射频消融第三脂肪垫对犬心房电生理参数及心房颤动诱发的影响

目的研究射频消融第三脂肪垫对犬心房电生理参数及心房颤动(房颤)诱发的影响。方法观察12只杂种犬在不同起搏周长下,消融第三脂肪垫前后心房不同部位有效不应期(AERP)、AERP离散度、AERP频率适应性,房颤诱发率及其诱发窗口的变化。结果与消融前相比,消融后心率变化差异无统计学意义(P>0.05)。随着起搏周长变短,AERP明显缩短,且差异具有统计学意义(均为P<0.05)。消融术后高位左心房、低位左心房、左心耳部位AERP明显缩短,高位右心房、低位右心房、右心耳部位AERP明显延长(均为P<0.05)。AERP离散度差异无统计学意义(P>0.05)。消融后不同测量部位的房颤诱发率均降低及房颤诱发窗口增宽。结论消融第三脂肪垫达到部分去迷走神经化,使左心房AERP缩短,同时使房颤诱发率降低及房颤诱发窗口增宽。     

消融犬Marshall韧带对刺激心房左后脂肪垫所致心房颤动的影响及机制

目的探讨消融犬Marshall韧带对刺激心房左后脂肪垫所致心房颤动(简称房颤)的影响及机制。方法成年杂种犬14条,随机分为实验组8条,对照组6条。实验组首先测量左肺静脉和左心耳的有效不应期,继而刺激心房左后脂肪垫诱发房颤。消融Marshall韧带上段后和下段后重复上述步骤。对照组除不干预Marshall韧带外,其它电刺激方案与实验组相同,同时对该组犬的心脏进行迷走神经染色。结果①实验组消融Marshall韧带后,左肺静脉和左心耳的有效不应期均显著延长(P0.05)。②和消融前比较,实验组消融Marshall韧带上段后的房颤诱发率有下降趋势(70.8%vs87.5%,P0.05);消融Marshall韧带全程后房颤诱发率显著下降(33.3%,P0.001)。对照组三次电刺激所测得的不应期和房颤诱发率无差异。③Marshall韧带与左下肺静脉、心房左后脂肪垫、左心耳之间存在迷走神经的直接联系。结论消融犬Marshall韧带可显著降低刺激心房左后脂肪垫所致房颤的诱发率。     

心脏脂肪垫在肺静脉引发房颤中的作用

目的探讨窦房结-心房脂肪垫(SAFP)在右上肺静脉灶性放电引发阵发性房颤(PAF)中的作用。方法12条新疆家养犬,苯巴比妥钠麻醉,经右侧开胸暴露右侧肺静脉。将1根8极标测电极导管固定在右上肺静脉,给予S1S1600bpm起搏刺激,另将1根8极(1.5×1.5cm)电极板固定在心外膜窦房结-心房脂肪垫上。术中监测II和aVR导联、血压和体温。以1～4V电压、1000bpm频率刺激窦房结-心房脂肪垫30～60s。结果12条家养犬在给予S1S11000ppm窦房结-心房脂肪垫刺激,随着电压从1增加到4V,心率从142±20bpm减少到75±30bpm(p<0.05),同时出现房性早搏、房性心动过速(房速)和房颤,同时予以右上肺静脉S1S1600ppm刺激,诱发房颤的房性早搏数随着刺激电压1～4V的增加从7个减少到2个,并以S1S1300ms,S1S2稍长于右上肺静脉不应期的早搏右上肺静脉刺激。S1S1600ppm刺激下房颤诱发率从基础状态的49.86%提高到70.59%,S1S2早搏刺激下从3.78%提高到16.6%(p<0.05)。7条狗在4%利多卡因4ml注射到窦房结-心房脂肪垫局部阻滞神经后,6条狗在同样右上肺静脉刺激诱发房颤电压的条件下不能诱发房颤,其中3条狗在电压增加大于9V时诱发房颤。房颤诱发的有效刺激部位在窦房结-心房脂肪垫2～3mm的范围内。结论有效部位窦房结-心房脂肪垫刺激,能够诱发慢频率依赖性阵发性房颤,刺激窦房结-心房脂肪垫增加右上肺静脉阵发性房颤的诱发率,局部神经阻滞降低或消除阵发性房颤的诱发.提示:增强窦房结-心房脂肪垫的自发神经放电,可能是临床右上肺静脉灶性放电转变成房颤的基础,消融窦房结-心房脂肪垫可能预防阵发性房颤的诱发。     

犬心脏第3脂肪垫对左心房及左上肺静脉电生理特性的影响

目的研究犬心脏第3脂肪垫（SVC-AO FP）对左心房及左上肺静脉有效不应期（PERP）及心房有效不应期（AERP）离散度的影响。方法10只犬麻醉后,自颈部离断并结扎双侧迷走神经,正中开胸暴露SVC-AO FP,右肺静脉（RPV）及下腔静脉（IVC）脂肪垫。消融RPV和IVC后,分别测定基础状态下、SVC-AO FP刺激后、SVC-AO FP消融后的左AERP、不应期离散度（dAERP）及左上PERP。结果SVC-AO FP刺激后AERP从基础状态下的（135±14）m s缩短至（106±16）m s（P<0.05）,消融后延长至（140±9）m s;dAERP从（15±4）m s,增加至（26±6）m s（P<0.05）,消融后为（11±9）m s;PERP从（131±12）m s缩短至（108±17）m s（P<0.05）,消融后的延长至（136±10）m s。结论刺激犬心脏SVC-AO FP缩短心房和肺静脉的有效不应期,增加心房有效不应期离散度。左心房及左上肺静脉的迷走神经支配部分可能直接来自SVC-AO FP。     

序列消融犬窦房结脂肪垫和房室结脂肪垫对迷走神经介导心房颤动诱发的影响

目的 研究旨在探索序列消融窭房结脂肪垫(sinus atrial node fat pad,SANFP)和房室结脂肪垫(atrialventricular node fat pad,AVNFP)对迷走神经介导的心房颤动(房颤)诱发的影响.方法 18只健康成年家犬分为二组,每组9只.A组优先消融SANFP,再联合消融SANFP+ AVNFP;B组优先消融AVNFP,再联合消融SANFP+ AVNFP.高频电刺激左、右侧迷走神经干制作迷走神经介导的房颤模型,测定消融前、后的房颤诱发率及心房和肺静脉不同部位有效不应期(effective refractory period,ERP).结果 (1)迷走神经干刺激可显著增加房颤的诱发率,且右侧迷走神经干刺激下的房颤诱发率高于左侧迷走神经干[(60.0±0.0)％比(18.4±22.1)％].(2)优先消融SANFP可显著降低左侧迷走神经干或右侧迷走神经干刺激下房颤的诱发率(分别降低了67.0％和72.0％),联合消融SANFP+ AVNFP可进一步降低2V电压的左侧迷走神经干或右侧迷走神经干刺激下房颤的诱发率(分别较消融前降低了100％和95.5％).而优先消融AVNFP也可显著降低2V电压的左侧迷走神经干或右侧迷走神经干刺激下房颤的诱发率(分别降低了95.7％和96.3％),但联合消融SANFP+ AVNFP并不进一步显著降低左侧迷走神经干或右侧迷走神经干刺激下的房颤诱发率(分别较消融前降低了98.0％和100％).(3)优先消融SANFP或AVNFP均可显著抑制迷走神经干刺激引起的右房、左房及右上肺静脉部位的ERP缩短效应.与单独消融SANFP相比,联合消融SANFP+AVNFP可进一步抑制迷走神经干刺激引起右房ERP的缩短效应,而联合消融AVNFP+ SANFP对迷 走神经干刺激引起左、右心房及肺静脉ERP的缩短效应的抑制作用与单独消融AVNFP比较差异无统计学意义.结论 心外膜脂肪垫消融可改变迷走神经干刺激对房颤诱发及心房肌、肺静脉ERP的影响,其中AVNFP是迷走神经干支配心房的汇聚点和主控区,因此AVNFP可能是房颤神经消融更有效的靶点.     

肺静脉在犬迷走神经介导性心房颤动维持中作用的研究

目的研究单纯肺静脉隔离在阵发性迷走神经介导性心房颤动(迷走性房颤)中的作用。方法杂种犬10只,分别刺激颈部迷走神经干诱发出持续性房颤。在心外膜进行肺静脉隔离,分别比较消融前后左、右心房的有效不应期(AERP),房颤的诱发率、持续时间和房颤波周长(AFCL)的变化。结果肺静脉隔离后,左、右心房AERP较消融前明显延长,AFCL明显延长,左、右心房AERP的差异明显缩短,房颤仍持续直至停止迷走神经刺激。结论肺静脉在迷走性房颤的维持上不起决定性的作用。     

射频消融心外膜脂肪垫治疗犬肺静脉左房交界处起源的心房颤动

目的探讨射频消融心外膜脂肪垫对左房-肺静脉交界触发的局灶性心房颤动(简称房颤)治疗的有效性。方法成年杂种犬10只,心外膜脂肪垫注射氯化乙酰胆碱(Ach)+左房短阵快速电刺激诱发犬左房-肺静脉交界触发的局灶性房颤模型。4极电极分别缝置于左房、右房、左肺静脉与左房交界处,记录最快激动部位。直视下射频消融心外膜脂肪垫。于房颤模型建立前后,及消融脂肪垫后测量左、右房有效不应期(ERP),肺静脉-左房交界处ERP、计算房颤诱发率。术毕处死实验犬行组织学检查。结果所有犬均能通过脂肪垫注射氯化Ach+左房短阵快速电刺激诱发出左房-肺静脉交界触发的局灶性房颤,建模后左房、右房、肺静脉-左房交界处的ERP均较建模前显著缩短(分别为94±33 ms vs 139±9 ms,104±17 ms vs 137±9 ms,104±17 ms vs 137±9 ms;P均<0.01)。脂肪垫消融后房颤诱发率与消融前比较显著降低(45%±16%vs 86%±4%,P均<0.01);左房、右房ERP无变化,肺静脉-左房交界处不应期显著延长(137±8 ms vs 104±17 ms,P<0.01)。组织学未发现除脂肪垫外的其它消融损伤灶。结论射频消融心外膜脂肪垫对肺静脉-左房交界触发的局灶性房颤治疗有效。     

肺静脉隔离对迷走神经功能及心房颤动易感性的影响

目的研究肺静脉隔离(PVI)对犬的心房迷走神经功能及心房颤动(简称房颤)易感性的影响。方法9条成年杂种犬,全麻下行颈交感-迷走神经干剥离术。静脉应用美托洛尔阻断交感神经活性。分别于肺静脉消融前后在基础状态及迷走神经刺激时测量窦性周长(SCL)、右心耳(RAA)、左心耳(LAA)、冠状静脉窦近端(CSp)和冠状静脉窦远端(CSd)的不应期(ERP)及心房易感窗口(VW)。结果①PVI前迷走神经刺激能明显降低SCL(P<0.001),PVI后迷走神经刺激对SCL影响较小(P>0.05)。②PVI前,迷走神经刺激能明显缩短心房各部位ERP(P均<0.05)。PVI后,迷走神经刺激对心房ERP的影响较小(P均>0.05)。③PVI前后基础状态下测得的VW无变化。PVI后迷走神经介导的房颤诱发率明显下降(P均<0.05)。结论PVI能导致迷走神经介导的窦房结抑制、心房不应期缩短能力及房颤易感窗口增加能力明显下降。     

迷走神经干预对犬心房电生理的影响

目的心房电重构可导致心房有效不应期缩短,通过测量心房有效不应期来研究迷走神经对心房电重构的影响。方法 10只成年犬给予酒石酸美托洛尔和阿托品阻断交感神经和迷走神经。分别测量心房电重构前后基础状态及迷走神经刺激下的心房有效不应期（ERP）和房颤易感窗口（VW）。结果①阿托品应用前后基础状态下的ERP无变化。阿托品应用前后迷走神经刺激下的ERP变化明显;②心房电重构后ERP：基础状态及迷走神经刺激下,无论右心房还是冠状静脉窦远端测得的ERP与重构前（阿托品应用后）ERP相比无明显差异（p值均〉0.05）;③VW的变化：阿托品应用前,迷走神经刺激下容易诱发房颤。阿托品应用后,心房电重构前后无论基础状态或迷走神经刺激均不能诱发房颤。结论迷走神经阻滞能减轻心房电重构所导致的心房不应期缩短,从而抑制迷走神经介导的房颤诱发。     

心脏脂肪垫在肺静脉灶性放电引发心房颤动中的作用

探讨心脏脂肪垫在肺静脉灶性放电与心房颤动 (简称房颤 )中的作用。 14条狗麻醉后经右侧开胸暴露右侧肺静脉。将 8极电极标测导管缝在右上肺静脉用于起搏。另放一 8极电极导管固定在临近右肺静脉和左房交接处脂肪垫。术中监测ECG的II和aVR导联、血压和体温。以 0 .1ms刺激间期 ,2 0Hz刺激频率的直方波刺激脂肪垫的迷走神经丛 30～ 5 0s,随着电压从 1～ 4 .5V ,心率逐渐减少 (P <0 .0 5 ) ,同时出现房性早搏、房性心动过速和房颤。在刺激迷走神经丛的同时 ,以 2 0 0～ 80 0次 /分的频率刺激肺静脉 (对照组没有迷走神经丛刺激 )均能诱发房颤。在迷走神经丛刺激下 ,以S1S1330ms,S1S2 稍长于肺静脉不应期的配对间期刺激肺静脉诱发房颤。与对照组比较 ,在迷走神经刺激下 ,肺静脉刺激诱发房颤的房性早搏数 ,随着刺激电压从 0 .6到 3V的增加 ,从 7个减少到 2个 (P <0 .0 5 )。 7条狗局部去神经后 ,6条狗在同样肺静脉刺激诱发房颤的电压条件下不能诱发房颤 ,其中有 3条在电压大于 9V时诱发房颤。结论 :在临近右肺静脉和左房交接处脂肪垫刺激可以将肺静脉灶性放电转变成房颤。因此 ,临床上自发的迷走神经丛的张力增高是肺静脉灶性放电转变成房颤的基础。     

Partial vagal denervation increases vulnerability to vagally induced atrial fibrillation

INTRODUCTION: Cervical vagal stimulation shortens the atrial effective refractory period (ERP) primarily in the high right atrium (HRA) and facilitates induction of atrial fibrillation (AF) by single premature HRA extrastimuli. We hypothesized that vagal denervation of the HRA prevents both ERP shortening in the HRA and AF induction during vagal stimulation. METHODS AND RESULTS: Vagal denervation of the HRA was achieved using radiofrequency catheter ablation (RFA) of the fat pad at the right pulmonary vein-atrial junction (RPV fat pad). Programmed stimulation was performed at each of four atrial sites to measure ERP and inducibility of AF during vagal stimulation. RPV fat pad RFA increased only the HRA ERP during vagal stimulation (70 +/- 8.7 vs 117 +/-14.8, P < 0.05). RPV fat pad RFA increased measures of dispersion of refractoriness, the standard deviation of ERP (24 +/- 2.1 vs 33 +/- 2.0, P < 0.01), and the standard deviation of AF cycle length (11 +/- 0.8 vs 22 +/- 1.7, P < 0.001) during vagal stimulation. RPV fat pad RFA increased the incidence of AF (15/28 vs 24/28, P < 0.05) and the vulnerability (22 +/- 4.7 vs 39 +/- 5.6, P < 0.01) to AF induction during vagal stimulation, particularly from left atrial premature beats. After RPV fat pad RFA, premature beats induced AF by causing conduction block primarily in the HRA and macroreentrant activation around the block. CONCLUSION: Partial right atrial vagal denervation facilitated rather than prevented initiation of vagally mediated AF.     

窦房结脂肪垫对犬右上肺静脉电生理特性影响的研究

目的研究不同水平刺激窦房结脂肪垫(SANFP)对右房(RA)及右上肺静脉(RSPV)的有效不应期(ERP)及心房颤动(简称房颤)诱发率的影响,探讨SANFP对房颤发生维持的作用。方法6只犬麻醉后经右侧开胸暴露RSPV及SANFP,以0.6～2,5,8mV三种不同电压强度水平、60ms频率刺激SANFP,同时以S1S2刺激观察三种水平下RA游离壁远、中、近端及RSPV远、中、近端ERP的变化;同样方法刺激SANFP以S1S1和S1S2程序刺激诱发房颤,测定房颤的诱发率。结果以5mV电压刺激窦房结脂肪垫RSPV近端ERP较基础时明显缩短(90±24msvs109±16ms,P<0.05),其房颤诱发率50%;以5,8mV电压刺激SANFP时RA游离壁近端、中端ERP变化较基础时明显缩短(96±20msvs117±14ms,65±20msvs117±14ms,P均<0.05),其房颤诱发率100%。结论窦房结脂肪垫可能在肺静脉起源的房颤的诱发和维持中起了重要作用。     

Vagal denervation and atrial fibrillation inducibility: Epicardial fat pad ablation does not have long-term effects

BACKGROUND: Major epicardial fat pads contain cardiac ganglionated plexi of the autonomic, predominantly vagal nerves. Vagal denervation may improve the success rate of atrial fibrillation (AF) treatment. OBJECTIVES: The purpose of this study was to elucidate the long-term effects of fat pad ablation on the electrophysiologic characteristics of the atrium and AF inducibility. METHODS: Six mongrel dogs were studied. Cervical vagal stimulation was applied to determine effects on the sinus node, AV node, atrial effective refractory period (AERP), and AF inducibility. AERP and AF inducibility were evaluated at both the right atrial and left atrial appendages and at the right atrial and left atrial free walls. Radiofrequency energy was delivered epicardially to the entire areas of two major fat pads: right pulmonary vein fat pad and inferior vena cava-left atrium fat pad. Cervical vagal stimulation then was applied to confirm the acute effects of fat pad ablation. The same evaluation was repeated 4 weeks later. RESULTS: The effects of vagal stimulation on the sinus node, AV node, and AERP were significantly eliminated immediately after fat pad ablation. However, these denervation effects disappeared after 4 weeks. At baseline, AF inducibility was increased by vagal stimulation (right atrial appendage: 72% +/- 31% vs 4.8% +/- 12%; right atrial free wall: 75% +/- 31% vs 0.0% +/- 0.0%; left atrial appendage: 60% +/- 29% vs 0.0% +/- 0.0%; left atrial free wall: 65% +/- 42% vs 0.0% +/- 0.0%). Fat pad ablation significantly reduced this vagal stimulation effect (8.3% +/- 20%, 10% +/- 22%, 17% +/- 29%, and 25% +/- 29%, respectively). However, similar to baseline, AF inducibility was strongly augmented by vagal stimulation 4 weeks after fat pad ablation (96% +/- 10%, 100% +/- 0.0%, 100% +/- 0.0%, and 95% +/- 11%, respectively). CONCLUSION: Radiofrequency fat pad ablation may not achieve long-term suppression of AF induction in this canine model.     

Autonomically induced conversion of pulmonary vein focal firing into atrial fibrillation

OBJECTIVES: This study was designed to determine the mechanism(s) whereby focal firing from pulmonary veins (PVs) is converted into atrial fibrillation (AF). BACKGROUND: The mechanism(s) whereby PV focal firing or even a single PV depolarization is converted into AF is unknown. METHODS: In 14 anesthetized dogs a right thoracotomy was performed to expose the right superior pulmonary vein (RSPV). An octapolar electrode catheter was sutured alongside the RSPV so that the distal electrode pair was adjacent to the fat pad containing autonomic ganglia (AG) at the veno-left atrial (LA) junction. An acrylic plaque electrode on the fat pad allowed AG stimulation at voltages ranging from 0.6 to 4.0 V. Multi-electrode catheters were sutured to the atria with their distal electrode pairs at the fat pad-atrial junctions. Right superior pulmonary vein focal firing consisted of S(1)-S(1) = 330 ms followed by as many as 11 atrial premature depolarizations (APDs) (A(2)-A(12)) whose coupling interval just exceeded RSPV refractoriness. RESULTS: Autonomic ganglia stimulation, without atrial excitation, caused a reduction in heart rate (HR): control 142 +/- 15/min, 4.0 V; 75 +/- 30/min, p /=9.3 V. CONCLUSIONS: The effects of AG stimulation at the base of the RSPV can provide a substrate for the conversion of PV firing into AF.     

房室结慢径区域消融对迷走神经功能及心房颤动易感性的影响

目的心房颤动（房颤）与房室结折返性心动过速有着某种程度的关联性,慢径区域消融可能影响了心房自主神经功能而导致窦性心动过速。但慢径区消融对心房自主神经功能的具体影响目前尚不清楚。本文旨在探讨慢径区消融对心房迷走神经调节功能及房颤易感性的影响。方法11条成年杂种犬,全身麻醉下行颈交感一迷走神经干剥离术。经右颈内静脉穿刺放置冠状静脉窦导管,经左股静脉穿刺放置右心室导管及右心房标测电极导管（Halo导管）,经右股静脉穿刺放置消融导管和希氏束导管。静脉应用美托洛尔阻断交感神经活性。测量慢径区域消融前后基础状态及迷走神经刺激下的窦性周长（SCL）及高位右心房（HRA）、低位右心房（IRA）、冠状静脉窦近端（CSp）和冠状静脉窦远端（CSd）的有效不应期（ERP）及心房易感窗口（VW）。结果（1）SCL的变化：消融前后迷走神经刺激导致的SCL缩短值无明显改变[（107±19）次／min对（108±8）次／min,P〉0．05],提示慢径区域消融没有明显改变迷走神经对窦房结的调节作用。（2）ERP的变化：消融前后迷走神经刺激导致的ERP缩短值在HRA分别为[（69±37）ms对（55±34）ms,P〉0．05],CSd分别为[（55±30）ms对（42±32）ms,P=0．08],IRA分别为[（66±24）ms对（19±21）ms,P〈0．001],CSp分别为[（46±24）ms对（7±18）ms,P〈0．001]。提示慢径区域消融对HRA及窦房结区域的迷走神经调节功能无明显影响,对CSd区域的迷走神经调节功能有一定的影响,而导致了IRA及CSp区域去迷走神经效应。（3）心房VW的变化：消融前后基础状态下各个部位刺激均较难诱发房颤（VW接近0）。消融后,HRA迷走神经刺激诱发房颤的能力较消融前没有明显变化[（63±31）ms对（63±25）ms,P〉0．05],CSd的VW有一定程度的降低[（35±37）ms对（57±28）ms,P     

Impact of pulmonary vein isolation on atrial vagal activity and atrial electrical remodeling

Objective Mechanisms of pulmonary vein isolation (PVI) for atrial fibrillation remain controversy.This study aimed to investigate the impact of PVI on vagal modulation to atria.Methods Eighteen adult mongrel dogs under general anesthesia were randomly divided into two groups.Bilateral cervical sympathovagal trunks were decentralized and sympathetic effects was blocked by metoprolol administration.Atrial electrical remodeling (AER) was established by rapid right atrial pacing at the rate of 600 bpm for 30 minutes.PVI was performed in group A.Atrial effective refractory period (ERP),vulnerability window (VW) of atrial fibrillation,and sinus rhythm cycle length (SCL) were measured at baseline and during vagal stimulation before and after atrial rapid pacing with and without PVI at fight atrial appendage (RAA),left atrial appendage (LAA),distal coronary sinus (CSd) and proximal coronary sinus (CSp).Results (1) Effects of PVI on vagal modulation:Shortening of SCL during vagal stimulation decreased significantly after PVI compared with that before PVI in group A (P＜0.001).Shortening of ERP during vagal stimulation decreaseed significantly after PVI compared with that before PVI (P＜0.05).VW of atrial fibrillation during vagal stimulation decreased significantly after PVI compared with that before PVI (P＜0.05).(2) Effects of PVI on AER:shortening of ERP before and after atrial rapid pacing increased significantly at baseline and vagal stimulation in group B compared with that in group A (P＜0.05).VW during vagal stimulation increased significantly after atrial rapid pacing in group B (P＜0.05).Conclusion PVI attenuates the vagal modulation to the atria,thereby decreases the susceptibility to atrial fibrillation mediated by vagal activity.PVI releases AER,which maybe contributes to the vagal denervation.Our study indicates that PVI not only can eradicate triggered foci but also modify substrates for AF.(J Geriatr Cardiol 2008;5:28-32)     

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 atr