Thrombolytic Therapy can Reduce the Arrhythmogenic Substrate After Acute Myocardial Infarction

Abstract

hrombolytic therapy has been shown to improve survival after acute myocardial infarction (AMI) primarily by decreasing infarct size and consequently preserving left ventricular function. [1][2][3][4][5][6] This mortality benefit has been reported to be greater than would be expected solely from the improvement of left ventricular function. 4,5 Some authors suggested that enhancement of electrical stability might contribute to the lower mortality, 6,7 but there is controversy about the electrophysiologic effects of early reperfusion achieved by thrombolytic therapy. [8][9][10][11][12][13][14][15][16][17][18][19][20] To evaluate electrical stability after myocardial infarction, several clinical techniques have been developed. The signal-averaged electrocardiogram (ECG) 21-31 and endocardial catheter mapping 32-37 are performed to detect delayed ventricular activation, which is required for the development of reentry. The induction of sustained monomorphic ventricular tachycardia by programmed ventricular stimulation is known to be one of the most useful predictors of future arrhythmic events. 24,[29][30][31][38][39][40] Previous studies, however, have used only one or two noninvasive methods, such as the ambulatory or the signalaveraged ECG, to evaluate the electrophysiologic effects of thrombolytic therapy. [9][10][11][12][13][14][15][16] In the present study, using the signal-averaged ECG, endocardial catheter mapping and programmed ventricular stimulation together, we investigated the electrophysiologic effects of early reperfusion achieved by thrombolytic therapy in patients who had recovered from their first AMI. Methods Study PatientsThe study group comprised 93 consecutive patients (80 men and 13 women; mean [± SD] age, 59.6±9.8 years; range, 39-75) who were admitted to hospital within 6h after the onset of the symptoms of their first AMI. The diagnosis of AMI was based on the typical chest pain lasting more than 30 min, ST elevation of more than 2mm in at least 2 leads on the ECG and an increase in serum creatine kinase MB isoenzyme. Patients older than 75 years old, with bundle branch block, atrial fibrillation or with contraindications to thrombolytic therapy were excluded. All patients underwent emergency coronary angiography using the Judkins technique. All of the patients were shown to have a culprit coronary artery with grade 0 or 1 flow of the Thrombolysis in Myocardial Infarction (TIMI) trial classification. 41 They received intracoronary urokinase (960,000 units over 40 min) or recombinant tissue-type plasminogen activator (100 mg over 40 min). Before the study, all patients gave informed, written consent. The Clinical Research Committee of the hospital approved the study protocol. To investigate the electrophysiologic effects of thrombolytic therapy, signal-averaged electrocardiography, endocardial catheter mapping and programmed stimulation were performed in 93 consecutive patients with their first AMI who underwent thrombolytic therapy. Early reperfusion was achieved in 75 patients (group 1),...