Autonomic mechanism for chronic atrial electrical remodeling induced by rapid atrial pacing in ambulatory danines

Objetives The mechanism for changes in the electrophysiological properties of the atria during rapid pacing induced atrial fibrillation(AF) is not well understood.We aimed to investigate the contribution of intrinsic cardiac autonomic nervous system(ICANS) in chronic atrial electrical remodeling and AF induced by rapid atrial pacing for 4 weeks. Methods Twelve adult mongrel dogs weighing 15 to 20 kg were assigned to two groups;group 1(experimental group,n= 7) and group 2(control group,n =5).All dogs were anesthetized with propofol and mechanically ventilated via endotracheal tubes.The chest was entered via bilateral mini-thoracotomy at the fourth intercostals space.Bipolar pacing electrode was sutured to the right atrial appendage.Four-electrode catheters(Biosense-Webster,Diamond Bar,CA) were secured to allow recording at the right and left atriaum.All tracings from the electrode catheters were amplified and digitally recorded using a computer-based Bard Laboratory System (CR Bard Inc,Billerica,MA).Electrograms were filtered at 50 to 500 Hz.Continuous rapid pacing(600 bpm, 2×threshold[TH]) was performed at the right atrial appendage. Ganglionated Plexi(GP) was localized by applying high frequency stimulation(HFS;20 Hz,0.1ms duration, 0.5 to 4.5 V)with a bipolar stimulation-ablation probe electrode (AtriCure,West Chester,OH).Group1 underwent ablation of bilateral GP and ligament of Marshall followed by 4-week pacing.Group 2 underwent sham operaton without ablation of GP and ligament of Marshall followed by 4-week pacing.The effective refractory period(ERP) and window of vulnerability(WOV) were measured at 2×TH before(baseline) and every week after GP ablation.WOV was defined as the difference between the longest and the shortest coupling interval of the premature stimulus that induced AF.GP consist of the anterior right ganglionated plexi(ARGP) located in the fat pad at the right superior pulmonary vein(RSPV)-atrial junction;the inferior right ganglionated plexi(IRGP) located at the inferior vena cava/right atrial junction;the superior left ganglionated plexi(SLGP) at the left superior pulmonary vein(LSPV) /left atrial junction and the inferior left ganglionated plexi(ILGP) at the left inferior pulmonary vein (LIPV)/left atrial junction.Results Immediately after ablation, the ERP in Group 1 became markedly longer and started to shorten gradually during the first 2 weeks,then stabilized at the 4th week.Compared to Group2,the ERP of Group1 was significantly longer in the first 3 weeks(P【 0.05),but no obvious difference at the 4th week in either the right or left atrium(P】0.05).In Group 1,AF could not be induced(WOV=0)in the first 3 weeks after ablation, and at the 4th week,AF was induced in 2 of 7 dogs.In Group2,WOV progressively widened during the 4-week period. AF could not be induced in 5 of 7 dogs in Group 1 and 1 of 5 dogs in Group 2 during the 4-week pacing period. Conclusions The intrinsic cardiac autonomic nervous system (ICANS) plays an important role in the early stage of atrial electrical remodeling induced by rapid atrial pacing.On the other hand,with time passing by,its effect on the formation of AF decreases gradually,which suggests that ICANS may account for a non-dominant factor in the late stage of the rapid pacing-induced chronic atrial fibrillation.

Effects of Amiodarone plus Losartan on Electrical Remodeling in Rapid Atrial Pacing in Rabbits

Objectives To investigate the electrical remodeling and the effects of amiodarone and losartan on electrical remodeling in rapid atrial pacing on rabbit model. Methods 40 normal rabbits were randomly divided into 4 groups ： the saline group （control group）, amiodarone group, losartan group, anti ＋ los group. All rabbits were raised drugs in a week. The atrial effective refractory period （AERP） was measured. Then, take a rapid atrial pacing （600 bpm） and the AERP was measured after 0.5, 1, 2, 4, 6 and 8 hours pacing and 30 minutes after the termination of rapid pacing. Results （1） In control group, after 8 hours rapid pacing, AERP200 and AERP150 were significantly shortened 16. 11% ± 3.1% （ P 〈 0. 01 ） and 9. 99 % ± 4. 2% （ P 〈 0. 01 ）. And the degree of AERP shortening induced by rapid pacing was greater at basic cycle lengths of 200 ms （BCL200） than that at BCL150. The AERP of amiodarone, losartan group and ami ＋ los group were not shortened during rapid pacing. （2） In the control group, after the termination of rapid pacing, the AERP gradually increased. The AERP at all of the BCLS examined recovered to almost the 95.78% and 96. 76% of baseline values within the first 10 minutes and recovered to almost the 99.07% and 99.39% of baseline values within the first 30 minutes. Conclusions Short-term atrial rapid pacing can induce the atrial electrical remodeling. Amiodarone and losartan can prevent the electrical remodeling.