El Enalapril Intravenoso No Evita El Desarrollo De Remodelado Eléctrico Auricular Agudo Secundario a Estimulación Rápida

Introduction and objectives. Recent clinical studies suggest a potential antiarrhythmic role of angiotensin-converting enzyme inhibitors in preventing atrial fibrillation. Studies in an animal model suggested that these drugs may prevent sustained atrial fibrillation by avoiding the occurrence of detrimental atrial electrical remodeling secondary to temporary episodes of fibrillation or atrial tachycardia. We sought to determine whether intravenous enalaprilat, administered at doses habitually used in clinical practice, prevented pacing-induced acute atrial remodeling.Patients and method. We analyzed 16 patients with no structural heart disease referred for electrophysiologic study due to supraventricular tachycardia. During the control period, right and left atrial effective refractory periods (ERP) were determined before and after a 10-minute period of rapid atrial pacing (250 ms) to quantitatively assess pacing-induced shortening of the ERP. After full recovery, a bolus dose of enalaprilat (0.015 mg/kg) was infused and the measurement and stimulation procedure repeated to quantify remodeling after enalaprilat administration.Results. In the control period, rapid pacing induced a significant 14% reduction (P< .01) in right atrial ERP and an 8% decrease (P< .01) in left atrial ERP as compared to baseline values. In the enalaprilat period, rapid pacing significantly reduced ERP by 15% in the right chamber (P< .01) and 7% in the left chamber (P< .01). There was no significant difference in the extent or time course of ERP shortening between the control and enalaprilat periods. The number of unintentionally induced atrial fibrillation episodes did not differ significantly between the two periods.Conclusions. Intravenous enalapril does not avoid the occurrence of pacing-induced acute electrical atrial remodeling, modify its time course, or impede the induction of atrial fibrillation.