The effects of the rate of intravenous infusion of streptokinase and the duration of symptoms on the time interval to reperfusion in patients with acute myocardial infarction.

Abstract

We studied the influence of the following variables on the time interval from initiation of an intravenous infusion of 750,000 U of streptokinase until reperfusion (reperfusion time) in 140 consecutive patients with an evolving acute myocardial infarction: (1) the rate of infusion of streptokinase, (2) the duration of chest pain before initiation of treatment, (3) patient age, (4) patient sex, (5) location of infarction, (6) history of previous myocardial infarction, and (7) pretreatment pathologic Q waves. The time of reperfusion was recognized by clinical criteria that were completely concordant with the anatomic findings in all 1 19 patients in whom patency or occlusion of the artery of infarction was established at delayed angiography (n = 116) or at postmortem examination (n = 3). The mean reperfusion time for the 129 patients for whom data were available was 49 36 min. The reperfusion time was inversely related to the rate of infusion of streptokinase (r = .41, p < .001), but this effect of infusion rate appeared to plateau at rates of greater than 500 U/kg/min. In the 64 patients receiving infusions at rates of 500 U/kg/min or less, the mean reperfusion time was 60 + 40 min, whereas in the 58 patients receiving the drug at rates greater than 500 U/kg/min it was 35 + 22 min (p < .001). The duration of chest pain before treatment was the only other studied variable found to influence the reperfusion time, but only at infusion rates of less than 250 U/kg/min (r= .6, p < .01). Our findings indicate that in patients with acute myocardial infarction who receive high-dose intravenous streptokinase, the time interval to reperfusion can be minimized by increasing the infusion rate up to at least 500 U/kg/min and by shortening the delay from onset of symptoms to treatment.Circulation 72, No. 5, 1053No. 5, -1058No. 5, , 1985 EARLY REPERFUSION of the artery of infarction may limit the extent of myocardial necrosis in patients with an evolving acute myocardial infarction' and improve ventricular function"5 and survival.i' 9 Both experimental' 02 and clinical"3-"' studies indicate that the critical determinant of the extent of myocardial necrosis and salvage is the duration of myocardial ischemia before reperfusion. In clinical practice, this ischemic period comprises (1) the time interval from the onset of infarction to the commencement of treatment, which is predominantly a logistical problem, 1620 and (2)-the time interval from commencement of treatment until reperfusion, which is predominantly a biological variable. In this study, we investigate the potential effect of the following factors on the time interval from treatment until reperfusion by intravenous streptokinase: (1) the rate of infusion of streptokinase, (2) the duration of chest pain before initiation of treatment, (3) patient age, (4) patient sex, (5) the location of infarction, (6) the presence of eletrocardiographic and/or historical evidence of a previous infarction, and (7)

Accelerated streptokinase in ST-elevation myocardial infarction — a romanian (ASK–ROMANIA) multicenter registry

“…An inverse relationship between the rate of streptokinase infusion and the time interval to reperfusion (non-invasively assessed) was found infusing 0.75 M.U. of streptokinase over 3-78 min (mean 26 ± 16) in 140 consecutive patients, with a plateau at infusion rates of 500 U/kg/min [32]. The mean reperfusion time was shorter (35 ± 22 min) at rates greater than 500 U/kg/min compared with 500 U/kg/min or less (60 ± 40 min, p b 0.001) [32].…”

“…of streptokinase over 3-78 min (mean 26 ± 16) in 140 consecutive patients, with a plateau at infusion rates of 500 U/kg/min [32]. The mean reperfusion time was shorter (35 ± 22 min) at rates greater than 500 U/kg/min compared with 500 U/kg/min or less (60 ± 40 min, p b 0.001) [32]. Thus, using the classical SK1.5/60 regimen, a rate greater than 500 U/kg/min can be obtained only in patients weighting 50 kg or less.…”

“…All major streptokinase trials used, however, only the slow infusion of this dose in 60 min [1][2][3][4][5]12,20,22,24,30]. Some data [31][32][33][34] and a personal experience accumulated before 1994 in the Spitalul de Urgenţă "Floreasca", Bucharest, suggested us that a faster infusion would increase the efficacy of streptokinase. The objective of this study was to test the hypothesis that a faster streptokinase infusion may result in a higher rate of coronary reperfusion and a lower mortality with no additional risk.…”

Aspect of Thrombolytic Therapy: A Review

“…The regular administration of steroids and antihistamines to prevent hypotension/bradycardia specially in association with Streptokinase complicates the administration procedures and is improbable to avert hypotension as the cause of Streptokinase induced hypotension is principally due to speed of administration [61, 62] and the exploit of bradykinin activated by Streptokinase [63]. …”

Adverse Reactions to Thrombolytic Agents

“…Arrhythmias occurring in the course of thrombolytic therapy of acute MI have been used as one of several non-angiographic markers of reperfusion (Lew et al 1985), but their sensitivity and specificity as such have not been clearly defined (Miller et al 1986). Other than the bradycardic responses previously described in association with hypotension, the most common rhythms observed are accelerated idioventricular rhythm and ventricular tachycardia.…”