SIGNIFICANCE OF ARRHYTHMIAS DURING THE FIRST 24 HOURS OF ACUTE MYOCARDIAL-INFARCTION TREATED WITH ALTEPLASE AND EFFECT OF EARLY ADMINISTRATION OF A BETA-BLOCKER OR A BRADYCARDIAC AGENT ON THEIR INCIDENCE

Background Although early intravenous beta-blocker therapy during acute myocardial infarction (AMI) reduces the incidence of fatal arrhythmias in patients not treated with thrombolytic agents, its antiarrhythmic effect in thrombolysed patients remains controversial. We investigated prospectively the arrhythmia incidence in 244 patients with AMI receiving alteplase and a double-blind randomized adjunctive therapy with intravenous atenolol, alinidine, or placebo. Moreover, the characteristics and prognostic significance of early arrhythmias and their relation with infarct size and coronary patency were evaluated. Methods and Results All patients underwent 24-hour Holter monitoring on day 1 and were clinically followed in the hospital for 10 to 14 days. Coronary angiography was per formed on day 10 to 14. Atenolol and alinidine significantly decreased the basic heart rate without causing more sinus arrest or higher-degree atrioventricular block. The prevalence of atrial fibrillation in alinidine patients was lower than in the atenolol patients (P=.007) but not lower than in placebo patients (P=.11). There was no effect of either agent on the incidence and frequency distribution of ventricular or supraventricular premature beats or on the incidence and characteristics of nonsustained ventricular tachycardia, accelerated idioventricular rhythm, sustained ventricular tachycardia (VT), or ventricular fibrillation (VF). On day 1, seven VF episodes were recorded in six patients (2.5%) and five VT episodes in five patients (2%). VF always started at <2.5 hours after start of thrombolytic treatment and VT always at >2.5 hours (average of 6 hours). Five of the seven VF and three of the five VT episodes started with an R-on-T. However, for all VT, the morphology of the first beat was the same as that of the following beats, suggesting that the sustained arrhythmia was not induced by an extrasystole. After day 1 and before hospital discharge, VF and VT developed in one and six patients, respectively. Three of the seven patients who developed VF during the first 2 weeks underwent coronary angiography; all three had an occluded infarct-related artery. In contrast, only one of nine patients with early or late VT had an occluded vessel. Patients with VT and VF on day 1 had a significantly larger enzymatic infarct size than those without the arrhythmia (P=.02), and a similar trend was noted for VT or VF after day 1 (P=.19). However, none of the patients with VT or VF on day 1 developed a life-threatening arrhythmia later during the hospital stay. Also, none of the seven patients with VT or VF after day 1 had experienced a major rhythm disturbance during the first 24 hours. Conclusions (1) Our data do not support the hypothesis that p-blockers or bradycardiac agents might reduce the incidence of major arrhythmias when used in conjunction with thrombolytic therapy. (2) The pathogeneses of VT and VF early during AMI are clearly distinct. (3) VT or VF during the first 2 weeks is a marker for a larger infarct. (4) We could not detect a relation between malignant arrhythmias on day 1 and recurrences within the following 2 weeks.