最紊乱的心房颤动波在心房内分布特点及肺静脉隔离对其影响

目的针对心房颤动(房颤)基质消融是房颤消融的最终目标,最紊乱的房颤波(Ⅲ型房颤)所在部位可能为房颤维持的关键所在。本文分析Ⅲ型房颤波在双侧心房的分布特点及肺静脉隔离对其影响。方法11例持续性房颤患者,用普通的电生理检查导管或64极Basket导管分别在上腔静脉、右心房游离壁、右心房后壁、右心耳、右心房间隔部、左心房后壁、左心耳、肺静脉及冠状静脉窦记录2分钟房颤心内电图。根据Wells对房颤电活动的分类,人工计算Ⅲ型房颤占所记录的2分钟心电图的百分比(房颤紊乱指数,DI)。比较肺静脉隔离前及房颤自动终止或电复律前冠状窦口及冠状窦中、远端房颤紊乱指数的变化。肺静脉隔离在房颤中进行。在窦性心律下证实仍然存在心房—肺静脉间电活动传导,在窦性心律或心房刺激下完成肺静脉隔离。结果在所有720次采样中,房颤紊乱指数成双峰分布,第二峰起始点为75%。在左心房后壁(包括肺静脉)采样326次,房颤紊乱指数大于75%占22.4%,在间隔部(包括冠状静脉窦开口部)采样118次,房颤紊乱指数大于75%占37.3%,在心房其它部位(包括右心房游离壁、右心房后壁、上腔静脉、左心耳及冠状静脉窦左房部)采样276次,房颤紊乱指数大于75%占6.2%。左心房后壁及间隔部与心房其它部位比较有统计学差异(P<0.001)。肺静脉隔离导致了冠状静脉窦远端的房颤电活动变化(房颤紊乱指数消融前14.34±25.01,消融后4.62±8.64,P=0.016),而对冠状静脉窦口无明显影响(房颤紊乱指数消融前37.49±38.09,消融后46.83±41.96,P=0.243)。平均随访7个月,6例患者维持窦性心律,5例患者转为阵发性或持续性房颤。结论Ⅲ型房颤多集中在左心房后部,包括肺静脉。肺静脉隔离可降低Ⅲ型房颤在左心房的百分比,而对右心房影响较小。提示Ⅲ型房颤的集中部位可能为房颤维持的关键部位,肺静脉隔离可能改变了房颤维持的物质基础。     

肺静脉隔离对迷走神经对心房电生理特性调节及对心房颤动易感性的影响

目的越来越多的证据表明肺静脉隔离(PVI)不仅去除了心房颤动(房颤)的触发病灶,也可能改变了房颤赖以维持的物质基础,但PVI如何改变了房颤的维持机制的研究较少.研究目的在于PVI对迷走神经对心房电生理特性调节及对房颤易感性的影响.方法11只成年杂种犬,全麻及机械通气下行颈部交感-迷走神经干剥离术,经右颈内静脉穿刺术放置右心室及冠状窦导管,经左股静脉放置右心房导管,经房间膈穿刺途径放置消融及标测导管于左心房.静脉应用普萘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右心耳(RAA)、左心房游离壁(LAFW)、冠状窦近段(CSP)及冠状窦远端(CSD)的不应期(ERP)及心房易感窗口(VW).不应期缩短值为基础状态下的ERP与迷走神经刺激时的ERP的差值,VW定义为引起房性早搏或房颤的最长与最短S1S2间期的差值.结果(1)有效不应期的变化消融术前,迷走神经刺激能明显缩短心脏各部位的ERP.消融术后,左心房内迷走神经刺激所致的ERP缩短值明显降低[LAFW(43.64±21.57)ms与(11.82±9.82)ms,78,P＜0.001;CSP(50.91±26.25)ms与(11.82±14.01)ms,P＜0.001;CSD(50±31.94)ms与(17.27±20.54)ms,P＜0.005]右心房内变化不明显[(58.18±28.22)ms与(50.91±22.12)ms,P=0.245].(2)VW的变化消融术后,基础状态下测得的VW无明显变化[RAA(32.5±37.32)ms与(21.25±27.48)ms LAFW(31.25±28.5)ms与(35±35.46)msCSP(20±23.3)ms与(22.5±26.05)ms;CSD(30±32.95)ms与(27.5±31.51)ms.P=0.21-0.74],而迷走神经刺激时左房内测得的VW明显降低[LAFW(36.25±11.88)ms与(11.25±16.42)msP＜0.001;CSP(52.5±19.82)ms与(13.75±19.96)msP＜0.005;CSD(43.75±19.23)mS与(17.5±19.82)ms,P＜0.05],右心房内无明显变化[(52.5±22.52)ms与(42.5±10.35)ms,P=0.316].结论PVI能导致左心房(包括冠心窦)去迷走神经反应,引起迷走神经刺激时的心房不应期延长及心房易感窗口缩短.提示PVI所致的左心房去迷走神经反应可能为PVI改变房颤赖以维持的物质基础的机制之一.     

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。     

经心外膜聚焦超声环肺静脉消融与左房盒式消融治疗犬心房颤动的比较研究

目的探讨聚焦超声经心外膜的环肺静脉消融(CPVa)和左房盒式消融(BOXa)两种不同术式对心房颤动(简称房颤)的影响。方法成年杂种犬20只,随机分为两组,建立肺静脉起源的阵发性房颤模型后,直视下分别行CPVa和BOXa。测定消融前、后左房有效不应期(LAERP)、计算房颤诱发率、房颤持续时间,术毕行组织学检查。结果所有犬均能诱发出肺静脉起源的阵发性房颤,房颤终止后的LAERP较基线水平显著缩短(CPVa组:140±10msvs102±10ms;BOXa组:139±11msvs105±8ms;P均<0.01),但消融前后的LAERP并无显著性差异。消融后两组的房颤诱发率均较消融前显著降低(CPVa组:98%vs28%;BOXa组:97%vs14%;P均<0.01),房颤持续时间均显著缩短(CPVa组:233±40svs70±29s;BOXa组:240±41svs34±22s;P均<0.01);部分犬可见肺静脉-心房双向电传导阻滞;消融后BOXa组房颤诱发率和房颤持续时间低于/短于CPVa组(P<0.05)。消融后焦域内的组织呈凝固性坏死。结论经心外膜聚焦超声CPVa可显著降低房颤诱发率和缩短房颤持续时间,而BOXa则可进一步提高成功率。     

经导管射频消融治疗局灶性心房颤动

报道19例局灶性心房颤动（简称房颤）射频消融治疗的结果,其中药物治疗无效且发作频繁（＞1次／日）的阵发性房颤17例、慢性房颤2例。17例患者尚同时合并有频发房性早搏（简称房早）（动态心电图显示＞700个／日）。同步记录高位有房、冠状静脉窦及左、右上肺静脉电图。根据房早或房颤开始发作时的心房激动顺序确定异位兴奋灶部位,以局部双极电图较体表心电图P'波起点最提前处为消融靶点。成功标准为消融后6Omin内房早／房颤消失及随访期内可以无须药物而维持窦性心律。结果：92．6％（25／27）的异位兴奋灶位于肺静脉,其中尤以双上肺静脉居多（21／25）。随访2．4±3．7个月后有13例患者（68．4％）达上述成功标准,其房早数目由术前的3720±2741个／日降至216±139个／日,除1例发生心房穿孔外无其他严重并发症。结论：射频消融治疗局灶性房颤效果较好,可以作为药物治疗无效的阵发性房颤患者的治疗选择。     

典型心房扑动射频消融术后发生心房颤动患者的心房电生理特性

分析典型心房扑动(简称房扑)射频消融术后发生心房颤动(简称房颤)患者的心房电生理特性,探讨心房内传导时间在房颤发生中的意义。56例典型房扑患者,其中19例有器质性心脏病,16例在消融前有房颤发作。所有患者均进行常规的电生理检查及标测,记录消融前后心房的电生理参数。根据消融术后随访是否有房颤的发生分为两组进行分析。结果:56例房扑患者全部消融成功,随访14±12(6～60)个月,中位数14个月。消融术后15例有房颤发作,其中3例进展为慢性房颤。15例有房颤发作患者的年龄较无房颤发作的患者大(57.1±13.6岁vs42.3±11.2岁,P<0.05),消融术前和术后的高右房至冠状窦的传导时间延长(分别为98.4±17.1msvs67.8±16.5ms;93.1±18.4msvs70.2±19.7ms;P均<0.05)。多因素Cox回归分析消融前有房颤发作的病史(危险比2.3,95%CI1.425～4.632,P=0.02)和窦性心律下高右房至冠状窦的传导时间超过90ms(危险比1.7,95%CI1.215～3.758,P=0.03)是预测射频消融术后发生房颤的独立的危险因素。结论:典型房扑射频消融术后发生房颤患者心房内传导延迟,并且房内传导延迟是预测射频消融术后发生房颤的重要电生理指标。     

环肺静脉口部线性消融治疗心房颤动的初期体会

目的报告环肺静脉口部线性消融治疗心房颤动(房颤)的初期体会和结果。方法56例药物治疗无效的房颤患者(阵发性房颤50例,持续性房颤6例)入选,平均年龄(50.6±9.6)岁。利用三维电解剖标测系统,围绕左和右侧肺静脉口部线性消融左心房,另外二条消融线分别连接左、右环状消融线以及左环状消融线至二尖瓣环。术后服用抗心律失常药3个月。结果55例患者接受消融治疗,其中53例完成预定的线性消融,操作时间和X线曝光时间分别为(193±56)min和(35±11)min。术中14例患者为房颤心律,其中8例(57.1%)消融过程中恢复窦性心律;20例出现迷走神经反射现象。随访时间>3个月(7.3±3.4)个月的41例,其中无房颤发作者25例(包括2例仍服用胺碘酮,61.0%),房颤发作次数和持续时间明显减少者11例(26.8%),无效者5例。无1例发生肺静脉狭窄。结论纯解剖方式的环肺静脉口部线性消融治疗房颤是安全可行的。其主要治疗机制是改变房颤的心房基质和去迷走神经作用。     

电生理标测指导下肺静脉电隔离术治疗慢性心房颤动

目的探讨电生理标测指导下的肺静脉电隔离术治疗慢性心房颤动(房颤)的可行性.方法 20例慢性房颤患者,男14例,女6例,年龄56～72岁(平均68±7岁);房颤病史1～9年(平均3±7年),经过至少一次的体外同步心脏电复律,房颤均在30 min内复发.电生理标测指导下的肺静脉隔离方法为(1)最早激动点指导下消融.肺静脉内的Basket导管记录的心房电活动显示节律较规整,激动顺序一致.(2)房颤长间歇(连续记录的最长心房电活动间期>300 ms)指导下消融.肺静脉内电位节律紊乱,激动顺序不一致,房颤长间歇后的第一次心脏搏动的最早激动部位为消融靶点.(3)3型房颤波指导下的消融.房颤频率快,肺静脉内Basket导管记录的电活动激动顺序紊乱,部分电极记录的心内电图等电位线消失而不能确定孤立的心房电活动(3型房颤),此部位作为消融靶点.在房颤过程中完成4支肺静脉电隔离后,房颤不能自发终止者应用体外同步电复律.重新将Basket 导管放入肺静脉,仍记录到肺静脉电位者将在窦性心律下完成电隔离.结果 (1)临床结果所有患者在肺静脉隔离后成功转复为窦性心律,其中1例患者自行转复为窦性心律,2例患者转为心房扑动,经右心房峡部消融后转为窦性心律,余患者经体外同步电复律转为窦性心律.随访3～19个月(平均8±9个月),维持窦性心律者9例(45%),11例(55%)患者复发,无有症状性的肺静脉狭窄.(2)消融结果20例患者的76 支肺静脉电隔离被完成.68支(89.5%)肺静脉电隔离在房颤中完成,其中的23支肺静脉在窦性心律时记录到肺静脉电位,继续在窦性心律下消融,均完成电隔离;8支(10.5%)在房颤时未能完成电隔离的肺静脉,在窦性心律下成功隔离.手术时间4.2～7.6 h(平均5.3±3.7 h),平均X线曝光时间2.7 h,无栓塞、心包填塞及肺静脉狭窄等严重并发症.结论 (1)电生理指导下的肺静脉隔离治疗慢性房颤仍能达到较高的临床成功率.(2)电生理指导下的肺静脉隔离是安全可行的.(3)房颤过程中隔离的肺静脉仍需要在窦性心律下被重新证实.(4)在房颤过程中较难隔离的肺静脉可在转复窦性心律后进行隔离.     

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。     

心房颤动消融术后二尖瓣峡部房性心动过速的发生机制及消融治疗

目的探讨心房颤动(简称房颤)患者环肺静脉左房线性消融术后二尖瓣峡部房性心动过速(简称房速)的发生机制及其消融策略。方法122例房颤患者采用EnSite-NavX和环状电极行环肺静脉左房线性消融,术后32例复发房颤或房速,8例经EnSite-NavX激动标测及拖带标测证实存在二尖瓣峡部房速,在三维导航下于左下肺静脉口部下缘至二尖瓣环之间行线性消融,对不能成功阻断二尖瓣峡部传导者予以冠状静脉窦内消融。术中同时探查双侧肺静脉电位,如传导恢复予以再次隔离。结果8例中2例呈无休止性发作,6例为阵发性,可被程序刺激诱发。房速的周长217.5±20.6ms,其中顺钟向折返5例,逆钟向折返3例。二尖瓣峡部线性消融至完全性双向传导阻滞5例,3例心内膜途径失败者经冠状静脉窦内消融,其中1例获得成功。术后随访5.5±4.3个月,6例无房颤及房速发作,1例仍有阵发性房速发作。另1例术后房速呈无休止发作,予以胺碘酮及美托洛尔控制心室率治疗。结论环肺静脉线性消融术后发生的二尖瓣峡部房速与左房线性消融治疗房颤的致心律失常作用有关,其主要的机制是消融线相关的大折返性心动过速,阻断峡部传导可以治疗此类房速。     

Shortening of fibrillatory cycle length in the pulmonary vein during vagal excitation.

OBJECTIVES: The goal of the present prospective study is to evaluate the impact of vagal excitation on ongoing atrial fibrillation (AF) during pulmonary vein (PV) isolation. BACKGROUND: The role of vagal tone in maintenance of AF is controversial in humans. METHODS: Twenty-five patients (18 with paroxysmal AF, 7 with chronic AF) were selected by occurrence of vagal excitation during AF (atrioventricular [AV] block: R-R interval >3 s) produced by PV isolation. Fibrillatory cycle length (CL) in the targeted PV and coronary sinus (CS) were determined before, during, and after vagal excitation. The CL was available at PV ostium during vagal excitation in 11 patients. RESULTS: Forty-eight episodes of vagal excitation were observed. During vagal excitation, CL abruptly decreased both in CS and PV (CS, 164 +/- 20 ms to 155 +/- 23 ms, p < 0.0001; PV, 160 +/- 22 ms to 143 +/- 28 ms, p < 0.0001), and both returned to the baseline value with resumption of AV conduction. The decrease in PVCL occurred earlier (2.5 +/- 1.5 s vs. 4.0 +/- 2.6 s, p < 0.01) and was of greater magnitude than that in CSCL (16 +/- 16 ms vs. 8 +/- 9 ms, p < 0.01). A sequential gradient of CL was observed from PV to PV ostium and CS during vagal excitation (138 +/- 29 ms, 149 +/- 24 ms, and 159 +/- 26 ms, respectively). The decrease in CL was significantly greater in paroxysmal than in chronic AF (CS, 11 +/- 9 ms vs. 5 +/- 7 ms, p < 0.05; PV, 23 +/- 25 ms vs. 8 +/- 14 ms, p < 0.05). CONCLUSIONS: Vagal excitation is associated with shortening of fibrillatory CL. This occurs earlier in PV with a sequential gradient to PV ostium and CS, suggesting that vagal excitation enhances a driving role of PV.     

Impact of catheter ablation of the coronary sinus on paroxysmal or persistent atrial fibrillation

Objectives: This study evaluated the impact of catheter ablation of the coronary sinus (CS) region during paroxysmal and persistent atrial fibrillation (AF).
Background: The CS musculature and connections have been implicated in the genesis of atrial arrhythmias.
Methods: Forty-five patients undergoing catheter ablation of AF were studied. The CS was targeted if AF persisted after ablation of pulmonary veins and selected left atrial tissue. CS ablation was commenced endocardially by dragging along the inferior paramitral left atrium. Ablation was continued from within the vessel (epicardial) if CS electrograms had cycle lengths shorter than that of the left atrial appendage.
RF energy was limited to 35 W endocardially and 25 W epicardially. The impact of ablation was evaluated on CS electrogram cycle length (CSCL) and activation sequence, atrial fibrillatory cycle length measured in the left atrial appendage (AFCL) and on perpetuation of AF.
Results: Endocardial ablation significantly prolonged CSCL by 17 ± 5 msec and organized the CS activation sequence (from 13% of patients before to 51% after ablation); subsequent epicardial ablation further increased local CSCL by 32 ± 27 msec (P < 0.001). AFCL prolonged significantly both during endocardial and epicardial ablation (median: 152 to 167 msec P = 0.03) and was associated with AF termination in 16 (35%) patients (46% of paroxysmal and 30% of persistent AF). AFCL prolongation ≥5 msec and/or AF termination was associated with more rapid activity in the CS region originally: P ≤ 0.04.
Conclusion: Catheter ablation targeting both the endocardial and epicardial aspects of the CS region significantly prolongs fibrillatory cycle length and terminates AF persisting after PV isolation in 35% of patients.     

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     

Spontaneous pulmonary vein firing in man: relationship to tachycardia-pause early afterdepolarizations and triggered arrhythmia in canine pulmonary veins in vitro

Introduction: Rapid firing originating within pulmonary veins (PVs) initiates atrial fibrillation (AF). The following studies were performed to evaluate spontaneous PV firing in patients with AF to distinguish focal versus reentrant mechanisms. Methods: Intracardiac recordings were obtained in 18 patients demonstrating paroxysmal AF. Microelectrode (ME) recordings were obtained from superfused canine PV sleeves (N = 48). Results: Spontaneous PV firing (566 ± 16 bpm; 127 ± 6 ms cycle length) giving rise to AF (52 episodes) was observed. Tachycardia‐pause initiation was present in 132 of 200 episodes of rapid PV firing and 34 of 52 AF episodes. The pause cycle length preceding PV firing was 1,039 ± 86 ms following tachycardia (420 ± 40 ms cycle length). The remaining episodes were initiated following a 702 ± 32 ms pause during sinus rhythm (588 ± 63 ms). Spontaneous firing recorded with a multipolar mapping catheter did not detect electrical activity bridging the diastolic interval between the initial ectopic and preceding post‐pause sinus beat. Tachycardia‐pause initiated PV firing (138 ± 7 ms coupling interval) in patients correlated with tachycardia‐pause enhanced isometric force, early afterdepolarization (EAD) amplitude, and triggered firing within canine PVs. Rapid firing (1,172 ± 134 bpm; 51 ± 8 ms cycle length) following an abbreviated coupling interval (69 ± 12 ms) was initiated in 13 of 18 canine PVs following tachycardia‐pause pacing during norepinephrine + acetylcholine superfusion. Stimulation selectively activating local autonomic nerve terminals facilitated tachycardia‐pause triggered firing in canine PVs (5 of 15 vs 0 of 15; P < 0.05). Conclusions: The studies demonstrate (1) tachycardia‐pause initiation of rapid, short‐coupled PV firing in AF patients and (2) tachycardia‐pause facilitation of isometric force, EAD formation, and autonomic‐dependent triggered firing within canine PVs, suggestive of a common arrhythmia mechanism.     

Stimulation of the intrinsic cardiac autonomic nervous system results in a gradient of fibrillatory cycle length shortening across the atria during atrial fibrillation in humans

Autonomic Stimulation Promotes AFCL Gradients in AF. Introduction: The intrinsic cardiac autonomic nervous system (ANS) is implicated in atrial fibrillation (AF) but little is known about its role in maintenance of the electrophysiological substrate during AF in humans. We hypothesized that ANS activation by high‐frequency stimulation (HFS) of ganglionated plexi (GP) increases dispersion of atrial AF cycle lengths (AFCLs) via a parasympathetic effect. Methods and Results: During AF in 25 patients, HFS was delivered to presumed GP sites to provoke a bradycardic vagal response and AFCL was continuously monitored from catheters placed in the pulmonary vein (PV), coronary sinus (CS), and high right atrium (HRA). A total of 163 vagal responses were identified from 271 HFS episodes. With a vagal response, the greatest reduction in AFCL was seen in the PV adjacent to the site of HFS (16% reduction, 166 ± 28 to 139 ± 26 ms, P < 0.0001) followed by the PV‐atrial junction (9% reduction, 173 ± 21 to 158 ± 20 ms, P < 0.0001), followed by the rest of the atrium (3–7% reduction recorded in HRA and CS). Without a vagal response, AFCL changes were not observed. In 10 patients, atropine was administered in between HFS episodes. Before atropine administration, HFS led to a vagal response and a reduction in PV AFCL (164 ± 28 to 147 ± 26 ms, P < 0.0001). Following atropine, HFS at the same GP sites no longer provoked a vagal response, and the PV AFCL remained unchanged (164 ± 30 to 166 ± 33 ms, P = 0.34). Conclusions: Activation of the parasympathetic component of the cardiac ANS may cause heterogenous changes in atrial AFCL that might promote PV drivers. (J Cardiovasc Electrophysiol, Vol. pp. 1‐8)     

Complete isolation of the pulmonary veins and posterior left atrium in chronic atrial fibrillation. Long-term clinical outcome

Aims: To evaluate the contribution of the posterior left atrium (LA)to chronic atrial fibrillation (AF). Methods and results: Twenty-seven patients with chronic-AF were studied. After pulmonaryvein (PV) isolation, the posterior-LA was isolated by ablationjoining the right- and left-PVs using an irrigated-tip catheter.Isolation was demonstrated by absent/dissociated posterior-LAactivity and the inability to pace the region. Ablation impactwas determined by the effect on cycle length (CL) and AF termination.Posterior-LA isolation was achieved using 35 ± 12 minof radiofrequency with total fluoroscopic and procedural durationsof 64 ± 16 and 199 ± 46 min, resulting in abolitionof electrograms (n = 21) or autonomous activity (n = 6; CL 820± 343 ms). AFCL increased from 156 ± 28 ms to162 ± 27 ms with PV-isolation and to 175 ± 32ms by posterior-LA exclusion (P < 0.0001). AF persisted inall after PV-isolation and terminated in 5 (19%) during posterior-LA-isolation.After 10 ± 6 months, 12 patients developed atrial tachycardia(four) or AF (eight); four underwent repeat posterior-LA-isolation,while the others required additional ablation/antiarrhythmics.After 21 ± 5 months, 17 (63%) were in sinus rhythm followingposterior-LA-isolation. Conclusion: This study demonstrates the feasibility of complete posterior-LAexclusion by catheter ablation. This strategy results in maintenanceof sinus rhythm in 63% at 2 years follow-up.     

典型心房扑动的经导管射频消融治疗

回顾分析 35例典型心房扑动 (简称房扑 )患者电生理检查和射频消融治疗的临床结果。心内激动标测显示沿三尖瓣环 (TA)逆钟向折返性房扑 2 7例 ,顺钟向折返 2例 ,同时存在二种折返 6例。 8例行TA峡部拖带起搏者均呈隐匿性拖带 ,起搏后间期与房扑周长差值为 1± 4(- 3～ 5 )ms。采用TA峡部双线性消融、后峡部或 /和间隔峡部消融的方法治疗所有患者均成功。 15例以房扑不能再诱发为手术终点 ,随访 10例 ,3例复发 ,复发率 30 % ;2 0例达到TA峡部双向阻滞 ,随访 19例 ,1例复发 ,复发率 5 % ,两组比较P <0 .0 5。随访的 2 9例中 ,7例发生心房颤动 (简称房颤 ) ,发生率 2 4%。与无房颤发作者相比 ,合并器质性心脏病、心房扩大和有房颤病史者的比例明显增加 (6 / 7比 9/ 2 2 ,6 / 7比 4/ 2 2和 7/ 7比 2 / 2 2 ,均P <0 .0 5 )。结果表明 ,心内激动标测结合拖带起搏技术可确定典型房扑的诊断 ,后峡部或间隔峡部消融是治疗房扑的有效方法 ,以TA峡部双向阻滞为手术终点较房扑不能被再诱发为终点可明显降低复发率。房扑消融术后发生房颤与合并器质性心脏病、心房扩大和术前存在房颤有关     

右侧神经丛消融对阵发心房颤动伴窦性心动过缓心率的影响

目的:探讨环肺静脉消融的基础上,进一步进行右侧神经丛消融以观察消融对心率的影响。方法:12例心动过缓伴心房颤动的患者,其中男性9例,女性3例,平均年龄(60.58±9.25)岁,在完成环肺静脉隔离的基础上,进行解剖指导下右侧神经丛的消融。结果:12例均完成四个肺静脉隔离及上腔静脉去神经消融,消融上腔静脉过程中,心率由(72.92±5.30)次/min增加到(84.58±5.63)次/min,术后平均随访(18±8)个月,心房颤动成功率50%。心率由术前(56.67±4.87)次/min,增加到术后1w(68.92±6.20)次/min,术后6个月(65.75±4.09)次/min。心率变异性(SDNN)由术前(132.83±16.7)ms减少为术后1w(87.67±19.21)ms,术后6个月(109.75±18.65)ms。结论:在环肺静脉消融的基础上,进行解剖指导下的上腔静脉消融可以进一步提高心率,达到去迷走神经支配的目的。     

Reversal of pulmonary vein remodeling after catheter ablation of atrial fibrillation

Background Pulmonary veins (PV) and the atria undergo electrical and structural remodeling in atrial fibrillation (AF). This study aimed to determine PV and left atrial (LA) reverse remodeling after catheter ablation for AF assessed by chest computed tomography (CT). Methods PV electrophysiologic studies and catheter ablation were performed in 63 patients (68% male; mean ± SD age: 56 ± 10 years) with symptomatic AF (49% paroxysmal, 51% persistent). Chest CT was performed before and 3 months after catheter ablation. Results At baseline, patients with persistent AF had a greater LA volume (91 ± 29 cm³ vs. 66 ± 27 cm3; P = 0.003) and mean PV ostial area (241 ± 43 mm² vs. 212 ± 47 mm²; P = 0.03) than patients with paroxysmal AF. There was no significant correlation between the effective refractory period and the area of the left superior PV ostium. At 3 months of follow-up after ablation, 48 patients (76%) were AF free on or off antiar?rhythmic drugs. There was a significant reduction in LA volume (77 ± 31 cm³ to 70 ± 28 cm³; P < 0.001) and mean PV ostial area (224 ± 48 mm² to 182 ± 43 mm²; P < 0.001). Patients with persistent AF had more reduction in LA volume (11.8 ± 12.8 cm³ vs. 4.0 ± 11.2 cm³; P = 0.04) and PV ostial area (62 mm² vs. 34 mm²; P = 0.04) than those who have paroxysmal AF. The reduction of the averaged PV ostial area was significantly correlated with the reduction of LA volume (r = 0.38, P = 0.03). Conclusions Catheter ablation of AF improves structural remodeling of PV ostia and left atrium. This finding is more apparent in patients with persistent AF treated by catheter ablation.