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。     

心房肌易损性与阵发性心房颤动的发生机制

目的探讨左、右心房肌复极,及其易损性与阵发性心房颤动(AF)的发生与维持机制。方法应用单相动作电位(MAP)技术记录14只犬左、右心房肌的复极达90%动作电位时程(APD90),通过S1S2程序刺激,同时记录心房有效不应期(ERP)及相对不应期(RRP),观察反复心房激动(RAF,在S1S2的早搏刺激后,发生2个以上的连续心房活动,从心房刺激到RAF第一个激动的间期必须小于250 ms)及AF的诱发。结果14只犬S1S2间期递减至130±32 ms时,可出现RAF,随后当S1S2间期缩短为110±28 ms时AF发作。AF发作前大多数可记录到RAF(66.7%);共诱发出15阵RAF,左房11阵,右房4阵,左房RAF的发生率明显多于右房(P<0.05);共诱发出18阵AF,左房诱发出12阵,右房诱发出6阵。左房的AF诱发率明显多于右房(P<0.05)。结论AF发作前多伴有RAF发作;RAF是易发生阵发性AF的特征性表现,代表心房的易损性;左右心房易损性不同。     

心房肌的复极与阵发性心房颤动发生机制的实验研究

目的心房肌的复极对阵发性心房颤动(简称房颤)的诱发及维持起着重要的作用.本研究使用单相动作电位技术(MAP)对在体犬左、右房肌的复极时间及房颤的诱发进行研究,以探讨心房肌对阵发性房颤发生和维持的潜在机制.     

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     

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。     

新型Ⅲ类抗心律失常药物尼非卡兰对心房及肺静脉组织动作电位的影响

目的研究尼非卡兰对心房及肺静脉组织动作电位的影响,探讨尼非卡兰在房性心律失常中的作用。方法2006年3月至4月,阜外心血管病医院电生理中心及北京市朝阳医院心脏中心从15只大耳白兔取右心房、左心房和肺静脉组织制成0.5cm×1.5cm组织条,用2倍阈强度,脉宽3ms刺激引发动作电位,采用标准玻璃微电极技术记录心房及肺静脉肌袖组织动作电位,用分级递增刺激和程序刺激测定各部位组织在基础条件下的不应期。用质量浓度为2.13mg/L的尼非卡兰的台氏液灌流组织条15min后,采用同样方法引发动作电位和测定不应期,比较用尼非卡兰前后动作电位时相和不应期的变化。结果尼非卡兰灌流后,左心房APD90由(51±16)ms延长到(78±33)ms(P<0.05),右心房APD90由(53±12)ms延长到(71±13)ms(P<0.05,),肺静脉肌袖APD90由(59±7)ms延长到(98±11)ms(P<0.001,),ERP由(102±8)ms延长到(118±13)ms(P<0.05)。结论尼非卡兰的延长心房和肺静脉肌袖组织动作电位时相及不应期的电药理作用可能是其治疗房性心律失常的基础。     

心房肌的复极与阵发性房颤发生机制的实验研究

目的使用单相动作电位技术(MAP)对在体犬左、右心房肌的复极时间进行研究,以探讨阵发性心房颤动(房颤)发生与维持的潜在机制.     

大鼠左心房肌单相动作电位的增龄性变化

目的　研究年龄对大鼠左心房肌单相动作电位(monophasicactionpotential,MAP)的影响。方法　选取实验用Wistar大鼠4 0只,按出生年龄分为青年组、成年组、中年组及老年组,每组10只。体外Langendorff灌流心脏,右心室刺激。分别记录各组左心房肌在4 0 0ms刺激周长下动作电位复极到90 %、5 0 %及2 0 %时的单相动作电位时程(MAPD90 )、MAPD50 、MAPD2 0 和心房有效不应期,以及在不同刺激周长下的MAPD90 、MAPD50 、MAPD2 0 。结果　MAPD各时相和有效不应期都随着年龄的增加而出现延长(P <0 .0 1) ;但老年组缩短。在同一年龄组中,刺激频率增加使动作电位时程都相应缩短,以MAPD90 明显;中年组MAPD改变明显。结论　年龄是影响心脏电活动重要的独立因素之一。     

心房神经节消融后心房结构重构与心房颤动诱发的关系

目的研究心房心外膜神经节丛（GP）消融后心房基质的变化,探讨其与心房颤动（房颤）诱发的关系。方法10只犬随机分为假手术组和GP消融组。所有犬均行超声心动图后无菌下右侧开胸,观察右心房短阵快速电刺激诱发房颤情况。之后GP消融组分别消融心房右前和右下GP,消融后即刻观察右心房短阵快速电刺激诱发房颤情况。所有犬喂养8周后,同样方法再观察房颤诱发情况。取出心脏分离左、右心房肌组织,采用放射免疫法检测脑钠肽（BNP）水平及免疫组化法检测神经密度;同样方法检测犬开胸前和开胸后8周血浆BNP水平和超声心动图。结果假手术组和GP消融后即刻右心房刺激未能诱发出房颤,但房颤在GP消融后8周易诱发;血浆和右心房组织BNP水平在GP消融后8周明显升高[（119．5±22．6）pg／mlV8（167．7±26．4）pg／ml,（213．2±34．9）pg／gVS（287．6±36．4）pg／g,P〈0．05],但左心房BNP水平无明显变化;两组犬术前和术后左右心房大小均无明显变化;GP消融8周后右心房GAP43、TH和ChAT阳性纤维的密度低于假手术组,差异有统计学意义[（791±714）permm2vs（2540±863）permm2,（448±582）permm。VS（1855±623）permm2,（580±726）permm2vs（2833±851）permm2,P〈0．05],但左心房无明显变化。结论心房心外膜GP消融后,心房基质发生重构,可能是GP消融后房颤易诱发的原因。     

胺碘酮对人在体心室复极离散度的影响

目的使用单相动作电位技术评价静脉推注胺碘酮对人在体心室复极离散度的影响。方法使用铂电极导管记录29例无器质性心脏病患者应用胺碘酮前后右室心尖部和右室流出道的单相动作电位图形,测量各标测点的激动时间(AT)、动作电位时程(APD_(90))、复极时间(RT)、舒张期基线和平台期峰点之间的电位差幅度(AMP),计算各指标的离散度ATd、APDd、RTd。结果 29例患者静脉推注胺碘酮20 min前后,右室心尖部的AT、APD_(90)、RT分别为(16.8±6.1)ms vs (24.3±5.5)ms、(248.3±10.6)ms vs (265.0±13.8)ms、(265.0±13.6)ms vs (282.1±17.3) ms(P均0.01),而右室流出道的AT、APD_(90)、RT分别为(19.1±5.7)msvs (26.2±6.6)ms、(260.0±18.6)ms vs (270.0±15.4)ms和(275.4±16.5)ms vs (294.7±16.4)ms(P均0.01)。而AMP、ATd、APDd、RTd值较用药前差别无统计学意义(P0.05)。结论静脉推注胺碘酮可延长不同部位AT、APD_(90)及RT,但对人在体心室复极离散度各指标无明显影响。     

Action potential duration restitution kinetics in human atrial fibrillation

OBJECTIVES: We undertook this study to determine whether human atrial fibrillation (AF) relates to steeply sloped action potential duration restitution (APDR) kinetics and whether the spatial nonuniformity of APDR promotes persistence of AF. BACKGROUND: A steeply sloped APDR curve is known to be an important determinant of the induction of more complex action potential duration (APD) dynamics and fibrillation. METHODS: Patients with chronic atrial fibrillation (CAF) (n = 18), paroxysmal atrial fibrillation (PAF) (n = 14) and normal control subjects (n = 9) were studied. The monophasic action potential duration at 90% repolarization (APD(90)) and the effective refractory period (ERP) were measured at six sites in the right atrium. After AF was electrically converted, APDR was assessed by delivering a single extrastimulus after a train of stimuli at a cycle length of 600 ms (S(1)S(2)) at six different sites of the right atrium, as well as rapid pacing at cycle lengths that induced APD alternans. RESULTS: The APD(90) and ERP in patients with CAF were shorter than those in patients with PAF and control subjects (p < 0.05); however, the dispersions of APD(90) and ERP in each group were similar. The maximal slopes of APDR by S(1)S(2) and rapid pacing in patients with CAF (1.2 +/- 0.4 and 1.7 +/- 0.2) and PAF (1.1 +/- 0.4 and 1.3 +/- 0.4) were higher than those in control subjects (0.5 +/- 0.3 and 0.8 +/- 0.2, respectively; p < 0.01). The maximal slope obtained by S(1)S(2) did not differ from that obtained by rapid pacing in any group. The inter-regional difference of the maximal slope in patients with CAF (1.6 +/- 0.4, p < 0.05) was greater than that in patients with PAF (1.2 +/- 0.3, p = NS vs. control) and control subjects (0.4 +/- 0.2). CONCLUSIONS: Atrial fibrillation was related to steeply sloped (>1) APDR kinetics. The spatial dispersion of APDR in patients with chronic AF was greater than that of patients with paroxysmal AF and control subjects, indicating that the heterogeneity of APDR of the atrium plays an important role in the persistence of AF.     

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。     

自主神经干预对心房恢复性质的影响

目的 研究心脏自主神经干预对心房恢复性质的影响.方法 正常成年杂种犬10只,开胸后将多极电生理导管缝置于肺静脉、左右心耳和左右心房处,应用Ag-AgCl电极记录标测部位单相动作电位,在基础状态和颈部迷走神经刺激条件下构建标测部位恢复曲线,分别对标测部位进行快速电刺激,记录心房颤动（房颤）诱发时的起搏周长和持续时间.心脏自主神经节（GP）消融后重复上述步骤.结果 GP消融前迷走神经刺激同基础状态相比显著缩短动作电位时限（APD）,降低恢复曲线最大斜率（Smax）,抑制APD电交替,但房颤容易发生（P＜0.05）.GP消融后,APD较消融前显著延长,恢复曲线Smax增大,APD电交替提前,但房颤不易诱发（P＜0.05）;GP消融后迷走神经刺激效应明显减弱.GP消融前迷走神经刺激能显著增加APD恢复曲线Smax离散度（0.5±0.2对0.3±0.1,P＜0.05）,而GP消融能显著降低APD恢复曲线Smax离散度（0.2±0.1对0.3±0.1,P＜0.05）.结论 恢复曲线的斜率并不能完全解释房颤的诱发和维持,心房APD电交替可能对房颤的诱发并无预测作用,恢复性质的离散可能是诱发房颤的重要因素.     

Dispersion of atrial repolarization in patients with paroxysmal atrial fibrillation.

To study the role of the dispersion of atrial repolarization (DAR) in the genesis of atrial fibrillation (AF), monophasic action potentials (MAP) were recorded simultaneously from a catheter at the high lateral right atrium (HLRA) and a catheter moving around the high, middle and low lateral right atrium (RA) the high, anterior and posterior septal RA and the RA appendage in 15 patients with paroxysmal AF and 15 patients with atrioventricular nodal re-entry tachycardia (AVNRT) or concealed Wolff-Parkinson-White syndrome (WPW) without history of AF. After recordings during sinus rhythm (SR), MAPs were recorded during programmed stimulation (PS) via the HLRA catheter at a drive cycle length (CL) of 500 ms. Thus, MAPs were recorded simultaneously from 2 sites at a time and sequentially from 4 to 12 sites during SR, drive pacing and PS. Taking the MAP at the HLRA as reference, the dispersion of repolarization time (dispersion of RT) and its two components, the dispersions of activation time (dispersion of AT) and MAP duration (dispersion of MAP duration) among the 4 to 12 sites were calculated and taken as parameters of DAR. RESULTS: During SR and PS, the maximal dispersion of RT was significantly greater in AF than in control patients, 113+/-49 ms vs 50+/-28 ms (P<0.001) and 114+/-56 vs 70+/-43 ms (P<0.05) respectively. The increased dispersion of RT in the AF group was caused by increases in both dispersion of MAP duration and dispersion of AT. CONCLUSION: During SR and PS, DAR increased in patients with paroxysmal AF due to increases in dispersion of MAP duration and dispersion of AT, which suggests the involvement of both repolarization and conduction disturbances in the development of paroxysmal AF.     

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。     

High-density activation mapping of fractionated electrograms in the atria of patients with paroxysmal atrial fibrillation

BACKGROUND: Areas of complex fractionated atrial electrograms (CFAEs) have been implicated in the atrial substrate of atrial fibrillation (AF). The mechanisms underlying CFAE in humans are not well investigated. OBJECTIVES: The purpose of this study was to investigate the regional activation pattern associated with CFAE using a high-density contact mapping catheter. METHODS: Twenty patients with paroxysmal AF were mapped using a high-density multielectrode catheter. CFAE were mapped at 10 different sites (left atrium [LA]: inferior, posterior, roof, septum, anterior, lateral; right atrium [RA]: anterior, lateral, posterior, septum). Local atrial fibrillation cycle length (AFCL) was measured immediately before and after the occurrence of CFAE, and the longest electrogram duration (CFAEmax) was assessed. RESULTS: Longer electrogram durations were recorded in the LA compared with the RA (CFAEmax 118 +/- 21 ms vs 104 +/- 23 ms, P = .001). AFCL significantly shortened before the occurrence of CFAEmax compared with baseline (LA: 174 +/- 32 ms vs 186 +/- 32 ms, P = .0001; RA: 177 +/- 31 ms vs 188 +/- 31 ms, P = .0001) and returned to baseline afterwards. AFCL shortened by >or=10 ms in 91% of mapped sites. Two different local activation patterns were associated with occurrence of CFAEmax: a nearly simultaneous activation in all spines in 84% indicating passive activation, and a nonsimultaneous activation sequence suggesting local complex activation or reentry. CONCLUSION: Fractionated atrial electrograms during AF demonstrate dynamic changes that are dependent on regional AFCL. Shortening of AFCL precedes the development of CFAE; thus, cycle length is a major determinant of fractionation during AF. High-density mapping in AF may help to differentiate passive activation of CFAE from CFAE associated with an active component of the AF process.     

阵发性心房颤动患者心房及肺静脉不应期离散度的变化

目的探讨阵发性房颤患者房颤相关组织的电生理特性改变情况。方法选取阵发性房颤患者10例(房颤组)和无房颤病史的左侧旁路有显性预激波患者15例(对照组)。将大头电极分别放置在两组患者左上肺静脉、左下肺静脉、右上肺静脉、右下肺静脉开口及左心房顶壁、前壁、后壁、高位右心房,分别测定各部位有效不应期(EPR)。结果①房颤组心房及肺静脉EPR离散度指数(DI)为0.117±0.028,对照组为0.074±0.029,两组比较,P<0.05。②房颤组左心房ERP为(234.00±28.72)ms,肺静脉ERP为(230.75±32.69)ms;对照组左心房ERP为(248.00±25.99)ms,肺静脉ERP为(244.33±26.78)ms,两组比较,P均<0.05。结论阵发性房颤患者DI明显增大,左心房、肺静脉ERP显著缩短。     

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。     

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.