Randomized comparison of intravenous versus intracoronary streptokinase for myocardial infarction

Alderman, Edwin L.; Jutzy, Kenneth; Berte, Larry E.; Miller, Rupert G.; Friedman, Joel P.; Creger, William P.; Eliastam, Michael

doi:10.1016/0002-9149(84)90297-2

Cited by 133 publications

(29 citation statements)

References 15 publications

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“…[1][2][3][4] Even in patients who reperfuse initially the clinical outcome is often complicated by a residual high-grade stenosis56 and by early reocclusion.7 8 Evidence from studies in experimental animal preparations suggest that this may in part be due to platelet activation since interventions that inhibit platelet function enhance the thrombolytic response to streptokinase9 and prevent reocclusion. 10 Whether platelet activation also plays a role in modulating the response to streptokinase in patients with acute myocardial infarction is unknown.…”

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confidence: 99%

Marked platelet activation in vivo after intravenous streptokinase in patients with acute myocardial infarction.

et al. 1988

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We assessed thromboxane biosynthesis as an index of platelet activation in 6 patients with acute myocardial infarction receiving intravenous streptokinase. Urinary 2,3-dinor-thromboxane B2 and plasma 1 1-dehydro-thromboxane B2, major enzymatic metabolites of thromboxane A2, were markedly increased after intravenous streptokinase (11,063 ± 2758 pg/mg creatinine and 33 ± 10 pg/ml, respectively) compared with levels in patients not receiving thrombolytic therapy (502 ± 89 pg/mg creatinine and 3 0.7 pg/ml). Prostacyclin biosynthesis also increased markedly after streptokinase coincident with the increase in thromboxane A2 formation. Administration of aspirin between the time of onset of coronary thrombosis and reperfusion both in man and in a canine preparation demonstrated that this reflected thromboxane biosynthesis de novo and not metabolism of preformed inactive thromboxane B2 washed out from the coronary circulation. Since the platelet is the major source of thromboxane A2, these findings suggest that there is marked platelet activation after coronary thrombolysis with streptokinase. Studies in vitro demonstrated that streptokinase enhanced platelet activation in a dose-dependent manner, resulting in the secondary release of thromboxane A2. The increase in platelet activation and thromboxane A2 biosynthesis may limit the therapeutic effect of intravenous streptokinase in acute myocardial infarction.

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confidence: 99%

Marked platelet activation in vivo after intravenous streptokinase in patients with acute myocardial infarction.

et al. 1988

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“…[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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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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“…Nine studies were reviewed (Alderman et al, 1984;Anderson et al, 1984;Blunda ef al., 1984;Geft et al, 1983;Rogers et al, 1983Rogers et al, , 1984Saltups el al., 1984;Taylor et al, 1984;Valentine et al, 1985), three of which were abstracts; two of these abstracts were presented at the American College of Cardiology meeting in March 1984, the third was presented at the 56th Annual Scientific Session of the American Heart Association in October 1983. The following are compared between ICSK and IVSK groups: (1) Duration from onset of symptoms to the initiation of treatment.…”

Section: Methodsmentioning

confidence: 99%

“…Only in four studies was angiography performed prior to and during treatment with IVSK (Alderman et al, 1984;Blunda et al, 1984;Rogers et al, 1983;Saltups et al, 1984). The rest of the trials did not document the infarct-related vessel prior to the initiation of IVSK therapy.…”

Section: Methodsmentioning

confidence: 99%

Intravenous versus intracoronary streptokinase in acute myocardial infarction

1985

Clinical Cardiology

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Summary: Nine studies specifically dealing with the comparison of intravenous streptokinase (IVSK) and intracoronary streptokinase (ICSK) in the treatment of acute myocardial infarction (MI) were analyzed to determine if IVSK is as efficacious as ICSK in achieving thrombolysis. Pooled data from the studies yielded success rates of 73% for IVSK and 72% for ICSK. Considering that the studies which did not perform preintervention angiogram may have overestimated the thrombolytic success rate in IVSK patients, there is a possibility that ICSK may be slightly more effective in achieving acute reperfusion. Bleeding complications were similar, and a systemic lytic state was observed in both treatment groups. No definitive conclusions can be drawn regarding the differences between groups in improvements of left ventricular function and mortality rates. ICSK has the advantage of direct documentation of reperfusion and spares the patient the risk of anticoagulation should the attempt fail. On the other hand, IVSK is cheaper, easier to administer, and can logistically be given earlier (even in the emergency room or ambulance) than ICSK; it is therefore more widely available, and may be the preferred mode of treatment in community hospitals where cardiac catheterization facilities are not readily available, if streptokinase is to be given at all.

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Randomized comparison of intravenous versus intracoronary streptokinase for myocardial infarction

Cited by 133 publications

References 15 publications

Marked platelet activation in vivo after intravenous streptokinase in patients with acute myocardial infarction.

Marked platelet activation in vivo after intravenous streptokinase in patients with acute myocardial infarction.

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

Intravenous versus intracoronary streptokinase in acute myocardial infarction

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