心房肌的复极与阵发性心房颤动发生机制的实验研究

目的　对在体犬左、右心房肌的复极时间进行研究 ,探讨阵发性心房颤动 (房颤 )发生与维持的潜在机制。方法　记录基础心律、非程序刺激及早搏刺激 (SR、S1 、S2 )时 1 4只犬左、右心房的单相动作电位 (MAP)和有效不应期 (ERP) ,测量每个动作电位的幅度和动作电位时程 [复极达90 %、80 %、5 0 %时的动作电位时程 (ms,APD90 、APD80 、APD50 ) ]。并在记录过程中同时观察房颤的诱发情况。结果　记录满意MAP信号 1 2例 ,共标测 2 6点 (右房 1 7点 ,左房 9点 ) ,MAP振幅平均(6 98± 1 76 )mV ,左心房APD90 和APD50 小于右心房 [(1 5 7 4± 4 3 5 0 )ms比 (1 70 9± 37 9)ms ,P <0 0 5 ;(88 4± 1 9 1 )ms比 (1 0 0 1± 2 1 2 )ms,P <0 0 5 )。其中左房刺激发作 38阵 ,明显多于右房 2 3阵 (P <0 0 5 )。由左房诱发房颤的早搏的偶联间期明显比在右房诱发的短 (P <0 0 5 )。起源于左房的房颤的早搏参数小于起源于右房的 (P <0 0 5 )。结论　左、右心房间具有MAP的异质性的复极特性 ,是诱发折返、发生和维持房颤的基质。     

心房肌复极的电整复性与阵发性心房颤动发生机制的实验研究

目的 研究在体犬左、右心房肌的电整复性即动作电位时程整复性(APDR),观察其与阵发性心房颤动(房颤)发生的潜在机制.方法 使用单相动作电位技术记录14只犬左、右心房复极达90%的动作电位时程(APD_(90)),并通过S_1S_2程序刺激,观察APDR变化,即每一个舒张间期与刺激后发生心房肌复极APD_(90)的关系,并观察房颤的诱发情况.结果 APD_(90)左心房为(157.4±43.5)ms明显小于右心房(170.9±37.9)ms,P<0.05.心房肌在S_1S_2递减程序刺激下,左心房与右心房具有不同斜率的APDR曲线,左心房的APDR曲线斜率1.3±0.4大于右心房0.9±0.3,P<0.05.进行心房快速起搏S_1S_2刺激时,14只犬中共诱发出18阵房颤,其中左心房刺激发作12阵,明显多于右心房6阵(P<0.05).结论 左、右心房间具有单相动作电位时程的异质性及APDR不均一的复极特性,是诱发折返、发生和维持房颤的基质之一.     

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。     

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。     

阵发性心房颤动患者心房内阻滞的评价

目的对阵发性心房颤动(房颤)患者心房内阻滞的情况进行评价.方法入选78例阵发性房颤患者和8创无阵发性房颤的射频消融患者,电生理检查时分别放置高位右心房、希氏束、冠状静脉窦电极导管作起搏和标测用,在高位右心房进行S1S2程序刺激,S1刺激固定于500ms,S2从450ms开始,-10ms扫描,记录不同刺激时心房内和心房间传导时间及心房不应期.结果S1刺激时阵发性房颤组和对照组S1-AHB间期分别为(56.7±15.4)ms和(60.8±14.2)ms;S1-ACSd间期在两组分别为(110.2±24.3)ms和(107.5±25.6)ms;差异均无显著性(P＞0.05).S2刺激时,心房内传导时间最长延长1倍以上的患者在两组分别为15/78例和11/80例,心房间传导最长延长1倍以上的患者在两组间分别为13/78例和9/80例,两组间差异无显著性(P＞0.05).心房不应期在两组分别为(218.0±28.2)ms和(216.0±24.7)ms,两者间差异无显著性(P＞0.05).结论多数阵发性房颤患者无明显的心房内阻滞和不应期改变,传导时间延长也并非特异地发生在阵发性房颤组,提示心房内阻滞和不应期缩短在阵发性房颤的发生中的作用尚不明确.     

选择性刺激犬心房窦房结脂肪垫的电生理观察

目的 位于右心房及右肺静脉交界处的窦房结(SAN)脂肪垫含有丰富的支配心房的副交感神经纤维节.本实验通过选择性直接刺激心脏SAN脂肪垫,观察其对SAN功能、房室传导、心房有效不应期(AERP)及心室有效不应期(VERP)、心房颤动(AF)诱发易感性等电生理参数的影响,以明确心房SAN脂肪垫的副交感神经功能分布特点及探讨AF发生机制.方法 入选杂种犬33只,右侧开胸暴露SAN脂肪垫.将标准的电生理导管置于右心房、希氏束、右心窒心尖部及右心室流出道,记录基础窦性周期长度(SCL)、AH及HV间期、房室结文氏点、AERP及VERP、AF诱发窗口(WOV)及快速右心房起搏诱发AF的RR间期.以逐级递增的能量直接刺激SAN脂肪垫直至AF诱发,测定不同能量状态下SCL及AF诱发阈值.以引起SCL较基线延长50%的固定能量再次刺激SAN脂肪垫,观察其对上述电生理参数的影响.AF诱发成功后,继续逐级增加刺激能量直至最人值10.0 mA.记录不同能量状态下诱发AF的连续10个RR间期,取其平均值.结果 100%犬在直接SAN脂肪垫刺激下诱发AF,AF诱发阈值为(4.0±1.3)mA.AF诱发前,SAN脂肪垫刺激导致窦性心率减慢[SCL:(588±77)ms对(994±293)ms,P<0.001].AF诱发后,直接刺激诱导AF RR间期进行性延长[(461±204)ms对最长(636±260)ms,P<0.001],个别犬出现高度房室阻滞.在以延艮SCL 50%的固定能量刺激SAN脂肪垫时,AERP与刺激前比较明显缩短(P<0.001)、WOV增宽(P<0.001),而AH、HV、房室结文氏点、VERP无变化(P>0.05).结论 直接SAN脂肪垫刺激延长SCL,缩短AERP,增加AF诱发易感性,而对房窒结下区传导及心室无影响.以前文献报道SAN脂肪垫只有单一调节SAN的功能,而本实验结果显示当刺激能量足够时,SAN脂肪垫还町减慢AF时房窜传导.     

地尔硫卓对心房急性电重构影响的临床研究

探讨地尔硫卓对心房快速激动诱发心房急性电重构的影响。将 31例导管射频消融成功的室上性心动过速患者随机分为两组 ,对照组 2 1例、地尔硫卓组 10例 ,以 15 0～ 2 0 0ms起搏周长 (PCL)诱发急性心房颤动 (AF)。以4 0 0msPCL分别在高位右房 (HRA)、低位右房 (LRA)、His束区 (HIS)等部位进行S1S2 扫描 ,测定基础状态、干预后和心房快速激动后心房有效不应期 (AERP) ;以三种不同PCL (35 0 ,4 0 0和 4 5 0ms)随机对右心耳 (RAA)进行S1S2 扫描 ,观察AERP频率自适应性的变化。对照组心房快速激动后HRA、LRA、HIS和RAA的AERP较基础状态、给盐水后有明显缩短 ;而地尔硫卓组心房快速激动后上述指标变化无显著性差异。将RAA处AERP与相应PCL进行曲线拟合 ,对照组基础状态下斜率为 0 .0 5 8、给盐水后斜率为 0 .0 6 8和心房快速激动后斜率为 0 .0 15。地尔硫卓组则分别为0 .0 30 ,0 .0 7和 0 .0 6 0。对照组诱发继发AF 13例 (13/2 1,6 1.9% ) ,明显高于地尔硫卓组 3例 (3/10 ,30 .0 % ) ,继发AF平均时限两组无明显差别。结论 :预先给予地尔硫卓可以阻止心房快速激动诱发的心房急性电重构的发生     

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。     

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     

右心房静止与心肌疾病

目的分析右心房静止患者的心脏电生理与临床表现特点。方法9例拟行永久起搏器植入术患者,年龄48.7±18.6岁。分别记录体表心电图、右房心内电图并经冠状静脉窦电极导管或食管电极记录左房电位,并给予心房刺激。结果9例患者的右房多部位均未记录到心房电位,10V电刺激不能激动局部心房肌。左房电位记录显示5例患者未记录到左房电位,2例为房扑,房颤、房速各1例。体表心电图7例未记录到房波,1例为房扑,1例为房颤,心房波振幅≤0.05mV。1例植入双心室起搏起搏器,1例植入右室双部位起搏器,其他病例植入右室起搏器。结论部分病例右心房的病变重于左心房,可以表现为右房静止;右心房静止者,左心房可以存在电活动,而体表心电图多数表现为心房静止。体表心电图表现为心房静止不能说明左右心房都不存在电活动。     

持续快速肺静脉起搏对犬心房结构及心电生理特性的影响

目的探讨快速起搏肺静脉(PV)建立持续性心房颤动(房颤)犬模型的心房结构及心电生理特性。方法 30只犬随机分为实验组和对照组,实验组以20Hz的固定频率行肺静脉持续起搏,建立持续时间24h的房颤动物模型。超声心动图测量实验组基础状态和起搏结束后左右心房面积,对所有犬的左右心房游离壁、左上肺静脉、左下肺静脉、右上肺静脉和右下肺静脉进行心外膜电生理标测,测量各标测部位的有效不应期(ERP)和平均房颤波周长(AFCL),观察肺静脉起搏对心房面积的影响以及各部位ERP和AFCL的变化。结果实验组11只犬完成实验,在(28.2±3.0)d内诱发出持续超过24h的房颤。超声心动图测量显示起搏结束后心房面积明显扩大(P0.05);与对照组相比,左右心房及各肺静脉的ERP明显缩短(P0.05);实验组各部位ERP和AFCL呈明显的梯度分布,自短至长依次为:肺静脉、左房游离壁和右房游离壁。结论在犬快速肺静脉起搏房颤模型中,心房面积的增大及各部位电生理特性的变化可能是持续性房颤诱发和维持的发生机制。     

已达到消融终点的长程持续性心房颤动复发危险因素分析

目的：探讨已达到消融终点的长程持续性心房颤动（房颤）患者复发的危险因素。方法：纳入达到消融终点的长程持续性房颤患者256例,消融终点定义为双侧肺静脉电隔离,二尖瓣峡部和左心房顶部线性消融双向阻断且碎裂电位消失。根据随访结果将患者分为房颤复发组（n＝43）和无复发组（n＝213）。通过多因素 COX 回归分析探讨房颤复发的独立危险因素。结果：经过（19．5±3．6）个月随访,与无复发组相比,房颤复发组患者右心房内径较大,为（53．31±6．55）mm 对（48．74±5．87）mm;房颤持续时间较长,为（81．83±45．75）个月对（53．16±40．23）个月;左心房内径较大,为（49．85±6．82）mm 对（46．77±5．83）mm,P 均＜0．01。多因素 COX 回归分析发现,左心房内径增大（OR＝1．01,95％CI：1．01～1．28,P ＜0．05）,右心房内径增大（OR＝2．85,95％CI：1．15～7．03,P ＜0．05）、房颤持续时间延长（OR＝1．01,95％CI：1．01～1．02,P ＜0．05）是房颤复发的独立危险因素。结论：除左心房内径和房颤持续时间外,右心房内径增大也是已达到消融终点的长程持续性房颤复发的独立危险因素。     

Limited benefit of septal pre-excitation in pace prevention of atrial fibrillation

BACKGROUND: Pre-excitation of the intra-atrial septum (IAS) by pacing at the ostium of the coronary sinus (CSO) can prevent atrial fibrillation (AF) in case of single atrial premature beats (APBs). We investigated whether pre-excitation of IAS, either by pacing at CSO or at the right ventricle in the presence of retrograde conduction (RV), can prevent atrial tachyarrhythmia triggered by single and multiple APBs. AF vulnerability was compared to pacing at the right atrium (RA) and sinus rhythm (SR). METHODS: Seventeen patients, age 52 +/- 21 years, who exhibited retrograde VA conduction and reproducible induction of atrial tachyarrhythmia during an electrophysiological procedure, were studied. Both during SR and pacing (S1-S1:600 ms) at RA, CSO, and right ventricle (RV), single (A1-S2:200 ms) and multiple premature stimuli (A1-S2-S3-S4:200-180-180 ms) were delivered at RA (4 x diastolic threshold). RESULTS: During pacing at RA, single and multiple APBs invariably induced runs of atrial tachyarrhythmia (mean duration 34 +/- 67 sec and 37 +/- 69 sec, range 1 sec to 20 min). During preventive pacing at CSO and RV, single APBs (A1-S2:200 ms) did not induce atrial arrhythmia (0 +/- 0 sec, 0 +/- 0 sec, P < 0.05 vs pacing at RA). In contrast, when multiple APBs were applied, pacing at CSO or RV failed to prevent initiation of AF (mean duration 36 +/- 63 sec, 38 +/- 65 sec, NS). Also during SR, single APBs did not induce AF (0 +/- 0 sec, P < 0.05 vs pacing at RA) whereas multiple APBs invariably induced AF (39 +/- 74 sec, NS). CONCLUSIONS: Compared to pacing at RA, pre-excitation of IAS either by pacing at CSO or at RV with retrograde conduction can prevent initiation of paroxysms of atrial tachyarrhythmia triggered by single but not by multiple right APBs. These findings imply that the potential benefit of choosing an optimal pacing site in patients requiring atrial-based pacing is limited. Moreover, in the absence of bradycardia, no specific pacing site offers incremental benefit over the natural "protective" effect of sinus rhythm.     

肺静脉起源的局灶性心房颤动模型：心房颤动触发机制与维持机制的分离

目的建立非肺静脉起源的局灶性心房颤动（房颤）模型,观察该房颤的诱发和维持特点并探讨其可能的电生理机制。方法21只健康成年犬静脉麻醉后行右侧开胸手术,暴露靠近右上肺静脉的心脏脂肪垫（内含神经丛）,将1根多电极导管固定贴靠于右上肺静脉,使其头端电极贴靠右上肺静脉与左心房交界处,另外将2根多电极导管分别固定于右心房中部和右心耳一侧。用一根细塑料管固定于右心耳与右心房交界处,将二者隔离开,隔离出的右心耳面积大约为240mm2。另将一根单向动作电位（MAP）导管经股静脉送至右心耳内以记录局部的单向动作电位。其中6只犬在右房中部用胶水固定一塑料的中空圆柱体,其内部面积大约为8mm2。分别以不同浓度（1、10、100mmol/L）的乙酰胆碱（Ach）浸润分离出的右心耳和圆柱体内部的心房表面。结果21只犬中有16只犬应用100mmol/L Ach浸润右心耳可重复发生自发持续性局灶性房颤（〉10min）。右心耳处房颤的平均周长为30.6±4.6 ms,心房部位房颤的平均周长为105.2±32.0 ms（P〈0.05）。房颤发生前均伴有MAP时程〉90%的缩短。在房颤发作中,沿右心耳与右房交界处采用血管钳钳夹可导致全部16只犬右心耳处电活动的消失,但其中14只犬的房颤仍然在心房内持续存在,另2只犬的房颤在30 s内终止。6只犬在行右上肺静脉附近的神经丛内注射甲醛溶液后,再行100mmol/L Ach浸润右心耳仅造成MAP时程的明显缩短,不再能发生自发持续性房颤;全部6只犬Ach浸润圆柱体内部的心房表面不能发生自发持续性房颤。结论采用100mmol/L的Ach浸润足够面积的右心耳可建立右心耳起源的局灶性房颤模型。内源性自主神经系统在该房颤的触发和维持机制中起作用。     

心房颤动24h和48h对犬心房肌有效不应期及L型钙电流的影响

目的 研究犬心房颤动（房颤）持续24h和48 h,心房肌有效不应期和L型钙电流变化的一致性及其机制.方法 健康成年杂种犬18只,分为对照组、24 h房颤组、48 h房颤组,每组6只.600次/min起搏高右心房建立犬房颤模型,应用程序刺激的方法测定右心房有效不应期（ERP）,通过Langendorff左回旋支灌流分离心房肌细胞,并通过全细胞膜片钳技术记录L型钙电流（ICa-L）变化.应用免疫组织化学方法检测各组心房组织L型电压依赖性钙通道（LVDCC）α1c蛋白表达.用图像分析系统对组织化学抗原表达进行半定量分析.结果 所有实验动物均可诱发出房颤.心房ERP的变化在最初6h较对照组明显缩短,后直至48 h呈进行性缩短.快速起搏6h后ERP（129.50±8.64）ms较对照组（141.00±15.23）ms缩短（12.13±2.24）ms（P＜0.01）,24 h后心房ERP（123.00± 13.37） ms缩短（19.23±2.14）ms（P＜0.01）,48 h缩短（28.15±4.26）ms（P＜0.01）.同时在房颤持续过程中24h房颤可引起ICa-L电流密度（-4.83±0.30）pA/pF较对照组（-6.69±0.08）pA/pF减小,48 h（-3.70±0.50）pA/pF减少的程度更重.24 h房颤及48 h房颤犬的左、右心房组织LVDCC α1c蛋白表达均较对照组明显减少（P＜0.05）,48 h房颤组减少程度更重（P＜0.01）.结论 房颤持续24 h,心房肌ERP显著缩短、ICa-L密度降低.房颤持续48 h仍然维持L型钙通道改变特征.提示：钙通道阻断剂可用于持续24 h房颤,预防房颤复发.     

Biatrial and three-dimensional mapping of spontaneous atrial arrhythmias in patients with refractory atrial fibrillation

INTRODUCTION: While atrial fibrillation (AF) initiation in the pulmonary veins has been well-studied, simultaneous biatrial and three-dimensional noncontact mapping (NCM) has not been performed. We hypothesized that these two techniques would provide novel information on triggers, initiation, and evolution of spontaneous AF and permit study of different AF populations. METHODS AND RESULTS: The origin of atrial premature beats (APBs), onset of spontaneous AF and its evolution were analyzed in 50 patients with AF in the presence or absence of structural heart disease (SHD) and in different AF presentations (group A: Persistent, group B: Paroxysmal). In 45 patients, spontaneous APBs in the right atrium (RA; n = 60) and left atrium (LA; n = 25) with similar regional distributions regardless of heart disease status were demonstrated. In total, 22 patients (44%) had > or =2 disparate regional origins. Biatrial regional foci were seen with equal frequency in patients with SHD (31%), without SHD (40%), in group A (32%), and in group B (36%). Biatrial mapping and NCM showed organized monomorphic atrial tachyarrhythmias arising in the RA (17), septum (17), or LA (21) and were classified as atrial flutter (RA = 34, LA = 8), macro-reentrant atrial tachycardia (RA = 1, LA = 3) or focal atrial tachycardia (RA = 2, LA = 7). Their regional distribution was more extensive in patients with SHD and persistent AF compared with patients without SHD or paroxysmal AF. Simultaneous biatrial tachycardias were observed only in group A patients and those with SHD. CONCLUSIONS: Simultaneous biatrial and NCM permits successful AF mapping in different AF populations and demonstrates a biatrial spectrum of spontaneous triggers and tachycardias. Organized monomorphic tachycardias with multiple unilateral or biatrial locations are commonly observed in human AF. Patients with heart disease or persistent AF have a more extensive distribution as well as simultaneous coexistence of multiple tachycardias during AF.     

Differences in organization between acute and chronic atrial fibrillation in dogs

OBJECTIVES: The purpose of this study was to determine differences in acute and chronic atrial fibrillation (AF) "organization" in canine models. BACKGROUND: Electrophysiologic changes occur during atrial remodeling, but little is known about how remodeling affects AF organization. We hypothesized that atrial remodeling induced by long-term rapid atrial rates heterogeneously decreases AF organization. METHODS: In seven dogs, acute AF was induced by atrial burst pacing, and in eight dogs chronic AF was created by six weeks of continuous rapid atrial pacing. Atrial fibrillation was epicardially mapped from the right atria (RA) and left atria (LA). Atrial cycle length (CL), spatial organization and activation maps were compared. Spatial organization was quantified by an objective signal processing measure between multiple electrograms. RESULTS In acute AF, mean CL was slightly shorter in the LA (124 +/- 16 ms) than it was in the RA (131 +/- 14 ms) (p < 0.0001). In chronic AF, LA CL (96 +/- 14 ms) averaged 24 ms shorter than RA CL (121 +/- 18 ms) (p < 0.0001). Right atria and LA in acute AF had similar levels of organization. In chronic AF, the LA became approximately 25% more disorganized (p < 0.0001) while the RA did not change. In acute AF, a single broad wave front originating from the posterior and medial atrium dominated LA activation. In chronic AF, LA activation was more complex, sustaining multiple reentrant wavelets in the free wall and lateral appendage. CONCLUSIONS: Acute and chronic AF exhibit heterogeneous differences in CL, organization and activation patterns. The LA in chronic AF is faster and more disorganized than it is in acute AF. Differences in the models may be due to heterogeneous electrophysiologic remodeling and anatomic constraints. The design of future AF therapies may benefit by addressing the patient specific degree of atrial remodeling.     

Long-term changes in sequence of atrial activation and refractory periods: no evidence for "atrial memory".

OBJECTIVES: The purpose of this study was to test whether the spatial distribution of the atrial refractory period (AERP) and the vulnerability to atrial fibrillation (AF) are altered by long-term changes in the sequence of atrial activation. BACKGROUND: The spatial distribution of the AERP plays an important role in AF. Changes in the activation sequence have been postulated to modulate atrial repolarization ("atrial memory"). METHODS: Six goats were chronically instrumented with epicardial atrial electrodes to determine activation time and AERP at 11 different areas of the right (RA) and left (LA) atrium and the Bachmann bundle. Activation time and AERP were measured during sinus rhythm and during prolonged RA and LA pacing (1 week RA pacing, 2 weeks LA pacing, 1 week RA pacing; 150 bpm). Inducibility of AF was determined by the number of atrial sites where single premature stimuli induced AF paroxysms >1 second. RESULTS: During sinus rhythm (106 +/- 4 bpm), AERP was longest at the Bachmann bundle and shortest at the LA free wall (185 +/- 6 ms and 141 +/- 5 ms, P < .001). In five of six goats, an inverse correlation between local activation time and AERP was found during sinus rhythm (r = -0.53 +/- 0.05; P < .05). The increase in atrial rate during RA and LA pacing caused an overall shortening of AERP from 167 +/- 6 ms to 140 +/- 6 ms (P < .001). However, a switch between long-term RA and LA pacing did not significantly change AERP at any of the 11 atrial regions and had no significant effect on AF inducibility. CONCLUSIONS: During sinus rhythm, an inverse relationship exists between the sequence of atrial activation and the local refractory period. However, long-term changes in the sequence of atrial activation do not alter the spatial distribution of AERP or the inducibility of AF.     

肺静脉电隔离术联合碎裂电位消融治疗持续性房颤疗效观察

目的：观察肺静脉电隔离术（ pulmonary vein isolation , PVI ）联合碎裂电位（ complex fractionated atrial electrograms , CFAE）消融对持续性房颤的疗效。方法对比观察23名于本院行房颤射频消融术的持续性房颤患者,所有患者均行PVI及左房顶部线性消融,其中12例联合CFAE消融,术后随访1年;观察两组手术时间、X线曝光时间、消融时间、手术并发症、左房大小、左房血栓、一次手术成功率等指标。结果联合CFAE消融组总手术时间（252±35） min、X线曝光时间（42±9．1）min、消融时间（94±11）min,单纯行PVI 组分别为（176±22）min、（34±7．6）min、（63±8）min,联合CFAE消融组手术各时间均明显延长（P＜0．01）;两组手术并发症、对左房大小及左房血栓的影响比较差异均无统计学意义;联合CFAE消融组一次手术成功率（75％）明显高于单纯行PVI组（64％）（ P＜0．05）。结论 PVI联合CFAE消融治疗持续性房颤虽增加手术、消融及X线曝光时间,但并不会提高并发症发生率,可提高房颤消融的一次手术成功率。