massive intracoronary thrombus. Therefore, coronary interventional strategy for intracoronary thrombolysis in patients with acute myocardial infarction should include measurement of hematocrit score.     

An angiographic study of intracoronary streptokinase versus intravenous tissue plasminogen activator after failed coronary thrombolysis with intravenous streptokinase

Objective The medical treatment of failed intravenous streptokinase in patients with acute transmural myocardial infarction using angiographic endpoints.Design Prospective open angiographic comparison of intracoronary streptokinase with intravenous tissue plasminogen activator. Setting: Single center study in a tertiary institution.Subjects Eighty-five patients with acute myocardial infarction within 4 hours after symptom onset. Treatment regimens: The subjects received 1.5 million U intravenous streptokinase. Coronary angiography within 48 hours (median 19 hours) showed infarct-related vessel patency in 65 patients (76%). In the catheterization laboratory the 20 patients (24%) with failed intravenous streptokinase received repeat thrombolysis immediately after angiography. The first 10 patients with failed intravenous streptokinase received intracoronary streptokinase at a dose of 4000 U/min in the occluded infarctrelated artery for a maximum of 1 hour. The subsequent 10 patients received high-dose front-loaded intravenous tissue plasminogen activator (100 mg in 1 hour).Results In none of the patients receiving repeat streptokinase was reperfusion obtained. In 6 of 10 (60%) of the patients receiving tissue plasminogen activator, reperfusion was seen within 60 minutes (p < 0.005 vs. intracoronary streptokinase). One patient (5%) died and two refused follow-up angiography. Seventeen (88%) patients underwent angiography 3 months later according to the protocol. Two patients showed a persistently reperfused infarct-related artery, three reoccluded, four spontaneously reperfused, and eight had a persistently occluded infarct-related artery. The left ventricular ejection fraction was slightly higher at 3 months, and there were no differences between the patients with open vessels (increase + 7.7 ± 5.8%) and those with persistently occluded vessels (increase +5.8 ± 6.8%)Conclusions Repeat thrombolysis after failed intravenous streptokinase can be achieved with front-loaded intravenous tissue plasminogen activator but not with intracoronary streptokinase. Although patient numbers are small and repeat thrombolysis was performed rather late, this study leads the way to affordable optimization of thrombolysis, which needs large-scale testing.     

Prevention of subsequent exercise-induced periinfarct ischemia by emergency coronary angioplasty in acute myocardial infarction: comparison with intracoronary streptokinase

To compare the efficacy of emergency percutaneous transluminal coronary angioplasty and intracoronary streptokinase in preventing exercise-induced periinfarct ischemia, 28 patients presenting within 12 hours of the onset of symptoms of acute myocardial infarction were prospectively randomized. Of these, 14 patients were treated with emergency angioplasty and 14 patients received intracoronary streptokinase. Recatheterization and submaximal exercise thallium-201 single photon emission computed tomography were performed before hospital discharge. Periinfarct ischemia was defined as a reversible thallium defect adjacent to a fixed defect assessed qualitatively. Successful reperfusion was achieved in 86% of patients treated with emergency angioplasty and 86% of patients treated with intracoronary streptokinase (p = NS). Residual stenosis of the infarct-related coronary artery shown at predischarge angiography was 43.8 +/- 31.4% for the angioplasty group and 75.0 +/- 15.6% for the streptokinase group (p less than 0.05). Of the angioplasty group, 9% developed exercise-induced periinfarct ischemia compared with 60% of the streptokinase group (p less than 0.05). Thus, patients with acute myocardial infarction treated with emergency angioplasty had significantly less severe residual coronary stenosis and exercise-induced periinfarct ischemia than did those treated with intracoronary streptokinase. These results suggest further application of coronary angioplasty in the management of acute myocardial infarction.     

Concomitant use of intraaortic balloon counterpulsation and streptokinase in acute anterior myocardial infarction.

Using a prospective, nonrandomized design, the authors sought to determine whether concomitant use of intraaortic balloon counterpulsation (IABP) and streptokinase in acute anterior myocardial infarction (MI) would improve the in-hospital mortality rate and angiographic findings. The study included 45 patients with an acute anterior MI. All patients received intravenous streptokinase. Among these, 25 patients had concomitant IABP while the remaining 20 patients had streptokinase alone. All patients underwent cardiac catheterization. Patients treated with concomitant IABP had a significantly higher frequency of thrombolysis in myocardial infarction (TIMI) grade 3 flow (n: 11; 44% vs n: 1; 5%, p<0.05), and there was a trend toward a lower in-hospital mortality rate in the IABP group (n: 0; 0% vs n: 3; 15%, p=0.08). The angiographic presence of thrombus image and grade > or =2 coronary collateral circulation to the infarct-related coronary artery for the IABP and non-IABP groups did not differ significantly. The preliminary results of this study suggest that concomitant use of IABP and streptokinase in acute anterior MI increases the incidence of TIMI grade 3 flow and may have decreased the in-hospital mortality rate without unacceptable rates of vascular or hemorrhagic complications.     

Systemic markers of fibrinolysis after unsuccessful intracoronary streptokinase thrombolysis for acute myocardial infarction: Does nonreperfusion indicate failure to achieve a systemic lytic state?

Reasons for the failure of intracoronary streptokinase (STK) to result in coronary thrombolysis were examined in 45 patients with acute myocardial infarction presenting with angiographic evidence of total coronary occlusion. In 25 patients (group A), clot lysis was initially successful; in 20 (group B), reperfusion was unsuccessful. The STK dosage in group A ranged from 84,000 to 310,000 units (mean 188,000 +/- 12,000); STK dosage in group B ranged from 160,000 to 360,000 units (mean 267,000 +/- 11,000 [p less than 0.05]). Before therapy, levels of fibrin degradation products and serum fibrinogen were normal in all patients. After intracoronary STK, fibrin degradation products and serum fibrinogen levels changed similarly in both groups. Eight-five percent of patients in group B had evidence of a systemic fibrinolytic state. These data suggest that higher doses of STK administered in the same manner are unlikely to result in an increased reperfusion rate. Systemic hematologic markers of fibrinolysis are not helpful in explaining the success or failure of intracoronary thrombolysis.     

Emergency coronary artery bypass surgery after intracoronary thrombolysis for evolving myocardial infarction.

Sixteen patients underwent emergency coronary artery bypass surgery immediately after intracoronary streptokinase infusion for acute evolving myocardial infarction. Of these, 11 patients had 70% residual stenosis in the recanalised vessel, and in five thrombolysis was unsuccessful. There were no hospital deaths. All the patients sustained myocardial necrosis, the peak activity of creatine phosphokinase correlating with the time to reperfusion. Chest tube drainage (mean 960 ml) was significantly higher than for control patients but did not correlate with the total dosage of streptokinase. No patients had further myocardial infarction or developed recurrent angina. Selected patients may benefit from coronary bypass surgery after intracoronary streptokinase infusion. If necessary this may be performed immediately with low mortality and morbidity.     

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.     

Intravenous streptokinase in acute myocardial infarction at the community hospital: a six-year experience

The efficacy of intravenous streptokinase in the initial management of acute myocardial infarction was evaluated over a 6-year period in 130 patients admitted to 3 community hospitals. Most patients were admitted within 2 hours of onset of symptoms and received 1.5 million units of streptokinase over a 30- to 60-minute period. Clinical observations and serial creatine phosphokinase-MB were indicative of vessel patency in 115 (88%) of the patients after initiation of thrombolysis. Of this group, 105 underwent catheterization, and recanalization was demonstrated in 97 (92%). Fifty percent of the patients who underwent reperfusion were subsequently maintained with medical therapy; 50% underwent either percutaneous transluminal coronary angioplasty or coronary artery bypass surgery. Major morbidity was confined to hematomas; no cerebral bleeding was encountered. There was 1 early death from cerebral thrombosis and 2 late deaths, 1 to cancer and 1 to myocardial infarction. These findings suggest the benefit of intravenous streptokinase thrombolysis in patients with acute myocardial infarction presenting within 3 hours of onset of pain, unless specific potential bleeding problems exist or in the case of certain very elderly persons. In addition, the trial demonstrated the feasibility of triaging patients who have undergone lytic therapy to a central facility for catheterization and management.     

Reduced incidence of left ventricular thrombi with intravenous streptokinase in acute anterior myocardial infarction: prospective evaluation by cross-sectional echocardiography

Forty-five consecutive patients with transmural anterior acute myocardial infarction were prospectively studied to determine the effect of intravenous streptokinase on the incidence of left ventricular thrombi. Three patients died. The remaining patients were divided into 2 groups. Group 1 patients (n = 22) received 750,000 units of intravenous streptokinase within 6 hours of onset of symptoms. Neither thrombolytic therapy or anticoagulants were administered to 18 patients in group 2. Cross-sectional echocardiography was performed 8 to 10 days following acute myocardial infarction to detect left ventricular thrombus. Technically satisfactory echocardiography was not possible in 2 patients. Apical akinesia or dyskinesia was observed in all patients. No patient in the treated group developed left ventricular thrombus compared with 8 of 18 (44.4%) in group 2 (P less than 0.05). One patient in the control group sustained an embolic cerebrovascular accident. Thus intravenous streptokinase significantly reduces the incidence of left ventricular thrombus formation in patients of transmural anterior acute myocardial infarction.     

Coronary thrombolysis after intracoronary and intravenous administration of streptokinase to myocardial infarct patients

Coronary thrombolysis by intracoronary and intravenous streptokinase (SK) is reported in myocardial infarction patients. Forty-two patients were examined within the first 6 hours of infarction: they were subjected to coronary-angiography on admission and 24 hours later, and their plasma fibrinogen levels were measured repeatedly for 2 days. SK administration was intracoronary in 24 patients and intravenous in 18. Rapid intravenous SK injection was not inferior to intracoronary administration in terms of efficiency. Although coronary reperfusion takes a somewhat longer time in cases of intravenous SK treatment, its technical simplicity and relative safety, as well as the fact that it can be started early suggest that it is a promising method of treatment for myocardial infarction.     

Coronary thrombolysis with recombinant human tissue-type plasminogen activator: a prospective, randomized, placebo-controlled trial

Forty-five patients with acute transmural myocardial infarction and angiographically confirmed complete coronary occlusion were prospectively randomized, two for one, to treatment of acute coronary thrombosis with intravenous recombinant human tissue-type plasminogen activator (rt-PA) or placebo. Each of five additional consecutive patients was treated with a high dose of rt-PA for 2 hr. Twenty-five of 33 patients (75%) receiving 0.5 to 0.75 mg/kg of rt-PA over 30 to 120 min had angiographically proven recanalization within 90 min of initiation of therapy. Only one of 14 patients given placebo had spontaneous recanalization within 45 min (p less than .001). Thirteen placebo-treated patients were crossed over to the intracoronary rt-PA group. Nine (69%) exhibited subsequent recanalization within 45 min. Levels of circulating fibrinogen decreased after treatment with rt-PA by an average of only 8% of baseline values. None of the patients manifested a depletion of fibrinogen level to below 100 mg/dl. Six patients who were completely unresponsive to rt-PA were subsequently treated with intracoronary streptokinase and none responded. Thus, either intravenous or intracoronary rt-PA induced coronary thrombolysis without eliciting clinically significant fibrinogenolysis in patients with evolving myocardial infarction due to thrombotic coronary occlusion.     

Emergency coronary artery bypass surgery after intracoronary thrombolysis for evolving myocardial infarction

Sixteen patients underwent emergency coronary artery bypass surgery immediately after intracoronary streptokinase infusion for acute evolving myocardial infarction. Of these, 11 patients had 70% residual stenosis in the recanalised vessel, and in five thrombolysis was unsuccessful. There were no hospital deaths. All the patients sustained myocardial necrosis, the peak activity of creatine phosphokinase correlating with the time to reperfusion. Chest tube drainage (mean 960 ml) was significantly higher than for control patients but did not correlate with the total dosage of streptokinase. No patients had further myocardial infarction or developed recurrent angina. Selected patients may benefit from coronary bypass surgery after intracoronary streptokinase infusion. If necessary this may be performed immediately with low mortality and morbidity.     

Prehospital thrombolysis in a rural community: Short- and long-term survival

Summary In order to assess the feasibility and outcome of using prehospital thrombolysis in acute myocardial infarction in a rural community, we performed an open randomized study of patients with symptoms of acute myocardial infarction of less than 6 hours. One hundred and forty-five patients with acute myocardial infarction were allocated to receive IV streptokinase prehospital by means of a mobile coronary care unit (MCCU) (n=43) or to receive IV streptokinase in hospital (n=102). The mean delay time to treatment was 138 minutes (MCCU group) and 172 minutes (hospital group) (p<0.02). Reperfusion time was 88 minutes for the MCCU group and 92 minutes for the hospital group. Mortality at 14 days was 2.3% for the MCCU group and 11.7% for the hospital group (p<0.05). Six month mortality was 4.9% for the MCCU group and 17.3% for the hospital group (p=0.03). Mortality at 1 year was 6.1% for the MCCU group and 20.0% for the hospital group (p=0.04). There were no significant adverse events in either treatment group. Thus, prehospital thrombolysis by streptokinase is feasible and allows significant reduction in the delay time to treatment initiation. There are encouraging improvements in both short- and long-term survival with no apparent reduction in safety profile.     

Randomized, double-blinded multicenter study. Comparison of intracoronary single-chain urokinase-type plasminogen activator, pro-urokinase (GE-0943), and intracoronary urokinase in patients with acute myocardial infarction

Coronary recanalization rates and changes in the coagulation and fibrinolysis system were evaluated in a randomized fashion in patients with acute myocardial infarction after intracoronary administration of single-chain urokinase-type plasminogen activator (pro-urokinase: GE-0943) or urokinase. Three groups of patients were studied: group H (n = 50), 6,000 units pro-urokinase i.c.; group L (n = 44), 3,000 units pro-urokinase i.c.; and group U (n = 54), 960,000 IU urokinase i.c. Coronary recanalization rates determined angiographically after 45 minutes of intracoronary infusion averaged 90% in group H, 59% in group L, and 61% in group U. The differences were statistically significant between group H and the latter two groups. Pro-urokinase affected plasma proteins of the fibrinolytic system to a lesser degree than urokinase. Bleeding complications were present in one patient in group L, in none in group H, and in five in group U. Thus, intracoronary administration of 6,000 units pro-urokinase is more effective in coronary thrombolysis and causes less systemic fibrinogenolysis than intracoronary administration of urokinase.     

Effect of intracoronary thrombolytic therapy on exercise-induced ischemia after acute myocardial infarction

Intracoronary streptokinase (SK) therapy increases vessel patency rate after acute myocardial infarction (AMI) and thus may lead to a greater exercise-induced myocardial ischemia. This hypothesis was tested in 39 patients enrolled in an angiographically randomized trial of intracoronary SK (19 treated with SK and 20 control subjects); all patients underwent thallium-201 scintigraphy at rest before acute angiography, as well as at rest and during stress 5 to 6 weeks after AMI. The patients were classified into 2 groups based on the presence (n = 13) or absence (n = 26) of complete obstruction of the infarct-related coronary artery at the end of the acute angiography. Semiquantitative score of myocardial thallium uptake was expressed as percent of maximal defect score. Thallium defect score at rest between admission and 5 to 6 weeks' study decreased from 10 +/- 16% units in the control group and from 23 +/- 14% units in the SK group (p = 0.01). This decrease was related to opening of the infarct-related artery (opening 23 +/- 16% vs occlusion 5 +/- 10%). The change in exercise-induced defect score was significantly (p = 0.01) larger in patients in the SK group (11 +/- 6% units) than in those in the control group (5 +/- 7% units). The perfusion defect during exercise was larger (p = 0.006) in patients with incomplete obstruction or reperfusion (10 +/- 6% units) than in patients with complete obstruction (3 +/- 7%). This difference was independent of the number of diseased coronary vessels.(ABSTRACT TRUNCATED AT 250 WORDS)     

Late effects of intracoronary streptokinase on regional wall motion, ventricular aneurysm and left ventricular thrombus in myocardial infarction: results from the Western Washington Randomized Trial

To determine whether intracoronary streptokinase improves late regional wall motion or reduces left ventricular aneurysm or thrombus formation in patients with acute myocardial infarction, two-dimensional echocardiography was performed at 8 +/- 3 weeks after infarction in 83 patients randomized to streptokinase (n = 45) or standard therapy (n = 38) in the Western Washington Intracoronary Streptokinase Trial. Among the patients treated with streptokinase, the average time to treatment was 4.7 +/- 2.5 hours after the onset of chest pain, and 67% had successful reperfusion. Regional wall motion was assessed in nine left ventricular segments on a scale of 1 to 4 (normal, hypokinetic, akinetic and dyskinetic). Left ventricular thrombus formation was interpreted as positive, equivocal or negative. All patients received anticoagulant therapy in the hospital and 52 received such therapy after hospital discharge. The mean (+/- SD) global (1.5 +/- 0.4 in both groups) and regional wall motion scores in the streptokinase-treated and control groups were not significantly different. The prevalence of aneurysm was 16% in both groups. Left ventricular thrombus was identified in only five patients (positive identification in four, and equivocal in one), all in the streptokinase-treated group (p = NS). There were also no differences between streptokinase and control treatment in any of the echocardiographic variables in subgroups of patients with anterior infarction, inferior infarction, no prior infarction or reperfusion with streptokinase. It is concluded that intracoronary streptokinase given relatively late in the course of acute myocardial infarction does not result in improved global or regional wall motion or a reduction in left ventricular thrombus or aneurysm formation in survivors studied 2 months after myocardial infarction.     

Clinical benefits of intracoronary high-dose tirofiban therapy in patients with acute ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention

To investigate the benefits of intracoronary high-dose tirofiban during primary percutaneous coronary intervention (PCI) for patients with acute ST-segment elevation myocardial infarction (STEMI) .Methods Fifty-eight patients with STEMI presented within 12 h of symptoms were randomly allocated to study group (n = 28,intracor-onary high-dose tirofiban) and control group (n = 30,intravenous high-dose tirofiban) .The culprit vessels were targe-ted with primary PCI in all patients.Clinical characteristics,angiographic findings,brain natriuretic peptide (BNP) at 7-day and in-hospital outcomes were compared between groups,as well as left ventricular ejection fraction (LVEF) and major adverse cardiac events (MACE,including death,reinfarction,worsening heart failure and target vessel revascu-larization) at 30-day clinical follow-up.Results Compared with the control group,the study group showed better thrombolysis in myocardial infarction (TIMI) flow grades immediately after PCI (96.4% vs 76.7% ,P = 0.02) .The 30-day composite major adverse cardiac events rate was lower in the study group (3.6% vs 23.3% ,P = 0.02) ,and the LVEF and BNP in the study group at 7 days was better than that in the control group (P = 0.01 and 0.02,respec-tively) .No significant difference in hemorrhagic complications in hospital between groups was noted (P = 0.61) .Conclusions The study indicates that intracoronary high-dose bolus administration of tirofiban for patients with STEMI who underwent primary PCI can significantly improve the reperfusion level in the infarct area and clinical outcomes at 30 days follow-up.It is better and safer to apply intravenous bolus injection for improving coronary flow,LVEF and short-term clinical outcomes.     

Comparison of intracoronary and intravenous methods of thrombolytic streptokinase therapy of patients with myocardial infarct

Intracoronary streptokinase (250.000 units over 60-90 min) was administered within 7.8 +/- 0.4 hrs after the onset of myocardial infarction symptoms to 85 patients, and intravenous streptokinase (500.000 units over 5-10 min) was given within 4.8 +/- 0.4 hrs to 46 myocardial infarction patients. Coronary angiography was conducted 1 to 3 hours after intravenous streptokinase administration. Coronary arterial reperfusion was achieved in 62% of patients in the former group, and in 66% in the latter one. Reperfusion was seen in 84% of patients in the first 3 hours after the onset of infarction, and in 60-66% at later dates. Hypofibrinogenemia did not become critical and persisted for one more day in cases of intravenous streptokinase infusions, as compared to the intracoronary route. Intravenous administration of 500.000 units streptokinase at the rate of 100.000-50.000 U/min is an effective and safe method for the treatment of myocardial infarction, and its prospective application in health practices appears quite promising.     

Time from onset of symptoms to thrombolytic therapy: a major determinant of myocardial salvage in patients with acute transmural infarction

To determine whether myocardial salvage after successful intracoronary or intravenous thrombolysis is time dependent, the relation between left ventricular wall motion and the time to treatment was studied in 69 patients admitted less than 3 hours after onset of acute transmural myocardial infarction (42 patients with reperfusion by intracoronary streptokinase, 27 by intravenous urokinase). A similar significant relation between the time to treatment and the severity of regional hypokinesia at follow-up was found in the intracoronary and intravenous groups. To better define this relation, particularly during the early phase of infarction, the groups were combined. In patients in whom thrombolytic treatment was initiated within 2 hours after symptom onset, wall motion at follow-up was within 2 standard deviations of the normal mean in 82% (14 of 17 patients). If treatment was started 2 to 5 hours after symptom onset, the probability of improved wall motion decreased to 46% (24 of 52 patients, p less than 0.025). The time/wall motion relation appeared to be independent of infarct location, angiographically visible collateral vessels and the presence of subtotal coronary artery occlusion. The severity of hypokinesia at follow-up study correlated with the magnitude of peak serum creatine kinase (r = -0.71), indicating that thrombolytic therapy initiated within 2 hours after the onset of symptoms improves regional left ventricular function and reduces infarct size more than later therapy does.