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Effects of Verapamil and Procainamide on Acute Atrial Electrical Remodeling Induced by Short-Term Rapid Atrial Pacing in Humans

Verapamil及Procainamide對於人體心房組織短期快速電刺激所誘發的電氣重塑效應之影響

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摘要


Atrial electrical remodeling (ER) after spontaneous or pacing-induced atrial fibrillation has been previously described in humans. We investigated atrial ER induced by a 5-minute period of rapid atrial pacing and the pharmacologic effects of verapamil and procainamide on this atrial ER phenomenon. The atrial effective refractory periods (ERPs) at drive cycle lengths of 400 (ERP400) and 600 (ERP600) ms, at five representative atrial sites (high right atrium [HRA]; proximal, middle and distal coronary sinus; interatrial septum), were determined in 20 patients at baseline and immediately after cessation of a 5-minute period of rapid pacing from the HRA at a rate of 150 bpm. The degrees of atrial ERP400 and ERP600 shortening after pacing were calculated as acute atrial ER. The same protocol was repeated in another 15 patients after intravenous administration of verapamil (0.15mg/kg) and in another 15 patients after intravenous administration of procainamide (15 mg/kg). The results demonstrated that, in the control state acute atrial ER can be significantly demonstrated at each atrial representative site (p<0.001). The mean ERP400 and ERP600 shortenings were 9±4% and 8±4%, respectively. After procainamide infusion, but not after verapamil, baseline ERP400 and ERP600 values were significantly prolonged at the five representative atrial sites (p<0.01). Acute atrial ER could still be demonstrated at each atrial site after procainamide or verapamil infusion (p<0.001). In conclusion, acute atrial ER can be demonstrated after only a 5-minute period of rapid atrial pacing in humans. Intravenous verapamil or procainamide does not abolish this ER process.

並列摘要


Atrial electrical remodeling (ER) after spontaneous or pacing-induced atrial fibrillation has been previously described in humans. We investigated atrial ER induced by a 5-minute period of rapid atrial pacing and the pharmacologic effects of verapamil and procainamide on this atrial ER phenomenon. The atrial effective refractory periods (ERPs) at drive cycle lengths of 400 (ERP400) and 600 (ERP600) ms, at five representative atrial sites (high right atrium [HRA]; proximal, middle and distal coronary sinus; interatrial septum), were determined in 20 patients at baseline and immediately after cessation of a 5-minute period of rapid pacing from the HRA at a rate of 150 bpm. The degrees of atrial ERP400 and ERP600 shortening after pacing were calculated as acute atrial ER. The same protocol was repeated in another 15 patients after intravenous administration of verapamil (0.15mg/kg) and in another 15 patients after intravenous administration of procainamide (15 mg/kg). The results demonstrated that, in the control state acute atrial ER can be significantly demonstrated at each atrial representative site (p<0.001). The mean ERP400 and ERP600 shortenings were 9±4% and 8±4%, respectively. After procainamide infusion, but not after verapamil, baseline ERP400 and ERP600 values were significantly prolonged at the five representative atrial sites (p<0.01). Acute atrial ER could still be demonstrated at each atrial site after procainamide or verapamil infusion (p<0.001). In conclusion, acute atrial ER can be demonstrated after only a 5-minute period of rapid atrial pacing in humans. Intravenous verapamil or procainamide does not abolish this ER process.

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