Thrombolytic therapy, infarct vessel patency and late potentials: can the arrhythmic substrate be altered?

Historical background. More than 15 years have passed since localized epicardial electrical signals beyond ventricular activation were recorded in dogs with ventricular arrhythmias after experimental myocardial infarction (I) and subsequently termed "late potentials." These observations became the basis for catheter and intraoperative electrical mapping in humans with sustained ventricular tachyarrhythmias following myocardial infarction to enable curative endocardial resection (2). During the past decade, signalaveraged surface electrocardiography has demonstrated the ability to record such late potentials noninvasively. Correlations between late potentials detected on the signalaveraged electrocardiogram (ECG) and spontaneous or induced sustained ventricular tachyarrhythmias in a variety of clinical states have been reproducibly confirmed. Thus, late potentials have been referred to as markers of an electrical substrate capable of sustaining malignant ventricular arrhythmias. Concomitantly, a decade of clinical investigations with administration of various thrombolytic agents during the evolutionary phase of acute myocardial infarction has proved fruitful. When administered within several hours after the onset of symptoms, thrombolytic agents have demonstrated improvement in the preservation of left ventricular function and survival. Successful reperfusion has been associated with spontaneous ventricular arrhythmias, most notably accelerated idioventricular rhythms. Decreased frequencies of ventricular premature beats have been reported after successful thrombolytic therapy. How-