快速心房激动对心房肌电生理特性的影响

比较快速心房起搏与急性心房颤动 (简称房颤 )诱发心房电生理特性的变化。以 15 0～ 2 0 0ms起搏周长(PCL)对 4 5例成功射频消融后 (RFCA)病人右房进行S1S1刺激诱发急性房颤 ,据能否诱发急性房颤分为非房颤组和急性房颤组 ;再以 4 0 0msPCL对心房快速激动前后高位右房、低位右房、His束周围等多部位进行S1S2 扫描 ,测定心房有效不应期 (ERP)、ERP离散度 (ERPd)、右房内及房间的传导时间的变化 ;另以 35 0 ,4 0 0和 4 5 0ms三个PCL随机对RAA进行S1S2 扫描 ,观察ERP频率自适应性的变化。两组心房快速激动后 4 0 0msPCL下右房各刺激部位及三种不同PCL右心耳ERP均较心房快速激动前有明显的缩短 ,并且缩短的程度相同。两组病人心房快速激动前后房内和房间传导时间及ERPd没有明显改变。两组心房快速激动前后斜率均值均较激动后明显下降 ;心房快速激动前、后斜率均值两组间无显明差别 (P >0 .0 5 )。结论 :两种方式的心房快速激动可诱发相似的心房电重构现象。     

地尔硫(艹卓)、普罗帕酮和胺碘酮对短阵心房快速除极诱发的心房有效不应期变化的影响

目的　研究地尔硫、普罗帕酮和胺碘酮对短阵心房快速除极诱发的心房有效不应期(ERP)变化的影响。方法　 6 9例室上性心动过速消融成功后的自愿者 ,被随机分为对照组、地尔硫组、普罗帕酮组和胺碘酮组。以 4 0 0ms起搏周长 (PCL)分别对高位右心房、低位右心房、希氏束周围等部位进行S1S2 程序刺激 ,另以 3个不同PCL(35 0、4 0 0和 4 5 0ms)对右心耳进行S1S2 程序刺激 ,应用双极记录法测定各组在基础状态、心房快速除极前、后心房ERP和ERP频率自适应性 (ERP RA)的变化 ,同时观察心房快速除极后程序刺激过程中意外诱发继发性心房颤动 (AF)的情况。结果　基础状态下 ,各组 4 0 0ms周长下心房各部位ERP差异不显著 ;心房快速除极前 ,对照组和地尔硫组心房各部位ERP无明显改变 ,而普罗帕酮组和胺碘酮组心房各部位ERP均明显延长 ;心房快速除极后 ,地尔硫组心房各部位ERP较除极前无明显缩短 ,对照组、普罗帕酮组和胺碘酮组心房各部位ERP较除极前均明显缩短。对照组、普罗帕酮组和胺碘酮组心房快速除极后斜率均值较除极前明显下降 ,地尔硫组心房快速除极后斜率均值较除极前无明显变化。地尔硫组、普罗帕酮组和胺碘酮组心房快速除极后继发AF发生阵数明显低于对照组。结论　预先给予地尔硫可以阻止心     

氯沙坦对心房急性电重构的影响

目的　以地尔硫为对照 ,探讨氯沙坦对心房快速起搏诱发急性电重构的干预作用。方法　 2 1只兔随机分为盐水组、地尔硫组和氯沙坦组。 2F电极导管分别置于高位右心房 (HRA)、低位右心房 (LRA)和希氏束区 (HIS) ,以最快 1∶1起搏频率心房起搏 3h。阻断自主神经后 ,观察各组心房快速起搏前后 ,不同部位心房有效不应期 (AERP)、AERP频率适应性、AERP离散度 (AERPd)及右心房内传导时间变化。结果　 (1)心房快速起搏后 ,盐水组AERP2 0 0 和AERP150 立即缩短 ;起搏 1h达最小值(P <0 0 5 ) ,起搏 0 5h内AERP2 0 0 和AERP150 缩短速率最快 [(30 2± 10 5 )ms/h ,(2 4 1± 9 1)ms/h];地尔硫组和氯沙坦组心房快速起搏后AERP无显著缩短。 (2 )心房快速起搏前 ,盐水组HRA处(AERP2 0 0 -AERP150 ) / 5 0ms为 0 17± 0 0 8,起搏 0 5、1、2、3h后分别为 0 0 8± 0 0 6、0 0 9± 0 0 6、0 0 8± 0 0 4、0 0 9± 0 0 5 ,P <0 0 5 ,提示AERP频率适应性降低 ;地尔硫组和氯沙坦组心房快速起搏前后 ,该值差异无显著性。 (3)盐水组心房快速起搏 2、3h ,AERPd明显增大 (P <0 0 5 )。地尔硫组心房快速起搏 3h ,与起搏前比较 ,AERPd显著增大 (P <0 0 5 )。氯沙坦组心房快速起搏后 ,AERPd无显著增加。     

地尔硫Zhuo、普罗帕酮和胺碘酮对短阵心房快速除极诱发的心房有效不应期变化的影响

目的 研究地尔硫Zhuo，普罗帕酮和胺碘酮对短阵心房快速除极诱发的心房有效不应期（ERP）变化的影响。方法 69例室上性心动过速消融成功后的自愿者，被随机分为对照组，地尔硫Zhuo组，普罗帕酮组和胺碘酮组。以400ms起搏周长（PCL）分别对高位右心房，低位右心房，希氏束周围等部位进行S1S2程序刺激，另以3个不同PCL（350，400和450ms)对右心耳S1S2,应用双极记录法测定各组在基础状态，心房快速除极前，后心房ERP和ERP频率自适应性（ERP－RA）的变化，同时观察心房快速除极后程序刺激过程中意外诱发继发性心房颤动（AF）的情况。结果 基础状态下，各组400ms周长下心房各部位ERP差异不显著；心房快速除极前，对照组和地尔硫Zhuo组心房各部位ERP无明显改变，而普罗帕酮组和胺碘酮组心房各部位ERP均明显延长；心房快速除极后，地尔硫Zhuo组心房各部位ERP较除极前无明显缩短，对照组，普罗帕酮组和胺碘酮组心房各部位ERP较除极前均明显缩短。对照组，普罗帕酮组和胺碘酮组心房快速除极后斜率均值较除极前明显下降，地尔硫Zhuo组心房快速除极后斜率均值较除极前无明显变化。地尔硫Zhuo组，普罗帕酮组和胺碘酮组心房快速除极后继发AF发生阵数明显低于对照组。结论 预先给予地尔硫Zhuo可以阻止心房快速除极诱发的心房ERP缩短和ERP频率自适应性削弱，提示细胞内钙超载可能是心房ERP重构的重要原因之一。地尔硫Zhuo，普罗帕酮和胺碘酮均可减少继发AF的发生，前者可能与其阻止快速除极诱发ERP缩短有关，后二者可能与其明显延长ERP的药理作用有关。     

依那普利对心房急性电重构影响的临床研究

目的　探讨依那普利对快速心房起搏诱发心房急性电重构的干预作用。方法　 2 7例阵发性室上性心动过速行射频消融术患者随机分为对照组 ( 16例 )和依那普利组 ( 11例 )。阻断自主神经后 ,以最快 1:1心房起搏 [( 349± 37) /min]诱发急性心房颤动 (房颤 ) ,观察各组患者心房快速刺激前后心房有效不应期 (AERP)、AERP频率自适应性、不应期离散度 (AERPd)的变化及房颤诱发情况。结果　①心房快速起搏后 ,对照组AERP明显缩短 ,依那普利组AERP无显著变化。两组患者心房快速起搏前后AERPd差异无显著性 ;②心房快速起搏前后 ,对照组右心耳 (RAA)处AERP与相应程控刺激基础周长拟合直线的斜率分别为 0 0 6 2和 0 0 18;依那普利组分别为 0 0 5 9和 0 0 5 3;③心房快速起搏后 ,对照组房颤诱发例数、次数显著增加 ,平均房颤持续时间明显延长 ;依那普利组心房快速起搏前后房颤诱发情况无显著差异。结论　依那普利能够防止心房快速激动引起的心房急性电重构 ,降低房颤诱发率     

地尔硫卓对心房有效不应期和单相动作电位重构的干预研究

为研究地尔硫卓对快速心房起搏诱发的心房肌急性电重构的影响 ,将 4 0例无器质性心脏病的室上性心动过速患者射频消融成功后 30min随机分为两组 ,地尔硫卓组 15例 ,对照组 2 5例 ;地尔硫卓组给予药物干预 ,对照组以生理盐水替代 ,应用双极记录及单相动作电位记录法检测基础状态下、药物负荷量后 (即快速心房起搏前 )及4 0 0ms周长心房起搏后右心耳、高位右房、低位右房和His束周围等部位有效不应期 (ERP)和右房单相动作电位复极 90 %的时程 (MAPD90 )。结果 :对照组快速心房起搏后心房各部位ERP和右房MAPD90 较刺激前有明显缩短 ,地尔硫卓组心房快速起搏前后各部位ERP和右房MAPD90 无明显改变。结论 :快速心房起搏可使无器质性心脏病和心房颤动病史的患者心房ERP和MAPD90 明显缩短 ,地尔硫卓可阻止快速心房起搏诱发的心房ERP和MAPD90 的缩短 ,提示细胞内钙超载可能是心房ERP和单相动作电位重构的重要原因之一。     

心房肌急性电重构的临床研究

目的探讨快速心房激动对心房电生理特性的影响.方法以150～200ms起搏周长(PCL)对21例射频消融术后患者右心房进行S1S1刺激诱发心房颤动,心房快速刺激前、后均以400ms周长分别对高位右心房(HRA)、低位右心房(LRA)、希氏束周围(HB)、右心耳(RAA)等多部位进行S1S2扫描,测定心房有效不应期(ERP)、有效不应期空间离散度(ERPd)、右心房内及心房间传导时间(CT)的变化;以350ms、400ms和450ms3个不同周长随机对RAA进行S1S2扫描,观察有效不应期频率自适应性(ERPA)的变化.结果快速心房激动后ERP较刺激前有明显缩短,HRA的ERP[(193.2±25.5)msvs(179.7±23.3)ms,P=0.001、LRA的ERP [(198.0±30.8)msvs(182.0±22.5)ms,P=0.026]、HB的ERP[(195.0±26.6)ms vs(182.0±16.8)ms,P=0.018]、RAA的ERP(194.0±20.1)msvs(180.0±29.0)ms,P=0.014].而ERPd则无明显变化[(25.0±17.8)ms vs(28.0±16.9)ms,P=0.576];3个不同周长下RAA的ERP均较心房快速激动前有显著缩短,S1S1为350ms、400ms和450ms.心房快速激动前后ERP分别为[(186.2±24.4)ms vs(168.7±30.9)ms,P=0.006]、[(194.0±20.1)ms vs(180.0±29.0)ms,P=0.014]和[(191.2±33.1)ms vs(170.0±28.3)ms,P=0.0001];心房快速激动前、后ERP与PCL相关系数分别为(rb=0.998,P=0.041;ra=0.397,P=0.74),心房激动前斜率接近正常0.058,激动后斜率为0.015.房内房间CT无明显变化,HRA-HB[(46.5±12.5)msvs(48.4±12.0)ms,P=0.125]、HB-CSD[(47.0±14.2)ms vs(49.6±14.8)ms,P=0.153].结论快速心房激动使右心房同一周长不同部位、同一部位不同起搏周长下ERP缩短,ERPA下降;ERPd及右心房内房间传导速度无明显改变.快速心房刺激使人心房肌发生电重构,ERP缩短、ERPA下降可能是心房颤动发生、维持和发展的重要原因.     

快速心房电刺激对人心房不应期的影响及卡托普利的干预作用

探讨快速心房电刺激对人心房有效不应期 (AERP)的影响及卡托普利的干预作用。选择本院行射频消融术的 38例成年患者为研究对象 ,随机分为卡托普利组 (14例 )、维拉帕米组 (12例 )及生理盐水对照组 (12例 )。分别在阻断心脏自主神经后 ,观察各组用药前、后及快速心房刺激后AERP的变化及AF诱发情况。结果 :①快速心房刺激可使 5 7.9%成人正常心脏诱发AF ;②诱发AF后AERP明显缩短 ,而未诱发AF者的AERP无明显变化 ;③卡托普利及维拉帕米均能显著延长诱发AF患者的AERP ;④卡托普利能减少AF诱发率 ,并缩短AF持续时间 ;而维拉帕米则使AF诱发率增加、持续时间延长。结论 :①快速心房刺激可使部分患者AERP缩短 ,并诱发这类患者发生AF ;②卡托普利可显著延长诱发AF患者的AERP ,并使AF诱发率降低、持续时间缩短     

离体兔心脏急性双心房扩张合并快速心房刺激时电生理变化及胺碘酮的干预作用

目的:观察离体兔心脏急性双心房扩张同时给予快速心房刺激后,电生理指标的变化以及胺碘酮的抗心律失常作用。方法:建立Langendorff灌流的离体兔心脏模型。把20只长耳白兔随机分为2组,组1:双心房压力依次升高为0cmH2O,6cmH2O,12cmH2O和20cmH2O,各压力水平分别给予10min快速心房刺激(频率50ms);组2:台氏液中加入胺碘酮(1.5mg/L)。观察在上述2种情况下心房有效不应期(AERP)、心房激动顺序的变化以及心房颤动(AF)的诱发情况。结果:随着双心房压力升高,每一压力水平合并10min快速心房刺激后,AERP明显缩短,心房激动顺序也发生改变(P<0.01),但个体间变化方向不一致,AF的诱发情况明显增加,甚至出现自发性AF。胺碘酮可以预防AERP的缩短以及心房激动顺序的改变,使AF的诱发情况明显减少。结论:在离体灌流的兔心脏,急性双心房扩张合并快速心房刺激后,AF的易患性增加,并且与AERP的缩短及心房激动顺序的改变相关,这些改变可以被胺碘酮抑制。     

辛伐他汀对老年犬急性心房电重构的影响

目的通过快速心房起搏(ATP)建立犬心房心动过速心房重构模型,观察辛伐他汀对急性心房电重构的影响,探讨辛伐他汀防治心房颤动(AF)的作用机制。方法健康成年杂种犬21只(雌雄不拘,体重10¹2.5 kg)。随机分为三组:对照组ATP组、药物干预组。药物干预组起搏前5 d给予辛伐他汀20 mg/d口服。右侧开胸将电极置于右心耳及右心房侧壁。ATP组和药物干预组以480次/min的频率快速起搏右心房,于实验开始及起搏后6 h对每只犬进行非开放性电生理检查,测定心房有效不应期(AERP)及burst刺激诱发AF频率和AF持续时间。结果对照组在整个时间内AERP无变化。ATP组ATP后,AERP明显缩短。药物干预组ATP后AERP亦缩短,但较ATP组变化明显减轻。各组起搏前AF的频率和持续时间没有差异。对照组在手术前后AF的频率和持续时间无变化。ATP组ATP后AF的诱发频率明显增多和持续时间延长。药物干预组与ATP组比较AF诱发频率及持续时间明显得到抑制。结论心房电重构造成的AERP等电生理变化促进了AF发生和维持。辛伐他汀对ATP引起的犬急性心房电重构具有一定的预防作用,并能削弱ATP对犬AF的促发作用。     

Suppression of atrial fibrillation by multisite and septal pacing in a novel experimental model

OBJECTIVES: To evaluate the preventive efficacy of multisite and septal atrial pacing in an experimental model. METHODS: Sterile right atrial pericarditis was induced in 12 foxhounds to provide an anatomical substrate for atrial fibrillation (AF). As a trigger mechanism, atrial extrasystoles were simulated by constant asynchronous pacing at a cycle length of 1000 ms from randomly selected right or left atrial electrodes, using a biatrial epicardial multielectrode with 128 bipoles. Additionally, a transvenous pacing lead was screwed into the interatrial septum. Four electrodes located in the high and low right (HRA/LRA) and left atrium (HLA/LLA) were selected for preventive multisite stimulation. Constant pacing at a cycle length 30 ms below sinus rate was applied from the following site(s): HRA, septal, HRA+LRA, HRA+LLA, HRA+LRA+LLA and HRA+LRA+HLA+LLA (order randomized). Number and duration of AF episodes were studied during 10 min intervals, separated by 5 min pauses, respectively. To validate the model, the protocol was repeated 10 min after i.v. bolus administration of D,L-sotalol (1 mg/kg body weight). RESULTS: The number of AF episodes decreased with increasing number of pacing sites, reaching statistical significance compared to HRA stimulation for quadruple-site and single-site septal pacing only (P<0.05). Single-site septal was as efficient as quadruple-site pacing in suppressing AF. The duration of AF episodes was not significantly affected by the pacing configuration. D,L-sotalol almost completely suppressed AF irrespective of the pacing configuration used. CONCLUSIONS: In this novel experimental model, quadruple-site and septal pacing effectively suppress paroxysmal AF.     

Determinants of Efficacy of Atrial Pacing in Preventing Atrial Fibrillation Recurrences

Atrial Pacing in Atrial Fibrillation. Introduction: Several studies have shown that single or dual site atrial pacing is effective in reducing he frequency of recurrent atrial fibrillation (AF) in selected patients. However, it is still unclear what the best predictors are of long-term efficacy of atrial pacing. Methods and Results: Forty-seven patients with paroxysmal AF requiring demand pacing underwent electrophysiologic study and dual chamber pacemaker implant. After 4 months of follow-up, patients were divided into two groups according to the presence (group 1) or absence (group 2) of symptomatic AF recurrences. Atrial pacing markedly reduced AF recurrences in all patients. Twenty-four patients were free of arrhythmia. The basal state conduction times (CT_s) and the incremental conduction times (ICT_s), during programmed electric stimulation between the high right atrium (HRA) and the coronary sinus ostium (CS_os) but not between the HRA and the His-bundle region, were significantly longer in group 1. There was no statistical difference in the effective refractory period (ERP) recorded at the HRA, the low right atrium (LRA), and the CS_s between the two groups, whereas the differences between the greatest and least recorded ERPs measured from the HRA, LRA, and CS_os (δERP) were significantly greater in group 1 patients. Two parameters were selected by discriminant multivariate analysis, namely δCT_os (ICT-CT between HRA and CS_os and δERP. The first bad a greater relative importance in predicting AF recurrence (r²= 0.33 and r²= O.1, respectively). Conclusion: Single site atrial pacing is effective in reducing AF recurrences, with decreasing efficacy in patients with greater right atrial conduction delay and wider refractoriness dispersion.     

Electrophysiologic actions of dl-sotalol in patients with persistent atrial fibrillation

OBJECTIVES: We sought to determine the electrophysiologic actions of sotalol in the remodeled atrium of humans. BACKGROUND: In experimental studies, sotalol has limited class III action in the electrically remodeled atrium and did not prevent atrial fibrillation (AF) induction. METHODS: We determined the effective refractory periods (ERPs) at three pacing cycle lengths (400, 500, and 600 ms) in the high right atrium (HRA) and distal coronary sinus (DCS) before and after intravenous infusion of dl-sotalol in 10 patients with persistent AF who underwent internal cardioversion. The same protocols were performed in 10 control subjects in sinus rhythm. RESULTS: In the HRA and DCS, the atrial ERPs at different drive cycle lengths were significantly shorter in patients with AF than in control subjects (p < 0.05). In patients with AF, the atrial ERP's adaptation to rate was nearly normal in the HRA, but was poor in the DCS. In both groups, dl-sotalol significantly increased the atrial ERPs at both the HRA and DCS, as compared with baseline (p < 0.05). However, the prolongation of atrial ERPs was significantly less at a drive cycle length of 600 ms in patients with AF versus control subjects (p < 0.05). After infusion of dl-sotalol, the atrial ERP's adaptation to rate at both the HRA and DCS was poor in patients with AF, and AF was still easily inducible in the majority of them, but not in control subjects. CONCLUSIONS: The results of the present study demonstrate that the electrophysiologic actions of dl-sotalol are significantly attenuated in the chronically remodeled human atrium, and these changes might represent a probable explanation for the low efficacy of dl-sotalol to prevent early AF recurrence after electrical cardioversion.     

左房快速起搏对肺静脉口及心房肌电重构的影响

目的探讨左房快速起搏对肺静脉口、左右心耳电重构的影响。方法运用快速起搏左心耳的方法建立心房颤动(AF)模型,在起搏前及起搏后的第1,3,5,7d对左、右心耳;左上、左下肺静脉口;右上、右下肺静脉口的有效不应期(ERP)、ERP频率适应性、ERP离散度及心房间的传导时间进行测定。采用S1S2程序刺激,基础起搏周长(PCL)分别为400,300,200ms,S2为200ms,以5ms的步长递减。程序刺激结合Burst刺激对上述心房部位进行AF的诱发,记录AF的发生率。在第8天关闭起搏器,采用上述相同方法对起搏停止后即刻;2,4,6,24h的上述各部位的ERP进行测定。结果起搏1d后各个基础起搏周长下各部位的ERP明显缩短,ERP频率适应性降低,ERP离散度增大(P<0.05),而心房间传导时间无明显变化(P>0.05);起搏终止后各部位的ERP逐渐延长,但起搏终止后6hERP与快速起搏前相比仍有明显缩短(P<0.05);24h后ERP基本恢复到起搏前水平,两者相比无明显差异(p>0.05);随着起搏时间的延长各部位AF的诱发率逐渐增高(P<0.05)。结论快速心房起搏不仅引起心房肌电重构,亦引起肺静脉电重构。     

迷走神经刺激和乙酰胆碱灌注对心房肌电生理特性的影响

研究在体情况下迷走神经刺激(VNS)和乙酰胆碱(Ach)灌注对心房肌不同部位的电生理影响,并探讨其诱发心房颤动(AF)的机制。10只杂种犬自身随机对照,运用单相动作电位(MAP)记录技术,同步记录10只开胸犬的右心耳(RAA)、高位右房(HRA)、低位右房(LRA)、左心耳(LAA)、高位左房(HLA)、低位左房(LLA)的MAP,分别给予切断迷走神经、VNS、Ach灌注(分别做为对照组、VNS刺激组、Ach灌注组)后,观察诱发AF的情况和动作电位时程APD50、APD90和APD离散(dAPD)的变化。结果:10只犬在VNS刺激和Ach灌注同时,右心耳单一刺激分别有7只和6只犬诱发AF;VNS明显缩短APD50、APD90,其中RAA缩短最明显(APD50从72±5ms到19±4ms,APD90从136±7ms到43±5ms,P<0.001);Ach灌注也明显缩短APD50和APD90,与VNS相比,LLA的APD90缩短更明显(47±6msvs62±8ms,P<0.01);VNS明显升高心房肌APD50和APD90的离散(17±5msvs7±3ms,25±7msvs8±5ms,P<0.01)。结论:VNS和Ach灌注可引起APD缩短和离散升高,但影响的部位和程度稍有差异,都易诱发AF。     

Effects of verapamil on superior vena cava electrical remodeling induced by short-term pacing from right atrium and superior vena cava in human

BackgroundAlthough the superior vena cava (SVC) may be involved in the triggering or maintenance of atrial fibrillation (AF), the electrophysiological properties of SVC in human are ill-defined.MethodsThe baseline effective refractory periods (ERPs) of high right atrium (HRA), SVC and the conduction time (CT) between HRA and SVC were measured at pacing cycle lengths (PCL) of 600 and 400 ms respectively in 20 patients (12 females, age 46 ± 13 years) with paroxysmal supraventricular tachycardia. Immediately after acute electrical remodeling (ER) induced by constant HRA or SVC pacing at PCL of 400 ms for 5 min, ERPs of HRA, SVC and the CT between HRA and SVC were determined. After verapamil was administered, the same protocols for determining ERPs of HRA, SVC and the CT between HRA and SVC were repeated.ResultsThe baseline ERP of SVC was significantly longer than that of HRA. The CT from SVC to HRA was significantly longer than that from HRA to SVC. After acute ER, both the ERPs of HRA and SVC were significantly shortened. However, no significant changes of the CT between HRA and SVC could be demonstrated. After verapamil infusion, significant shortening of the ERP of HRA and SVC still occurred following acute ER and the ERP of SVC was still longer than that of HRA.ConclusionsIn human, ER can occur both in HRA and SVC after a short and moderately rapid heart rate pacing either from HRA or SVC. Verapamil cannot prevent such ER from occurring.     

Evidence of mechanoelectric feedback in the atria of patients with atrioventricular nodal reentrant tachycardia

Objective Patients with atrioventricular nodal reentrant tachycardia (AVNRT) could serve as a clinical model to study the effects of mechanical stretch in the electrical properties of atrial myocardium.Materials and methods We studied 14 patients with AVNRT. Peak, mean and minimal atrial pressures, atrial refractoriness (ERP) in the right atrial appendage and high right atrial lateral wall and monophasic action potential duration at 90% of repolarisation (MAPd90) in the right atrial appendage were assessed during atrial pacing at 500 and 400 ms and after 2 min of pacing at the tachycardia cycle length. Measurements were repeated from the same positions after ventricular pacing at the same cycle lengths and after 2 min of tachycardia. Susceptibility to atrial fibrillation (AF) was assessed by noting whether AF was induced during ERP evaluation.Results Atrial pressure showed a statistically significant increase during ventricular pacing compared to baseline. This increase remained substantially unchanged when the tachycardia was induced. A significant reduction in atrial ERP and MAPd90 was also observed during ventricular pacing at all cycle lengths compared to atrial pacing. Two minutes of spontaneous tachycardia were enough to change the atrial ERP and MAPd90 to values significantly lower than those during atrial pacing at the cycle length of tachycardia. During the ERP evaluation AF was induced more often during the tachycardia (28%) than during ventricular (14%) and atrial pacing (0%).Conclusion In AVNRT patients, ventricular pacing and reentrant tachycardia significantly increase right atrial pressures and subsequently shorten ERP and MAPd90, leading to an enhanced propensity for AF.