Effects Of Antiarrhythmic Drugs On Acute Electrical Atrial Remodeling Induced By Tachycardia

Objective: The present study was performed to assess the effect of tachycardia-induced on atrial electrophysiological charateristics; To investigate the effect of antiarrhythmic drugs on acute electrical atrial remodeling induced by tachycardia, and providing clues for clinical prophylaxis of atrial fibrillation occurrence.Methods:1.Fifty one patients without structural heart disease suffering from paroxysmal supraventricular tachycardia were studied after successful radiofrequency catheter ablation (RFCA), All patients were randomized to four groups (control group, diltiazem group, propafenone group and amiodarone group). The quadrupolar electrode catheters positioned in the high right atrium (HRA), the coronary sinus (CS) and the His bundle area were reserved after RFCA. An electrode monophasic action potiential (MAP) catheter was placed in the right atrial free wall. Intravenous atropin (0.04mg/kg) and propranolol (0.2mg/kg) were adminstrated in all subjects with a duration of more than 5 min to prevent the sympathetic nerve activity before the study.2. The atrial ERP in HRA,LRA,RAA and HIS with a drive cylcelength of 400ms, ERP-RA in RAA with 3 different drive cycle length of 350, 400 and 450ms, and MAPD90 in the right atrial free wall at sinus rhythm were measured in baseline(after autonomic blockade), before(post-drug or saline) and after rapid atrial depolarization in all subjects;Results:1. There was a significant shortening of the post-tachycardia atrial ERP measured at a drive cycle length of 400 ms in each stimulating site including HRA, LRA and HIS, similarly, in RAA with 3 different cycle length of 350, 400 and 450ms within control group, the post-tachycardia ERPd was unchanged, as compared with pre-tachycardia ones. ERP-RAwas attenuated obviously in RAA site after rapid atrial depolarization.2.Atrial ERP was similar before each episode of rapid atrial depolarization between AF group and non AF group. The post-tachycardia atrial ERPs shortened significantly in each site of right atrium at 400ms drive pacing length and in RAA at three different drive pacing length( 350, 400 and 450), as compared with the corresponding pre-tachycardia ones, the extent of shortened value was similar in both groups.3. Post-tachycardia atrial ERP in each stimulating site of right atrium shortened significantly, and ERP-RA in RAA was inpaired obviously in control group, propafenone group and amiodarone group, however, both of which remained unchangeable in diltiazem group, as compared with those of pre-tachycardia. The MAP90 was similar before and after rapidatrial depolarization within diltiazem group, and shortened significantly after rapid atrial depolarization in both propafenone and amiodarone group, as compared with that before rapid atrial depolarization. The incidence of secondary AF was lower in the 3 drug interventional groups than in control group. Conclusions:1 Short episodes of rapid atrial depolarization may induce atrial electrical remodeling including shortening of atrial ERP and maladaptation of right atrial appendage ERP. There is no difference in shortening of atrial ERP induced either by rapid atrial pacing or by acute AF.2 Diltiazem, but not propafenone and amiodarone,could markedly attenuate this effect and right atrial MAPD90 shortening induced by tachycardia. However, diltiazem, propafenone and amiodarone could decrease the incidence and duration of secondary AF.