普罗帕酮和Ⅲ类新药Ambasilide对犬心房颤动的作用和电生理机制比较研究

目的应用心外膜标测技术观察Ⅲ类新药Ambasilide对迷走性持续心房颤动(房颤)的影响,并与普罗帕酮比较,研究其电生理作用机制。方法建立迷走神经性持续房颤模型,13只犬给予普罗帕酮(2mg/kg),另13只犬给予Ambasilide(2mg/kg),观察两药对房颤的终止情况,同时在用药前后进行心房电活动实时心外膜标测及心房有效不应期的测量。结果普罗帕酮2mg/kg负荷量可转复房颤11/13(84.6％),Ambasilide2mg/kg负荷量可转复13/13(100％)。当S1S1为400ms时普罗帕酮可使心房有效不应期从(149±6)ms增至(181±5)ms,增加率为23％±4％,而S1S1为200ms时,心房有效不应期从(120±6)ms增至(192±4)ms,增加率达66％±8％,心房有效不应期增加为正向频率依赖性(P＜0.01)。当S1S1为400ms时Ambasilide可使心房有效不应期从(164±3)ms增至(214±7)ms,增加率为31％±4％,而S1S1为200ms时,心房有效不应期从(126±5)ms增至(156±5)ms,增加率25％±6％,心房有效不应期增加为非频率依赖性(P＞0.05)。普罗帕酮在S1S1为200ms时可减慢心房传导速度达34％±4％,而Ambasilide对心房传导速度无影响。两药均可延长折返波长。结论(1)普罗帕酮和Ambasilide通过增加心房不应期和折返波长而终止迷走性持续房颤;(2)普罗帕酮延长心房不应期呈正向频率依赖性而Ambasilide呈非频率依赖性延长;(3)普罗帕酮减慢心房传导速度而Ambasilide对心房传导速度无影响。     

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.     

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.     

房性期前收缩及年龄因素对人心房传导速度的影响

目的:探讨房性期前收缩及年龄因素对人心房传导速度的影响。方法:入选30例无器质性心脏病,因室上性心动过速行心脏电生理检查及射频消融术的患者,按年龄分为青年组、中年组和老年组。按能否诱发房颤,分为诱发房颤组与未诱发组。窦性心律时测定P波宽度,电生理检查测量心房有效不应期,以及高位右房(HRA)-冠状静脉窦远端(CS)的传导时间(iaCT)。分别测量基础刺激S1(600 ms、500 ms、400 ms和300 ms)以及相应S1起搏时不同配对间期的期前刺激(心房有效不应期+2,4,6,8,10 ms)时的左右房传导速度。结果:共有9例诱发房颤,老年组房颤诱发率显著高于青年组,诱发房颤组iaCT的延缓率高于非诱发组(均P0.05)。老年组以及诱发房颤组P波明显增宽;期前刺激时心房传导速度明显减慢,iaCT明显延长(P0.01);期前刺激时老年组的心房传导速度较青年组减慢,老年组iaCT较青年组及中年组均明显延长(P0.05)。结论:老年人P波增宽,易出现房颤。各年龄组在房性期前收缩时心房传导速度均明显减慢;老年组较青年组减慢更明显。     

大鼠心房肌电生理特性的增龄性变化

目的探讨年龄对心房肌单相动作电位(MAP)和有效不应期(ERP)的影响,及其与心房颤动(房颤)的关系。方法选取Wistar大鼠40只分为青年组、成年组、中年组和老年组4组。Langendorff体外灌流心脏。分别测量各组心房肌在400ms刺激周长下MAP复极到90%、50%及20%时的时程(MAPD90、MAPD50、MAPD20)和ERP,以及其他不同刺激周长下的MAPD。结果在400ms刺激周长下,4组大鼠右心房肌MAPD90随年龄增长而逐渐延长〔(75±5)(、123±8)(、140±11)和(140±14)ms,均为P<0.01〕;而左心房肌青年组至中年组延长分别为〔(60±4),(120±3),(139±7)〕,老年组缩短〔(102±14)ms,均为P<0.01〕。心房肌ERP的增龄性变化规律与MAPD90相同。刺激周长从400ms缩短到250ms,右心房肌MAPD90缩短程度从青年组到老年组逐渐增加;左心房肌以老年组缩短程度最小。结论左右心房肌电生理特性增龄性变化规律不同。老年期心房电生理变化可能有利于房颤的发生。     

心脏血管内迷走神经丛刺激与阵发性心房颤动的动物模型制作

探讨心脏血管内迷走神经丛刺激与阵发性心房颤动 (简称房颤 )的动物模型制作。 32条Mongrel狗活体心脏大血管 :冠状窦、左右肺动脉、左房、上下腔静脉等处插入 7F蓝状电极进行迷走神经丛刺激 ,刺激频率为 2 0Hz,刺激间期 0 .1ms,刺激电压 1～ 4 0V ,刺激时间 30～ 5 0s。为了避免神经丛刺激直接对心房的影响 ,于刺激迷走神经丛的同时在P波后发放 2 0 0Hz、2 0～ 5 0ms的PS2 心房高频刺激 ,使迷走神经刺激落入心房的不应期。在这些心脏血管迷走神经丛刺激时减慢窦性心律 ,且减慢速度呈电压依赖。在一定的刺激强度下 ,窦性心律能够达到最大减低 (从75 0± 10 2ms至 15 6 0± 2 30ms) ,心房肌不应期显著缩短 (从 175± 13ms缩至 96± 2 3ms) ,同时出现房性早搏、房性心动过速和房颤 ,且重复性很好。应用 β 阻断剂 (esmolol1mg/kg)时 ,提高了房颤诱发域值 ;迷走神经阻断剂 (atropine1～ 2mg/kg)可以完全阻断房颤的诱发。结论 :蓝状电极非常有利于快速在静脉血管腔内找到迷走神经丛刺激位点 ;心脏大血管处存在迷走神经丛 ,刺激这些神经丛能够复制出与临床灶性阵发性房颤非常类同的房颤 ,迷走神经阻断剂可阻断这类房颤的诱发。     

房室结双径路1：2房室传导的电生理特性

目的　总结房室结双径路 1∶2房室传导的电生理特性。方法　分析诱发 1∶2房室传导的条件 ;测定患者的基础AH、HV、心房有效不应期、房室结快径有效不应期、快慢径传导时间之差等电生理参数 ,与无 1∶2传导者对比分析。结果　 11例有 1∶2传导者基础AH 5 0～ 80 (6 0 9± 7 0 )ms,HV 35～ 40 (38 6± 2 3)ms;心房有效不应期 130～ 2 40 (194 5± 31 4)ms,与对照组差异无显著性 ;房室结快径有效不应期 7例短于 2 2 0ms,其他 5例分别为 40 0、380、32 0、2 80、2 40ms。快、慢径传导时间之差为 30 0～ 740 (4 99 0± 12 1 8)ms,显著大于对照组。房性早搏、心房期前刺激、心房快速刺激、窦性搏动、房室结多径路发生房室结折返性心动过速时以及心室期前刺激等 6种方式可诱发 1∶2房室传导。结论　房室结远端共同传导通路的不应期短于快、慢径传导时间之差 ,是发生 1∶2房室传导的必要条件。     

室上速并发心房颤动的电生理研究

目的探讨室上速并发心房颤动(房颤)的电生理特性及其发生机制。方法对38例室上速患者,根据有无房颤史分为两组,即房颤组18例,无房颤组20例。分别测量两组室上速周长、心房内压、心房各部位有效不应期、心房不应期离散度、心房最大不应期与室上速周长的比值,所有对象均行射频消融术治疗室上速,并行为期半年的随访,观察两组病人房颤的发生情况。结果房颤组与无房颤组的室上速周长分别为（326±9）ms,（331±11）ms,P>0.05。在窦性心律与室上速发作时,房颤组的心房不应期离散度均较无房颤组增加,房颤组的心房最大不应期与室上速周长的比值比无房颤组明显增加（P<0.05）。房颤组的心房最大不应期比无房颤组增加（P<0.05）,但却发生在心房的不同部位。结论(1)室上速合并房颤与室上速周长无明显关系。(2)心房不应期离散度是室上速合并房颤发生和维持的一个重要机制。(3)心房最大不应期与室上速周长的比值可能是室上速诱发房颤的另一个机制。     

阵发性心房颤动患者心房复极离散度的研究

目的　通过记录阵发性心房颤动 (房颤 )患者心房单相动作电位 (MAP) ,分析心房复极离散度与房颤发生的关系。方法　特发性阵发性房颤患者与无自发房颤病史的阵发性室上性心动过速患者各 1 5例 ,均接受心内电生理检查和 /或导管射频消融治疗。两根 MAP电极于右心房共取 4～ 1 0个不同部位进行同步的窦性心律基础刺激 (S1)及期前刺激 S2 时的 MAP记录。测量、计算心房复极离散度(RTd)及动作电位时限和局部冲动时间的离散度 (APDd、ATd)。　结果　窦性心律时房颤组最大 RTd显著大于对照组 (1 2 3 .69± 54.67) ms比 (64 .2 5± 2 3 .2 9) ms,(P<0 .0 1 )。其差异主要来源于 APDd(1 1 5.0 0± 4 6.90 ) ms比 (57.56± 3 3 .57) ms,(P<0 .0 1 ) ,ATd差异无显著性。随 S1、S2 的加入 ,各组局部激动时间和离散度逐渐增大 ,而动作电位时限逐渐缩短 ,且房颤组的这种改变程度显著大于对照组。在S1时无房颤发生 ,加入期前刺激时 ,大多数房颤组患者均多次诱发出短阵房颤。其诱发率及次数均显著高于对照组。　结论　研究结果表明 ,MAP记录技术是临床观察、分析心房复极离散度及其在阵发性房颤中的作用的较佳方法。心房复极离散度的增加是阵发性房颤发生的重要因素。期前刺激时动作电位时限的缩短和离散以及传导障碍在     

射频消融房室交界区慢、快经区域对犬和人心房颤动时心室率的影响

本文观察经导管射频消融房室交界区慢、快径区域对大和人心房颤动时心室率的影响.方法 杂种犬4条,体重11±1.2kg.房室结折返性心动过速患者7例,年龄29～65岁.阵发性房颤患者4例,年龄62～70岁,其中2例为短P-R间期综合征.均先采用“下位法”消融慢径区域后,若房室结有效不应期或房颤时平均R-R间期无明显变化,则加行“快径”区域消融.房颤诱发采用猝发脉冲电刺激(人)或静滴氯化乙酰胆碱后猝发脉冲电刺激(犬).结果 7例房室结折返性心动过速患者中5例经下位法射频消融阻断慢径,房室结前传有效不应期及诱发房颤时平均R-R间期明显延长(222±33ms vs 285±42ms和539±44ms vs 656±53ms P<0.01),无并发症.4条大及4例阵发性房颤患者经心内电生理检查证实均无房室结双径路表现,选择性消融“慢径区域”后,房室结有效不应期和房颤时平均R—R间期无明显变化,加行“快径区域”消融后,房室结有效不应期和房颤时平均R—R间期明显延长(犬145±16ms vs 185±22ms和305±13ms vs 403±17ms P<0.01,人220ms vs 490ms和367ms vs 690msP<0.01),1例房颤患者术后3天出现Ⅲ°AVB,2周后恢复为Ⅰ°AVB.本文还在动物实验中观察到消融快径区域时,房侧靶点(A/V>1)较室侧靶点(A/V<1)更易于造成Ⅲ°AVB.结论 选择性射频消融慢径区域对减?     

Bundle branch block on alternate beats during atrial fibrillation

This article reports a case of tachycardia-dependent right bundle branch block (RBBB) occurring during atrial fibrillation. In some sections of the recording, an alternans occurs between complexes with a complete RBBB pattern and complexes showing normal intraventricular conduction or incomplete RBBB. Alternans is frequently observed during phases of fast and nearly regular rhythm, but it occurs even in the presence of a markedly irregular ventricular response. The RBBB alternans associated with short and regular RR intervals is likely to represent a manifestation of 2:1 bundle branch supernormal conduction, whereas alternans occurring with irregular cycles expresses a complex interaction between the RR cycle length and some mechanisms affecting intraventricular conduction, such as tachycardia-dependent bundle branch block, supernormal conduction and concealed retrograde activation of the anterogradely blocked bundle branch (the so-called "linking" phenomenon).     

Effects of acute atrial dilation on heterogeneity in conduction in the isolated rabbit heart

INTRODUCTION: Atrial dilation plays an important role in the development and persistence of atrial fibrillation (AF). The mechanisms by which atrial dilation increases the vulnerability to AF are not fully understood. METHODS AND RESULTS: In 11 isolated rabbit hearts, the right atrium was acutely dilated by increasing the intra-atrial pressure from 2 to 9 and 14 cm H2O. A rectangular mapping array of 240 electrodes (spatial resolution 0.5 mm) was positioned on the free wall of the right atrium. The atrium was paced from four different sites at intervals of 240 and 125 msec. At normal atrial pressure (2 cm H2O), conduction was uniform in all directions with an anisotropy ratio between 1.5 and 1.7. Increasing the pressure to 9 cm H2O decreased the normalized conduction velocity during rapid pacing by 18%. The incidence of areas of slow conduction and conduction block increased from 6.6% and 1.6% to 10.2% and 3.3%. At 14 cm H2O, conduction velocity decreased by 31% and the percentage of slow conduction and block further increased to 11.5% and 6.6% (P < 0.001). The appearance of lines of intra-atrial block was largely dependent on the pacing site. Whereas during pacing at the cranial part of the crista terminalis no increase in conduction delays occurred, pacing from the low right atrium unmasked several lines of block oriented parallel to the major trabeculae and the crista terminalis. In an additional series of six hearts the left atrium also was mapped. The effect of dilation of the left atrium was comparable to that of the right atrium. Increasing the atrial pressure to 14 cm H2O increased the amount of intra-atrial conduction block threefold to fourfold. CONCLUSION: Acute atrial dilation results in slowing of conduction and an increase of the amount of intra-atrial conduction block. The increase in spatial heterogeneity in conduction was related to the anisotropic properties of the atrial wall.     

三腔起搏器治疗快速性房性心律失常的临床应用(附二例报告)

目的观察三腔双心房起搏治疗快速性房性心律失常的临床效果。探讨三腔起搏的原理,适应症以及起搏模式的选择。方法患者2例均为男性,平均年龄50岁,诊断房间传导阻滞合并快速性房性心律失常,并植入三腔双心房同步起搏器。左心房起搏通过冠状静脉窦植入2188电极导线,左右心房电极导线通过Y形转接器与双腔起搏器连接。结果双房同步起搏后,患者快速房性心律失常的发作明显减少。结论初步临床应用提示,三腔双心房同步起搏治疗快速性房性心律失常可行且有效。     

双房同步起搏预防和治疗房性快速性心律失常

目的 观察双房同步起搏技术对伴有房间传导阻滞的阵发性快速性房性心律失常的疗效。方法 病态窦房结综合征合并房间传导阻滞的阵发性快速性房性心律失常患者7例，男4例、女3例，年龄58～78岁。其中4例行双房起搏(AAT)，3例行双房右室三腔起搏(DDD)，经穿刺左锁骨下静脉插入右房、右室和冠状静脉窦起搏电极导线，分别用于起搏右房、右室和左房。结果 起搏器及电极导线均顺利植入，未发生任何并发症。冠状静脉窦电极顶端距冠状静脉窦口2．5—3．5cm，P波振幅为1．6—5．5mV、阻抗624—808Ω,、单极起搏阈值0．5—0．7V。随访2—31个月，7例均健在，房性心律失常的临床发作得到明显控制。结论：双房同步起搏技术是房间传导阻滞合并快速房性心律失常的有效预防和治疗方法。     

Anterograde sinuatrial conduction evaluated by sinus node electrogram in atropine blocked retrograde atrial conduction

Two cases are described where atropine induced the disappearance of reset zone as response to premature atrial stimulation for blocked retrograde atrial conduction. Because of this, sinuatrial conduction time could not be estimated. The sinus node electrogram allowed the direct measurement of sinuatrial conduction and showed a facilitated anterograde conduction through the perinodal fibers after administration of the drug.     

房间隔起搏的初步临床应用经验

目的 探讨有适应证的阵发性心房颤动(房颤)患者永久性房间隔起搏的可行性和安全性。方法 先行心内电生理标测，寻找使双心房同步激动的房间隔最佳起搏点，采用主动固定方法将导线固定于该部位。结果 18例伴有房间传导阻滞的阵发性房颤患者，14例患者完成房间隔标测和永久性起搏导线植入手术，4例未能成功植入房间隔起搏导线。结论 在伴有房间传导阻滞的阵发性房颤患者中永久性房间隔起搏是安全可行的。     

Synergistic action of atrial dilation and sodium channel blockade on conduction in rabbit atria

INTRODUCTION: The aim of this study was to investigate the interaction of atrial dilation and blockade of the rapid sodium channel on atrial conduction and degree of anisotropy. METHODS AND RESULTS: The right atrium was acutely dilated by increasing intra-atrial pressure from 2 to 9 cm H2O in 14 isolated rabbit hearts. A rectangular mapping array of 240 electrodes (spatial resolution 0.5 mm) was positioned on the free wall of the right atrium during pacing from four different directions at intervals of 240 and 140 msec. In nondilated atria, 0.5 and 1.0 mg/L of the use-dependent INa blocker flecainide prolonged the total conduction time under the mapping electrode by 15% to 75%. In dilated atria, flecainide depressed conduction by 24% to 89% (P < 0.05). The incidence of intra-atrial conduction block increased from 0.6%-0.8% to 3.3%-7.2% in nondilated atria and from 3.9%-4.6% to 13%-21% in dilated atria (P < 0.05). The direction of activation relative to the crista terminalis and major pectinate muscles was of major importance for occurrence of conduction block. During rapid pacing, the degree of anisotropy in conduction increased by the combination of atrial dilation and flecainide (1.0 mg/L) from 1.7 +/- 0.1 to 2.2 +/- 0.4 (P < 0.05). The effects of dilation and flecainide on conduction were clearly synergistic. The effect of flecainide on the atrial refractory period also was enhanced by atrial dilation. CONCLUSION: In dilated atria, blockade of the rapid sodium channels caused a higher degree of local conduction delay and intra-atrial conduction block than in nondilated atria.     

Association of right bundle branch block or intraventricular conduction delay with recurrence of atrial fibrillation after catheter ablation

Background

The association between bundle branch block (BBB) and recurrence of atrial fibrillation (AF) after catheter ablation is unclear. The aim of this study was to determine whether AF combined with BBB is associated with AF recurrence after catheter ablation.

Methods

A total of 477 consecutive AF patients who underwent catheter ablation were included. The AF patients were divided into three groups according to BBB: AF without BBB (n = 427), AF with right bundle branch block (AF with RBBB) (n = 16), and AF with intraventricular conduction delay (AF with IVCD) (n = 34).

Results

Of the 477 AF patients (mean age 57 years, 81% men, median CHA₂DS₂-VASc score of 1), 16 (3.4%) patients had RBBB, and 34 (7.1%) patients had IVCD. During a mean follow-up of 15.2 ± 6.7 months, 119 patients (24.9%) had recurrence of AF. Of these, 111 (26%) patients were in the AF without BBB group, with 2 (12.5%) and 6 (17.6%) patients in the RBBB and IVCD groups, respectively. The Kaplan–Meier estimate of the rate of recurrent AF was not significantly different among the three groups (p = .39). Multivariable analysis showed that persistent AF (HR 1.7, 95% CI 1.15–2.50, p = .007), chronic kidney disease (HR 2.94, 95% CI 1.20–7.17, p = .01), and left atrial diameter (HR 1.04, 95% CI 1.009–1.082, p = .01) were significantly associated with AF recurrence.

Conclusion

AF with BBB was not significantly associated with the recurrence of AF after catheter ablation in middle-aged patients with low-risk cardiovascular profile.