Intravenous streptokinase in evolving acute myocardial infarction

Ganz, William; Geft, Ivor; Shah, Prediman K.; Lew, Allan S.; Rodriguez, Lois; Weiss, Teddy; Maddahi, Jamshid; Berman, Daniel S.; Charuzi, Yzhar; Swan, H.J.C.

doi:10.1016/0002-9149(84)90066-3

Cited by 214 publications

(38 citation statements)

References 43 publications

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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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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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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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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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“…A prominent elevation in CK activity has been reported to be associated with successful coronary arterial reperfusion in patients receiving thrombolytic agents for acute myocardial infarction. 21 Vatner et al 22 found a more rapid appearance of CK and an earlier time to peak in dogs undergoing reperfusion at 1 and 3 hr after coronary artery occlusion (time to peak CK activity = 4.2 ± 0.4 and 6.8 ± 0.5 hr, respectively) than in similar animals that did not undergo reperfusion (time to peak = 11.4 ± 0.5 hr). Similar results have been noted in patients treated with thrombolytic agents.46 Successful reperfusion in these studies has generally been associated with peaks in CK activity at average times of 13 to 16 hr (vs 20 to 26 hr for patients not undergoing successful reperfusion).…”

Section: Resultsmentioning

confidence: 95%

Patterns of myoglobin release after reperfusion of injured myocardium.

Ellis¹,

Little²,

Masud³

et al. 1985

Circulation

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Myoglobin is an intracardiac protein that is released into the blood after myocardial injury and is then cleared rapidly by the kidneys. This study was undertaken to determine whether successful reperfusion of damaged myocardium could be assessed by examination of blood myoglobin concentration-time patterns. After release of a 2 hr occlusion of the mid left anterior descending coronary artery in 11 dogs that had been instrumented over the long term, immunoreactive arterial plasma concentration of myoglobin, [Mb], rose rapidly to a peak within 25 + 2(SEM) min (range 20 to 40). Individual peaks were three to 165 times the myoglobin levels immediately before release of the occlusion. Myoglobin was cleared rapidly from plasma, falling to one-half its peak level 38 3 min after the peak. Similarly well-defined peaks in [Mb] were evident in plasma from the great cardiac vein (GCV), with a mean time to peak of 16 + 2 min and a magnitude of two to 177 times prerelease values. In contrast, arterial and GCV creatine kinase activity-time curves showed less defined peaks and they occurred later and with more variability (60 to 330 min after reperfusion). In nine patients with acute infarction, successful coronary artery reopening was also accompanied by a sharp four-to sixteenfold rise in plasma [Mb] within 1 to 2 hr. Elevations in plasma creatine kinase were slower and more prolonged, peaking at 2 to 18 hr. The sharp, early peaks in [Mb] after successful reperfusion were in contrast to the case in one patient in whom reperfusion was not successful and in whom there was only a gradual increase in [Mb]. T2o100 defined as the time required for [Mb] to rise from 25% to 100% of peak, averaged 48 + 9 min for the nine patients undergoing successful reperfusion. In contrast, T25-100 in published series of patients with acute infarction in whom reperfusion was not attempted averaged 5 to 6 hr. In summary, reperfusion of injured myocardium results in a rapid release of myoglobin into the blood in both experimental animals and man. An early peak in the myoglobin concentration-time curve appears to be an additional useful indicator of reopening of the vessel when reperfusion is undertaken and a coronary arteriogram is not available. Circulation 72, No. 3, 639-647, 1985. IT IS NOW generally agreed that most transmural myocardial infarctions are associated with fresh thrombi superimposed on atherosclerotic lesions of varying severity.' Although the thrombi can often be dissolved with lytic agents, it is frequently difficult to assess whether or not reperfusion has occurred if an immediate coronary arteriographic examination is not performed. Some authors have attempted to use the rate of rise, peak magnitude, and/or time to peak creatine kinase (CK) elevation after reperfusion, but there

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“…Discussion The results of the present study indicate that PAF mediates the hypotension as well as the alterations of PLT functions induced by the infusion of SK and t-PA. One limitation of the administration of the thrombolytic agents in patients with acute myocardial infarction is that they can cause a significant fall in systemic blood pressure. [44][45][46] Experimental studies indicate that SK and, in particular, the SK-plasmin complex produce a marked fall in blood pressure that is related either to a rapid increase in serum plasmin concentration or to bradykinin generation.18 Indeed, the infusion of plasmin17 or bradykinin47 produces a marked hypotensive effect. Clinical studies, moreover, demonstrate that the hypotensive reaction is not a specific effect of SK but that it also occurs after high-dose intravenous infusion of urokinase48 or t-PA. 15 The present study indicates that infusions of both SK and t-PA in rabbit induced a significant fall in blood pressure that started 30 minutes after the beginning of the infusion and persisted during the 120-minute observation period.…”

Section: Platelet Preparation and Aggregation Studiesmentioning

confidence: 99%

Role of platelet-activating factor in hypotension and platelet activation induced by infusion of thrombolytic agents in rabbits.

Montrucchio

Alloatti

Mariano

et al. 1993

Circulation Research

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Infusion of the thrombolytic agents streptokinase (SK, 666 units/kg per minute for 60 minutes) and tissue-type plasminogen activator (t-PA, 10 micrograms/kg per minute for 15 minutes) in rabbits induced a significant hypotension and decrease in platelet count that were completely prevented by treatment with platelet-activating factor (PAF) receptor antagonists SDZ 63-675 and WEB 2170. PAF synthesis by vascular tissue was suggested by its extraction from blood-free heart and aorta of rabbits treated in vivo with SK or t-PA but not of control rabbits. In contrast, PAF was not detected in peripheral blood. Ex vivo studies on platelet aggregation response to ADP and PAF performed on platelet-rich plasma obtained before and after SK and t-PA infusion demonstrated an early hyperaggregable phase, abrogated by PAF receptor antagonists and followed by reduced sensitivity of platelets to PAF. The ED50 values for the aggregation of washed rabbit platelets induced by PAF but not thrombin were significantly increased at 60 and 120 minutes after SK and t-PA infusion, suggesting a specific desensitization of platelets to PAF. In contrast to PAF receptor antagonists, aspirin did not significantly modify the hypotension and the platelet hyperaggregability induced by SK or t-PA or the platelet hypoaggregability induced by t-PA. Thrombocytopenia induced by t-PA, but not by SK, was partially prevented by aspirin. The effect of SK, t-PA, and plasmin on the aggregation of washed platelets from untreated rabbits and from humans was also studied. Whereas SK and t-PA were inactive, plasmin induced dose-dependent platelet aggregation that was inhibited by platelet pretreatment with PAF receptor antagonists. In conclusion, the effect of PAF receptor antagonists observed in the present experimental model suggests that the hypotension and activation of platelets induced by SK and t-PA infusion are mediated by PAF.

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Intravenous streptokinase in evolving acute myocardial infarction

Cited by 214 publications

References 43 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.

Patterns of myoglobin release after reperfusion of injured myocardium.

Role of platelet-activating factor in hypotension and platelet activation induced by infusion of thrombolytic agents in rabbits.

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