Coronary thrombolysis by intravenous streptokinase in acute myocardial infarction: Acute and follow-up studies

Spann, James F.; Sherry, Sol; Carabello, Blasé A.; Denenberg, Barry; Mann, Richard H.; McCann, William D.; Gault, James H.; Gentzler, Richard D.; Belber, Arthur D.; Maurer, Alan H.; Cooper, Emmett M.

doi:10.1016/0002-9149(84)90380-1

Cited by 151 publications

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“…The patient population consisted of 101 consecutive patients who were entered into a prospective study of intravenous streptokinase in acute myocardial infarction and in whom ie systemic blood pressure was continuously monitored duri the infusion of streptokinase. The study inclusion criteria were (1) chest pain of 3 hr or less duration, (2) ST segment elevation indicative of transmural ischemia, (3) unresponsiveness of both the chest pain and the electrocardiographic changes to sublingual nitroglycerin, (4) no contraindication to thrombolytic or anticoagulant therapy, and (5) consent of both the patient and his or her physician. The diagnosis of acute myocardial infarction was subsequently confirmed by a rise in serum levels of the creatine kinase MB isoenzyme in all patients.…”

Section: Methodsmentioning

confidence: 99%

“…[1][2][3][4][5][6][7][8][9] In most recent studies, intravenous streptokinase has been administered rapidly so as to achieve a high concentration of streptokinase in proximity to the coronary thrombus and thereby accelerate thrombolysis. '0- '3 One limitation of the administration of a rapid intravenous infusion of streptokinase is that it can cause a significant fall in systemic blood pressure.4' 5' This study investigates the frequency and severity of the hypotensive effect of intravenous infusion of streptokinase in patients with acute myocardial infarction and its relationship to the rate of the infusion.…”

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confidence: 99%

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

Lew¹,

Laramee

Cercek³

et al. 1985

Circulation

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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 < .00 1). 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 < .001). The fall in blood pressure was associated with an increase in heart rate (73 14 to 78 + 17 beats/min, p < .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 < .001) and the rate of fall of systolic blood pressure (r = .67, p < .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. Our data indicate that in patients with either anterior or inferior myocardial infarction, a rapid infusion of high-dose intravenous streptokinase may frequently cause transient and sometimes severe hypotension, the magnitude of which is directly related to the rate of infusion of streptokinase. Circulation 72, No. 6, 1321No. 6, -1326No. 6, , 1985 SHORT-TERM INTRAVENOUS INFUSION of high-dose streptokinase is an effective method of coronary thrombolysis and coronary artery reperfusion during an acute myocardial infarction.1-9 In most recent studies, intravenous streptokinase has been administered rapidly so as to achieve a high concentration of streptokinase in proximity to the coronary thrombus and thereby accelerate thrombolysis.'0-'3 One limitation of the administration of a rapid intravenous infusion of streptokinase is that it can cause a significant fall in systemic blood pressure.4' 5' This study investigates the frequency and severity of the hypotensive effect of intravenous infusion of streptokinase in patients with acute myocardial infarction and its relationship to the rate of the infusion. MethodsPatient population. The patient population consisted of 101 consecutive patients who were entered into a prospective study of intravenous streptokinase in acute myocardial infarction and in whom ie systemic blood pressure was continuously monitored duri the infusion of streptokinase. The study inclusion criteria were (1) chest pain of 3 hr or less duration, (2) ST segment elevation indicative of transmural ischemia, (3) unresponsiveness of both the chest pain and the electrocardiographic changes to sublingual n...

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Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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

Lew¹,

Laramee

Cercek³

et al. 1985

Circulation

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“…An increased rate of recanalization in the infarct-related coronary artery and a lower death rate at the acute stage have been reported with their use. [1][2][3][4][5] However, it has not been established whether coronary thrombolysis can reduce the size of the infarct. 8 The observed reduction in infarct size is markedly variable, even among patients in whom coronary thrombolysis is accomplished at the same time after the onset of acute myocardial infarction and in whom recanalization is of the same degree.…”

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confidence: 99%

Quantitative analysis of contraction band and coagulation necrosis after ischemia and reperfusion in the porcine heart.

Miyazaki¹,

Fujiwara²,

Onodera³

et al. 1987

Circulation

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To assess the importance of contraction band necrosis (CBN) in reperfusion, CBN, coagulation necrosis (CN), and infarct size, expressed as CBN + CN, were quantitatively analyzed in 25 porcine hearts without collateral circulation. The left anterior descending coronary artery was ligated for 20, 30, 60, and 120 min and then reperfused for 8 hr (groups 1 to 4, respectively). Five hearts were not reperfused (group 5). The areas of CBN and CN were traced at a magnification of X 100 under an inverted microscope and quantified with use of an image analyzer. There was no change in hemodynamics with either occlusion or reperfusion. Regional myocardial blood flow, measured by the generated hydrogen gas clearance method. decreased to almost zero after occlusion but recovered during reperfusion. Percent of risk area infarcted in groups 1 to 4 was 0 ± 0%, 1 1 + 7%, 80 ± 9%, and 96 ± 2%, respectively, and the percent of risk area infarcted in group 4 was the same as that in hearts subjected to permanent occlusion (95 ± 3%). The percent area of CBN was 100 ± 0% in group 2 68 ± 1 1% in group 3, 2 ± 1% in group 4, and 2 ± 2% in group 5. In group 3, the inner third of the ischemic left ventricular wall showed CN and the middle and outer third CBN. These findings show that in pig hearts without collateral circulation, the transmural infarct, two-thirds of which is occupied by CBN, is evident even when reperfusion is achieved after 1 hr occlusion. Therefore, protection against CBN might reduce infarct size after reperfusion.

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“…Intravenous heparin was continued for 8-14 days at a rate adjusted to maintain the activated partial thromboplastin time at 1 1/2-2 times control. At 24 hours after angiography, heparin was discontinued for [2][3][4] hours to allow removal of the sheaths, and it was then reinstituted with a bolus of 2,000-5,000 units. For at least 24 …”

Section: Patients and Methods Patient Selection Criteriamentioning

confidence: 99%

“…[1][2][3][4][5][6] Recombinant tissue-type plasminogen activator (rt-PA) has been shown to be a more effective thrombolytic agent than streptokinase7-9 and to produce less extensive systemic fibrinogenolysis. '0 In multicenter trials, intravenous rt-PA has been associated with coronary reocclusion rates of 10% to 30% despite heparin anticoagulation.…”

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confidence: 99%

Prevention of coronary artery reocclusion and reduction in late coronary artery stenosis after thrombolytic therapy in patients with acute myocardial infarction. A randomized study of maintenance infusion of recombinant human tissue-type plasminogen activator.

et al. 1988

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Sixty-eight patients with acute "transmural" myocardial infarction presenting within 6 hours (range, 1.3-5.8 hours) of onset of chest pain were given intravenous recombinant tissue-type plasminogen activator (rt-PA) at a dosage of 1 mg/kg during 90 minutes. Coronary angiography at 90 minutes revealed a patent infarct-related coronary artery in 52 patients (76%). These patients were randomized either to treatment by continuous infusion of heparin alone (27 patients) or to treatment by heparin and a maintenance infusion of rt-PA at a dosage of 0.8 mg/kg during 4 hours (25 patients). Coronary angiography was repeated 60 minutes after the start of the maintenance infusion and again after 8-14 days. Acute symptomatic reocclusion of the infarct-related artery occurred during the 1-hour observation period in five (19%) patients treated with heparin alone but in none of the patients treated with rt-PA (p = 0.05). The measured residual stenosis of the patent infarct-related coronary artery was similar in the heparin-treated and the rt-PA-treated groups at 90 minutes infusion: 66±14% versus 68±13% diameter stenosis, respectively (mean ± SD) and 1.1 ± 1.1 mm2 versus 0.82 ± 0.7 mm2 area (p = 0.35). At 8-14 days after infusion, residual stenosis was unchanged in the heparin-treated group, but it improved to 55 ± 17% (p = 0.001) and 1.6 ± 1.2 mm2 (p = 0.003) in the rt-PA-treated group. At 90 minutes of infusion, residual intraluminal thrombus was observed in 29 of the 52 patients (56%) with a comparably measured distribution in the two groups (p= 0.43). At 150 minutes, however, the extent of intraluminal thrombus was significantly reduced in the rt-PA-treated group as compared with the heparin-treated group (p= 0.03). In-hospital ischemic events (symptomatic reocclusion, unstable angina, or cardiovascular death) occurred in 12 patients of the heparin-treated group but only in three patients of the rt-PA-treated group (p = 0.03). Fibrinogen levels decreased to 65 ± 21% of baseline at 90 minutes of rt-PA infusion. During the rt-PA maintenance infusion, fibrinogen fell slightly from 63 ± 26 to 57 ± 28% (p = 0.18). This study shows that after successful reperfusion with 1 mg/kg rt-PA during 90 minutes, a maintenance infusion of 0.8 mglkg rt-PA during 4 hours prevents acute symptomatic coronary artery reocclusion, and it reduces the frequency of ischemic events and the severity of residual coronary artery stenosis at hospital discharge. (Circulaton 1988;78:546-556) S uccessful thrombolytic therapy of acute myoin-hospital reocclusion rate after reperfusion with cardial infarction does not always produce intravenous streptokinase has ranged from 10% to stable coronary artery patency. The reported

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Coronary thrombolysis by intravenous streptokinase in acute myocardial infarction: Acute and follow-up studies

Cited by 151 publications

References 20 publications

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

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

Quantitative analysis of contraction band and coagulation necrosis after ischemia and reperfusion in the porcine heart.

Prevention of coronary artery reocclusion and reduction in late coronary artery stenosis after thrombolytic therapy in patients with acute myocardial infarction. A randomized study of maintenance infusion of recombinant human tissue-type plasminogen activator.

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