Myocardial Salvage after Intracoronary Thrombolysis with Streptokinase in Acute Myocardial Infarction

Markis, John E.; Malagold, Michael; Parker, J. Anthony; Silverman, Kenneth; Barry, William H.; Als, Ann V.; Paulin, Sven; Grossman, William; Braunwald, Eugene

doi:10.1056/nejm198110013051401

Cited by 269 publications

(46 citation statements)

References 17 publications

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“…Even among clinical studies, varied incidence of reperfusion arrhythmias has been demonstrated. 2,[27][28][29][30][31] These results suggest that mechanisms responsible for AIVR and VT in clinical cases might be somewhat different from those observed in experimental models. In the present study, we clinically demonstrated for the first time that AIVR and VT that occur after reperfusion are probably cAMP-mediated arrhythmias and are therefore likely to be triggered arrhythmias.…”

Section: Electrophysiological Mechanisms Of Reperfusion Arrhythmiasmentioning

confidence: 84%

Antiarrhythmic Efficacy of Dipyridamole in Treatment of Reperfusion Arrhythmias

et al. 2000

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Background-Intracellular calcium overload is believed to play an important role in development of reperfusion arrhythmias. Dipyridamole, an inhibitor of cellular uptake of adenosine, may prevent or terminate reperfusion arrhythmias by reducing intracellular calcium overload. Methods and Results-First, we tested for a preventive effect of dipyridamole. Sixty-one patients who underwent primary PTCA for treatment of acute anterior wall myocardial infarction were enrolled in this prospective study. Patients were divided into dipyridamole (DP) and nondipyridamole (non-DP) groups. The 2 groups had similar baseline characteristics. In the DP group, dipyridamole 0.5 mg/kg was infused intravenously for 3 minutes immediately before reperfusion during primary PTCA. Arrhythmias after reperfusion were analyzed from continuous ECG recordings. None of the patients in the DP group (nϭ23) had accelerated idioventricular rhythms (AIVR) or ventricular tachycardia (VT). In contrast, 7 (18.4%) had AIVR and 3 (7.9%) had VT in the non-DP group (nϭ38; PϽ0.01). Second, we tested for a termination effect of dipyridamole. Dipyridamole 0.5 mg/kg was infused intravenously while continuous ECG recordings were obtained in 9 patients who had either sustained AIVR (nϭ7) or sustained VT (nϭ2) after reperfusion of occluded coronary artery. Arrhythmias were terminated in all patients. Conclusions-These results indicate that administration of dipyridamole can prevent and terminate reperfusion arrhythmias such as AIVR and VT. cAMP-mediated triggered activity may, at least in part, be responsible for reperfusioninduced AIVR and VT. (Circulation. 2000;101:624-630.)

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Section: Electrophysiological Mechanisms Of Reperfusion Arrhythmiasmentioning

confidence: 84%

Antiarrhythmic Efficacy of Dipyridamole in Treatment of Reperfusion Arrhythmias

et al. 2000

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“…Intracoronary streptokinase therapy provided within 4-6 h of the onset of acute myocardial infarction had been shown to limit myocardial necrosis, lower mortality and morbidity, and improve left ventricular function (Markis et al, 1981). However, it is crucial that this form of therapy be started as soon as possible after the onset of symptoms (Schwarz et al, 1982), and logical that earlier reperfusion would result in greater salvage of myocardium.…”

Section: Discussionmentioning

confidence: 99%

Intracoronary streptokinase therapy in the coronary care unit for acute myocardial infarction

Natarajan

Karlekar

Turkevich

et al. 1984

Clinical Cardiology

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Intracoronary streptokinase was offered and preliminary coronary angiography performed in 14 patients who were seen with the clinical diagnosis of acute myocardial infarction within 4 h of onset of symptoms. The procedure was performed in the Coronary Care Unit (CCU) of St. Peter's Medical Center with the use of a portable C‐arm fluoroscope. Angiography was recorded on video tape. Service was provided by an “on‐call” team consisting of two physicians, a CCU nurse, and a radiology technician, on a 24‐h service basis. Adequate visualization of coronary anatomy was obtained in all patients. Patency of occluded vessels was achieved in 10 of 11 patients who received intracoronary streptokinase. The initial streptokinase bolus was administered at a mean interval of 4.1 h from onset of symptoms. It is concluded that speedy and effective coronary thrombolytic therapy can be provided in the CCU on a 24‐h service basis by an on‐call team. The use of CCU for this purpose will make this therapy widely available across the country, without the need for Cardiac Catheterization Laboratory.

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“…The study population consisted of 140 consecutive patients with acute myocardial infarction (107 men, 33 women) who were 62 + 12 years old (range 32 to 86) and were included in a prospective study of intravenous streptokinase. All fulfilled the following criteria: (1) In 15 patients, the chest pain had resolved before commencement of the streptokinase infusion, in two patients there was no CK data, and in six patients the onset of the abrupt and rapid rise in CK was delayed. In these 23 patients.…”

Section: Methodsmentioning

confidence: 99%

“…However. this reperfusion syndrome, consisting of relief of chest pain, resolution of ST segment elevation, and CK washout, has a sound physiologic basis and its validity is supported by (1) experimental studies,479 (2) the complete concordance between the occurrence of this syndrome and the finding of patency of the artery of infarction in our study, and (3) the excellent concordance between these signs and angiographically recognized reperfusion in several intracoronary streptokinase studies.29 5 In the intracoronary studies of Lee, Rentrop, Mathey, and Ganz and their colleagues,9 50 > the clinical signs of reperfusion usually occurred within minutes of the angiographic demonstration of arterial patency and in some studies, these clinical signs were used to indicate when to check the patency of the artery of infarction by angiography.9°08-5' Furthermore, these clinical signs of reperfusion have also been adopted by several other investigators using intravenous streptokinase. '6 19.…”

mentioning

confidence: 90%

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.

Lew¹,

Laramee²,

Cercek³

et al. 1985

Circulation

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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)

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Myocardial Salvage after Intracoronary Thrombolysis with Streptokinase in Acute Myocardial Infarction

Cited by 269 publications

References 17 publications

Antiarrhythmic Efficacy of Dipyridamole in Treatment of Reperfusion Arrhythmias

Antiarrhythmic Efficacy of Dipyridamole in Treatment of Reperfusion Arrhythmias

Intracoronary streptokinase therapy in the coronary care unit for acute myocardial infarction

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.

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