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Course and Interrelation of ReperfusionInduced ST Changes and Ventricular Arrhythmias in Acute Myocardial Infarction Manfred Zehender, MD, Stefan Utzolino, MD, Armin Furtwangler, MD, Wolfgang Kasper, MD, Thomas Meinertz, MD, and Hanjt)rg Just, MD
With the increasing use of thrombolytic therapy, the presence and time course of reperfusion-induced ventricular arrhythmias and ST-segment changes have become of particular interest. Technical improvements in bipolar Holter monitoring offer the opportunity to record both parameters continuously and simultaneously. Time course and interaction of both parameters in dependence on the onset of thrombolysis and time of reperfusion were investigated in 30 patients with acute myocardial infarction. Reperfusion was achieved in 20 patients after 49 f 23 miautes and in another 2 patients after 120 minutes (73%, group A). Vascular occlusion persisted in 8 patients for >24 hours (group B). Sudden STsegment changes (>0.2 mV/lS min) in the bipolar leads indicated reperfusion in 7 of 22 patients (32%). ldioventricular rhythms, most frequent in reperfused patients (group A: 18 of 22 patients, mean 121 beats/hour), were unspecific reperfusion markers (group B: 5 of 8 patients, 1 beat/hour) unless frequent (p 0.2 mV in >_2 chest leads. In all consenting patients with acute myocardial infarction and without contraindications for thrombolytic therapy, 24 hour Holter recording was initiated immediately after admission. Coronary angiography was performed in all patients within 60 minutes after admission. Patients with spontaneous reperfusion at that time were excluded from the study. The occluded vessels were the Ramus interventricularis anterior in 14 patients, the Ramus circumflexus in 4 and the right coronary artery in 12. Thrombolytic therapy was administered intravenously using therapeutic doses of pro-urokinase, recombinant tissue plasminogen activator or acylated streptokinase-plasminogen activator in combination with heparin (bolus: 10,000 U, 1,250 U/24 hours). Thrombolytic therapy was begun in all patients 3 repetitive beats with a rate between 60 and 120 beats/min), ventricular premature beats, and nonsustained ventricular tachycardia (rate > 120 beats/min) defined as >3 QRS complexes lasting O.l mV and lasting >30 seconds (minimal time between 2 episodes: 3 minutes). Measurements were obtained for the isoelectric section of the PQ interval, the J point and a third point that was coupled 60 ms later. To determine the time of reperfusion, ST changes >0.2 mV within 15 minutes after the invasive diagnosis of reperfusion were examined. Statistical criteria: Values are mean f standard deviation. Differences in the frequency and time course of ventricular arrhythmias, and ST-segment changes between both groups were compared using Student’s unpaired t test for parametric data, and the x2 evaluation for proportional data. Statistical significance level was p
ST-segment elevation depended on the occluded vessel (89%, left descending artery; 59%, left circumflex artery [p
Course and Interrelation of ReperfusionInduced ST Changes and Ventricular Arrhythmias in Acute Myocardial Infarction Manfred Zehender, MD, Stefan Utzolino, MD, Armin Furtwangler, MD, Wolfgang Kasper, MD, Thomas Meinertz, MD, and Hanjt)rg Just, MD
With the increasing use of thrombolytic therapy, the presence and time course of reperfusion-induced ventricular arrhythmias and ST-segment changes have become of particular interest. Technical improvements in bipolar Holter monitoring offer the opportunity to record both parameters continuously and simultaneously. Time course and interaction of both parameters in dependence on the onset of thrombolysis and time of reperfusion were investigated in 30 patients with acute myocardial infarction. Reperfusion was achieved in 20 patients after 49 f 23 miautes and in another 2 patients after 120 minutes (73%, group A). Vascular occlusion persisted in 8 patients for >24 hours (group B). Sudden STsegment changes (>0.2 mV/lS min) in the bipolar leads indicated reperfusion in 7 of 22 patients (32%). ldioventricular rhythms, most frequent in reperfused patients (group A: 18 of 22 patients, mean 121 beats/hour), were unspecific reperfusion markers (group B: 5 of 8 patients, 1 beat/hour) unless frequent (p 0.2 mV in >_2 chest leads. In all consenting patients with acute myocardial infarction and without contraindications for thrombolytic therapy, 24 hour Holter recording was initiated immediately after admission. Coronary angiography was performed in all patients within 60 minutes after admission. Patients with spontaneous reperfusion at that time were excluded from the study. The occluded vessels were the Ramus interventricularis anterior in 14 patients, the Ramus circumflexus in 4 and the right coronary artery in 12. Thrombolytic therapy was administered intravenously using therapeutic doses of pro-urokinase, recombinant tissue plasminogen activator or acylated streptokinase-plasminogen activator in combination with heparin (bolus: 10,000 U, 1,250 U/24 hours). Thrombolytic therapy was begun in all patients 3 repetitive beats with a rate between 60 and 120 beats/min), ventricular premature beats, and nonsustained ventricular tachycardia (rate > 120 beats/min) defined as >3 QRS complexes lasting O.l mV and lasting >30 seconds (minimal time between 2 episodes: 3 minutes). Measurements were obtained for the isoelectric section of the PQ interval, the J point and a third point that was coupled 60 ms later. To determine the time of reperfusion, ST changes >0.2 mV within 15 minutes after the invasive diagnosis of reperfusion were examined. Statistical criteria: Values are mean f standard deviation. Differences in the frequency and time course of ventricular arrhythmias, and ST-segment changes between both groups were compared using Student’s unpaired t test for parametric data, and the x2 evaluation for proportional data. Statistical significance level was p
ST-segment elevation depended on the occluded vessel (89%, left descending artery; 59%, left circumflex artery [p
