快速起搏犬左心房对肺静脉有效不应期的影响

目的：观察10 min快速刺激左心耳对肺静脉有效不应期的影响。方法：20条成年杂种犬在左上肺静脉根部血管外膜处放置自制环状电极,首先测量基础状态下起搏周长（PCL）为300 ms时肺静脉有效不应期。接着以400次/min的频率起搏左心耳10 min。分别于起搏中止后即刻、5 min、10 min时重复测量肺静脉有效不应期。结果：肺静脉有效不应期在10 min快速起搏中止后即刻,5 min时与起搏前相比有显著差别（P〈0.05）,10 min时与快速起搏前相比无显著差别（P〉0.05）。结论：10 min快速起搏左心耳可以导致肺静脉有效不应期明显缩短,这种变化在10 min内可以完全恢复。     

异搏定对快速起搏犬肺静脉有效不应期的影响

目的:观察阻断钙离子通道对快速起搏犬肺静脉对肺静脉有效不应期及有效不应期频率适应性的影响。方法:20条成年杂种犬随机平均分为两组。给药组静脉注射维拉帕米,对照组静脉注射生理盐水。两组首先测量起搏周长(PCL)分别为400 ms时肺静脉有效不应期接着以每分钟400次的频率刺激左心房20 min,分别在刺激中止后即刻、5min、10 min时再次测量PV-ERP。结果:刺激终止后即刻及5 min时异搏定组与对照组比较有效不应期明显延长,差异有显著性(P<0.05)。10 min时差异无显著性(P>0.05)。结论:钙离子通道阻断剂异搏定可以减轻肺静脉电重构的程度。     

快速心房起搏对家兔心房肌L型钙离子通道的影响及氯沙坦干预的研究

目的 探讨以人工心脏起搏的方法制备家兔急性心房纤颤(atrial fibrillation,AF)模型时心房发生电重构的机制和干预方法.方法 家兔45只随机分为生理盐水(NS)组、生理盐水起搏(NSP)组、氯沙坦起搏(LP)组.观测每组基础状态、快速心房起搏时心房有效不应期(AERP)及心房肌L-型钙通道的电流密度(ICa-L),并进行统计学处理.结果 [1]快速起搏时NSP组较NS组各个基础周长下的AERP均显著下降(P＜0.01);NSP组快速起搏6小时和8小时与NS组AERP的差距随着基础周长的下降而减少.[2]而快速起搏8小时后LP组AERP的下降较NSP组显著减轻(P＜0.01);LP组快速起搏后与NS组AERP的差距随着基础周长的下降未见减少趋势.[3]NSP组较NS组心房肌ICa-L降低;LP组较NS组和NSP组心房肌ICa-L差异无统计学意义(P＞0.05);而LP组较NSP组心房肌ICa-L的标准差显著降低(P＜0.05).结论 快速心房起搏可引起AERP缩短及AERP频率适应性不良为特征的心房肌电重构.氯沙坦可以抑制这种电重构及心房肌ICa-L离散度增加,从而降低AF的发生.     

经皮右心室临时起搏22例的临床应用体会

目的：分析经皮右心室临时起搏技术的临床应用。方法：选择符合病例22例。采用Seldinger法右锁骨下静脉穿刺，置入6F或7F血管鞘，在X线引导下，送人6F四级起搏电极导管至右心室稳定部位，参数满意后，连接临时起搏器，设置起搏参数进行起搏。结果：本组完成22例经皮右心室临时起搏；临床疗效好、并发症少，并发症发生率4．1％。结论：该技术方法起搏疗效肯定，创伤小、省时、合并症少，导管操作方法易行，便于在基层医院开展。     

心脏神经结丛消融联合低强度耳屏迷走神经刺激对犬房颤电生理特性的影响

目的研究心脏神经节丛消融联合低强度耳屏迷走神经刺激对阵发性犬心房颤动(简称房颤)电生理特性的影响,探讨低强度耳屏迷走神经刺激对房颤消融术后的治疗价值。方法 21条健康成年比格犬随机分为3组:RAP组(500次/min快速心房起搏,n=7)、ABL组(心脏神经节消融+500次/min快速心房起搏,n=7)、LL-ST组(心脏神经节消融+低强度右侧耳屏刺激+500次/min快速心房起搏,n=7)。其中,RAP组为单纯快速心房起搏,ABL组为右上神经节丛(ARGP)和左上神经节丛(LSGP)消融后快速心房起搏,LL-ST组为ARGP+LSGP消融后低强度刺激右侧耳屏迷走神经+快速心房起搏。于起搏前及起搏后2、4、6、8、10、12、14、16 h测定犬心房和肺静脉不同部位的房颤诱发率、房颤持续时间、有效不应期(ERP)及有效不应期离散度(dERP)。结果 (1)与RAP组相比,LL-ST组房颤诱发率显著降低,房颤持续时间显著减少,ERP显著延长,dERP显著降低,差异有统计学意义(P均<0.05)。(2)与ABL组相比,LL-ST组房颤诱发率显著降低,房颤持续时间显著减少,ERP显著延长,dERP显著降低,差异均有统计学意义(P<0.05)。结论低强度右侧耳屏迷走神经刺激联合心脏神经节丛消融可以有效控制房颤消融术后的复发。     

经皮右心室临时起搏23例的临床应用分析

目的：分析经皮右心室临时起搏技术的临床应用意义。方法：选择符合病例23例，采用Seldinger法股静脉穿刺，置入6或7F血管鞘，在X线透视下，送入6F四极起搏电极导管至右心室稳定部位，参数满意后，连接临时起搏器，设置起搏参数进行起搏。结果：本组完成23例经皮右心室临时起搏，临床疗效好，并发症少4．3％。结论：该技术方法起搏效果肯定，创伤小，省时，合并症少，导管操作方便易行。     

心房快速起搏对兔心房颤动心电生理的影响

目的探讨心房快速起搏对兔心房有效不应期（effective refractory period,ERP）和心肌组织场电位时程（field potential duration,FPdur）的影响。方法成年新西兰兔40只,以500次/min行快速起搏并测量ERP,根据起搏时间分为5组,0,4,8,12,24h组各8只。起搏结束时开胸取心,应用微电极阵列技术记录场电位形态及Fpdur,比较各组心房组织FPdur与ERP变化趋势。结果 8h组ERP缩短为（82.11±1.74）ms,24h组缩短至（80.09±2.18）ms,与0h组比较差异均有统计学意义（P〈0.05）;8h组FPdur延长为（121.18±3.55）ms,24h组延长至（85.91±5.4）ms,与0h组比较差异有统计学意义（P〈0.05）;R-R间期在起搏4h后缩短至最低,振幅在起搏后12h降至最低,搏动频率在起搏后4h降至最低,与0h组比较差异均有统计学意义（P〈0.05）。结论心房颤动时心房ERP缩短,FPdur延长,微电极阵列技术可对心房颤动时的电重构提供准确电生理变化信息。     

起搏器治疗对左室功能尚好房室传导阻滞患者的心功能影响

目的：评价左室功能尚好的房室阻滞患者植入心脏起搏后心力衰竭和左室收缩功能，探讨起搏器术后对左室功能的影响及其预测因素。方法：对象为48例因房室传导阻滞（AVB）行永久起搏治疗的患者，对其手术前后12导联心电图、超声心动图、心功能NYHA分级进行随访评估。结果：48例患者均行右室心尖起搏，其中男性26例、女性22例，平均随访12&#177;9月。术后随访期间，13例患者发展为充血性心力衰竭，NYHA分级较术前增高（1．64&#177;0．7对2．27&#177;0．8，P〈0．001），左室射血分数（LVEF）明显较术前降低（60％&#177;6％对51％&#177;13％，P〈0．001）。对LVEF≤40％（A组）和〉40％（B组）的患者对比分析发现，A组较B纽患者的起搏QRS时限为长（181&#177;32ms对151&#177;26ms，P〈0．01）．室间延迟也较长（44&#177;29ms对27&#177;18ms，P=0．02）；起搏QRS时限=180ms时，其检测左室功能异常的敏感性为54％，特异性为93％。结论：左室储备功能正常的房室阻滞患者，起搏后LVEF明显下降，起搏QRS时限可用以预测起搏后左室功能障碍的发生与否。     

阿托伐他汀对心房颤动预防作用及其电生理机制的实验研究

目的探讨阿托伐他汀对心房颤动（房颤）电生理机制的影响。方法 30只新西兰大白兔随机分为对照组、房颤组和阿托伐他汀组,各10只。房颤组和阿托伐他汀组采用快速心房起搏（频率600次/min）制作急性房颤模型,对照组仅植入电极不起搏,阿托伐他汀组起搏前用阿托伐他汀2mg/（kg.d）灌胃7d。观察起搏0,4,8,12,16,20,24h时房颤诱发率、房颤持续时间、心房有效不应期和频率适应性的变化。结果起搏后8,12,16,20,24h房颤组和阿托伐他汀组房颤诱发率高于对照组（P〈0.05）,房颤组高于阿托伐他汀组（P〈0.05）;房颤组和阿托伐他汀组房颤持续时间较对照组延长（P〈0.05）,阿托伐他汀组房颤持续时间的延长较房颤组减少,但差异无统计学意义（P〉0.05）;与对照组比较,起搏4h后房颤组心房有效不应期缩短（P〈0.05）,心房有效不应期频率适应性降低（P〈0.05）,随起搏时间延长呈进行性加重;阿托伐他汀组起搏12h后心房有效不应期高于房颤组（P〈0.05）,起搏8h后心房有效不应期频率适应性的降低较房颤组减少（P〈0.05）。结论阿托伐他汀可有效抑制快速心房起搏兔心房肌的电重构,表现为抑制心房有效不应期缩短和心房有效不应期频率适应性不良,可有效预防房颤发生,但并不影响房颤维持时间。     

经心外膜聚焦超声消融治疗犬心房颤动的实验研究

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)对房颤的影响.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,直视下分别行环肺静脉消融和左房盒式消融.消融前、后记录左房有效不应期(LA-ERP)、计算房颤诱发率、记录房颤持续时间,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LA-ERP较基线水平显著缩短[CPVa组:(140±10)ms vs(102±10)ms,P＜0.01;BOXa组:(139±11)ms vs(105±8)ms,P＜0.01],但消融前后的LA-ERP并无显著性差异[CPVa组:(102±10)ms vs(110 8)ms,P=0.070;BOXa组:(106±7)ms vs(111±7)ms,P=0.225].消融后两组的房颤诱发率均较消融前显著降低[(98±4)%vs(28±10)%,P＜0.01,(97±4)%vs(14±7)%,P＜0.01],房颤持续时间均显著缩短[(233±40)s vs(70±29)s,P＜0.01;(240±41)s vs(34±22)s,P＜0.01];部分犬可见肺静脉一心房双向电传导阻滞;两组间消融前房颤诱发率、房颤持续时间无统计学差别,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 经心外膜聚焦超声环肺静脉消融可显著降低房颤诱发率和缩短房颤持续时间,而左房盒式消融则可进一步提高成功率.     

Characteristics of rapid rhythms recorded within pulmonary veins during atrial fibrillation

Rapid rhythms often arise in the pulmonary veins during atrial fibrillation (AF). The activation patterns within pulmonary veins during these rapid rhythms are not well described. In 39 patients with paroxysmal AF, ostial recordings were obtained during AF in 110 pulmonary veins with a decapolar distal ring catheter. Pulmonary vein tachycardia (PVT) was defined as a pulmonary vein (PV) rhythm that had a cycle length shorter than at the adjacent left atrium. During AF, PVT was recorded in 93% of PV's, usually in the form of intermittent bursts that had a mean duration of 1,325 +/- 647 ms and mean cycle length of 125 +/- 20 ms. The mean cycle length of continuous PVT's (141 +/- 25) was longer than the mean cycle length of intermittent bursts of PVT (P < 0.05). The intermittent PVT's were associated with a shorter left atrial cycle length than were the continuous PVT's. In 90% of PVTs, complex activation patterns attributable to simultaneous recordings from two or more overlapping fascicles were present at a segment of the pulmonary vein ostium, and the mean cycle length of these recordings was 80 +/- 32 ms. PVT during AF is much more often intermittent than continuous. The relationship between PVT cycle length and left atrial cycle length suggests that PVT's influence the left atrium during AF. PVT must be distinguished from recordings within PV's that have a short cycle length as a result of simultaneous recordings from two or more overlapping fascicles.     

The Maximum Effect of an Increase in Rate on Human Ventricular Refractoriness

The purpose of this study was to determine the maximum shortening of ventricular refractoriness that occurs following an increase in rate and to quantitate the duration of ventricular pacing required to obtain this maximum shortening of refractoriness. The subjects of the study consisted of 41 patients who underwent a clinically indicated electrophysiologic study. Ventricular refractory periods were measured with an extrastimulus (S2) at basic cycle lengths of 600 and 400 ms by Method A (8 beat basic drive trains and 4 second intertrain paue and Method B (drive train duration of 3 minutes, then an S2 after every eighth basic drive beat, with no pause after the S2). In 23 subjects, the mean ventricular effective refractory period determined by Method B was 12 +/- 7 ms (+/- standard deviation) shorter than when determined by Method A at a basic drive cycle length of 600 ms (p less than 0.0001) and 33 +/- 9 ms shorter at a basic drive cycle length of 400 ms (p less than 0.001). In these 23 subjects, the drive train duration required for maximum shortening of ventricular refractoriness was estimated by counting the number of drive train beats preceding ventricular capture by an S2 inserted after every fourth basic drive beat at a coupling interval fixed at 5 ms longer than the ventricular effective refractory period determined in that subject by Method B. The mean number of basic drive beats preceding capture by S2 was 114 +/- 84 beats at a basic drive cycle length of 600 ms and 233 +/- 85 beats at a BDCL of 400 ms. In six subjects the ventricular effective refractory period was measured by Methods A and B before and after autonomic blockade with propranolol and atropine, and the amount of shortening in the ventricular effective refractory period with Method B was not affected by autonomic blockade. In conclusion, the basic drive train has a cumulative effect on ventricular refractoriness in humans, and a drive train duration substantially longer than 50 beats often is required to obtain the maximum shortening of ventricular effective refractory period after an increase in rate. Therefore, ventricular effective refractory periods determined conventionally using 8 beat drive trains and a 4 second intertrain pause often may be overestimates of the actual ventricular effective refractory period. The shortening of ventricular refractoriness with long drive train durations is probably related to a prolonged duration of pacing required to obtain a steady-state action potential duration after an increase in rate.     

Mechanisms underlying sustained firing from pulmonary veins: evidence from pacing maneuvers and pharmacological manipulation

Atrial Fibrillation (AF) is often initiated by pulmonary vein (PV) depolarizations. However, sustained PV firing (PVF) is infrequently observed in this population and has not been characterized. In 15 patients undergoing AF ablation we report the response of sustained PVF to pacing and pharmacological maneuvers. Sustained PVF was defined as discrete, repetitive, electrical activity during sinus rhythm that did not correspond with other electrical events (P, QRS, T wave), persisting > or =5 minutes and recorded at/or distal to PV ostium prior to ablation. During sustained PVF, pacing was performed from coronary sinus and/or posterior right atrium at different cycle lengths (900 to 400 ms; duration: 30 to 60 s) following which, if PVF persisted, in random order, isoproterenol and adenosine were administered and carotid sinus massage (CSM) was performed. PVF response was classified as: suppressed (complete quiescence), augmented (increase in frequency of PVF/AF initiation) and "no effect." Sustained PVF was observed in 16 veins. In 13 (81%) patients, PVF was suppressed during overdrive pacing with early recurrence (< or =5 s) postpacing regardless of pacing cycle length in 11 (85%) patients. PVF was augmented by isoproterenol in the majority of patients (88%) and showed mixed response to adenosine (augmented 40%, suppressed 20%, and no effect 40%). CSM appeared to have no effect on PVF in the majority of patients (86%). Sustained PVF is seen infrequently in patients undergoing AF ablation. Its response to pacing maneuvers argues against sustained reentry and supports triggered activity and/or abnormal automaticity as the mechanisms underlying the phenomenon.     

Acute Effects of Different Atrial Pacing Sites in Patients with Atrial Fibrillation: Comparison of Single Site and Biatrial Pacing

It has been reported that a trial single site or biatrial pacing can suppress the occurrence of AF. However, its mechanism remains unclear. The study population included 32 patients with AF (n = 20: AF group), or without paroxysmal AF (n = 12: control group). The mechanism and efficacy of atrial pacing were investigated by electrophysiological studies to determine which was more effective for suppressing AF induction; single site pacing of the right atrial appendage (RAA) or distal coronary sinus (CS-d), or biatrial (simultaneous BAA and CS-d) pacing. In the AF group, AF inducibility was significantly higher with BAA extrastimulus during RAA (12/20; P < 0.0001) or biatrial paced drive (7/20; P < 0.01) than during CS-d paced drive (0/20). In the control group, AF was not induced at any site paced. In the AF group, the conduction delay and other parameters of atrial vulnerability significantly improved during CS-d paced drive. The atrial recovery time (ART) at RAA and CS-d was measured during each basic pacing mode. ART was defined as the sum of the activation time and refractory period, and the difference between ARTs at RAA and CS-d was calculated as the ART difference (ARTD). The ARTD was significantly longer during BAA pacing in the AF group than in control group (155.0 +/- 32.8 vs 128.8 +/- 32.9 ms, P < 0.05). In the AFgroup, ARTDs during biatrial (52.0 +/- 24.2 ms) and CS-d pacing (51.7 +/- 26.0 ms) were significantly shorter than ARTD during RAA pacing. The CS-d paced drive was more effective for suppressing AF induction than biatrial or RAA paced drive by alleviating conduction delay. CS-d and biatrial pacing significantly reduced ARTD compared with RAA pacing.     

Procainamide Induced Change of the Width of the Zone of Entrainment and its Relation to the Inducibility of Reentrant Ventricular Tachycardia

Procainamide depresses conduction velocity and prolongs refractoriness in myocardium responsible for reentrant VT, but the mechanism by which the induction of VT is suppressed after procainamide administration remains to be determined. In the present study, the relationship between electrophysiological parameters and the noninducibility of VT was assessed during procainamide therapy with a special reference to the change of an excitable gap. Clinically documented monomorphic sustained VT was induced in 30 patients and, utilizing the phenomenon of transient entrainment. the zone of entrainment was measured as the difference between the cycle length of VTand the longest paced cycle length interrupting VT (block cycle length) which was determined as the paced cycle length decreased in steps of 10 ms, and used as an index of the excitable gap. The effective refractory period was measured at the pacing site and the paced QBS duration was used as an index of the global conduction time in the ventricle. The cycle length of VT, the block cycle length, and the width of the zone of entrainment were determined and compared between the responders and nonresponders. In 15 patients, these parameters were determined at the intermediate dose and related to subsequent noninducibility at the final dose. At the final doses of procainamide, VT was suppressed in 8 (26.7%) of 30 patients. However, the cycle length of VT, the block cycle length, and the width of the zone of entrainment were unable to predict the drug efficacy, i.e., noninducibility. The change in the effective refractory period at the pacing site or the width of the paced QRS duration was not different between the responders and nonresponders. Among the variables, only the width of the zone of entrainment showed a significant narrowing in the responders at the intermediate dose of procainamide, and it was smaller than that of the nonresponders. The significant narrowing of the width of the zone of entrainment was associated with the subsequent noninducibility of VT at the final dose. The present study showed that the baseline cycle length of VT, the block cycle length, the drug induced change of the effective refractory period, or the paced QRS duration was not a predictor of the noninducibility after procainamide administration. However, a significant narrowing of the width of the zone of entrainment at the intermediate dose was associated with the noninducibility of VT at the final dose.     

Influence of Duration of Rapid Ventricular Pacing on Ventricular Refractoriness in the Presence of Propafenone and Lidocaine

Propafenone and lidocaine have a rate dependent negative dromotropic effect on intraventricular conduction. We investigated the use dependent actions of propafenone and lidocaine on intraventricular conduction in isolated guinea pig hearts perfused by the method of Langendorff. Of primary interest was how the number of stimuli of the conditioning train (S1) might influence the ventricular effective refractory period (VERP) when refractoriness is assessed at a high pacing rate. Propafenone (0.3 μM) and lidocaine (50 μM) caused a comparable prolongation of the intraventricular conduction time during sinus rhythm. During ventricular pacing in the presence of propafenone an abrupt decrease of the pacing cycle length (220 to 120 ms) resulted in an initial peak of rate dependent prolongation of the QRS interval that subsequently decreased to a stable steady-state level. Lidocaine also induced a rate dependent increase of the intraventricular conduction time up to a steadystate level. The time constant, characterizing the changes of the intraventricular conduction time after shortening the ventricular pacing cycle length from 220 to 120 ms was significantly (P < 0.01) longer in the presence of propafenone (τ= 31 ± 4 beats; mean ± SEM; n = 11) than for lidocaine (τ= 3 ± 1; n = 10). Both drugs caused the greatest increase of tbe VERP when the number of conditioning stimuli (S1, interstimulus interval = 120 ms) was in the range of their respective time constant. However, when the number of conditioning stimuli was further increased, VERP progressively diminished. These effects may be explained by a shortening of the action potential during high rates that results in a decreased binding of propafenone to Na⁺ channels and by the direct shortening of repolarization period by lidocaine (Class IB drug).     

快速心室起搏犬心房颤动模型研究

目的建立快速起搏心室致心力衰竭犬房颤模型,研究其电生理及心房结构和功能改变。方法 15只健康杂种犬分两组:对照组6只,实验组9只[240次/min心室起搏(25±3)d]。超声心动图测定起搏前后心房面积、面积缩小分数及左心室功能,利用心内电极测定心房有效不应期、传导速度及房颤诱发情况。结果实验组7只犬完成了实验。快速心室起搏(25±3)d后,犬的收缩末期和舒张末期左、右心房面积显著增大(与起搏前比较,P<0.01),左、右心房面积缩小分数显著减小(左心房:(35.7±1.9)%和(20.7±2.7)%,P<0.01;右心房:(35.0±2.3)%和(18.0±2.3)%,P<0.01),左室射血分数从(65.3±2.1)%降至(31.6±2.8)%(P<0.01)。实验组犬左、右心房有效不应期显著延长,心房内传导速率较对照组减慢。实验组有5只犬诱发出超过30 min的房颤,平均房颤持续时间较对照组显著延长(687±290)s和(13±9)s,P<0.01)。实验组平均房颤持续时间与左、右心房面积及面积缩小分数相关(P<0.05)。结论 快速心室起搏致心衰模型能稳定地诱发出房颤,房颤持续时间与心衰引起的显著心房结构和功能异常相关。     

Refractory Period Extension During Ventricular Pacing at Fibrillatory Pacing Rates

Refractory period extension (RPE) bas been proposed as a basic mechanism for defibrillation but it remains unclear if RPE exists at the fast rates associated with ventricular fibrillation. In 7 pentobarbital anesthetized dogs, we measured refractory periods with and without 8 ms rectangular transcardiac shocks at left ventricular pacing rates of 200–600 beats/min. To achieve these high rates, an incremental rate pacing method was used to produce pacing train timing sequences requiring 4.5–27 seconds. A variably timed premature stimulus followed the last stimulus in each pacing train. To determine refractoriness, a 128 electrode arrav (4 × 4 cm) was used to detect the presence, or absence of an activation sequence sweeping away from the pacing site. At each rate, a control refractory period (RPc) was measured and refractory periods were also measured for 8 and 12 V/cm shocks with coupling intervals of 60% to 90% of RPc. RPc decreased as the rate increased with a minimum RPc of 94 ms at a rate of 600 beats/min (100 ms cycle length). RPE/RPc versus shock coupling interval was similar at all pacing rates. RPE/RPc increased with increased coupling interval or higher shock intensity. We conclude that during ventricular pacing at fibrillatory rates tissue is nearly always in a refractory state: that RPE exists at fibrillatory activation rates; and that RPE/RPc versus shock coupling interval does not vary strongly with pacing rate. These findings support the hypothesis that RPE contributes to defibrillation.     

Summation of Excitation with a Single Conditioning Stimulus in the Canine Heart

A subthreshold stimulus was reported to become effective in producing a propagated ventricular response when preceded by another subthreshold stimulus or stimuli, a phenomenon that is known as summation of excitation but has not been studied systematically. Effect on summation of current intensity and coupling interval of a conditioning stimulus (Sc, protocol #1) and that of stimulation site of Sc (protocol #2) were determined in anesthetized, open-chest dogs. Effective refractory period (ERP) was determined with an extrastimulus (S2) at a ventricular pacing cycle length (S1S1) of 500 msec. Pulse width of S1, S2 and Sc was 2 msec. For pacing protocol #1 (12 dogs), current intensity of S1 and S2 was equal (twice diastolic threshold, 2, 5, or 15 mA), and that of Sc was equal to or lower than that of S1. S1S2 interval was fixed 1 msec shorter than ERP, and Sc was delivered 5 msec prior to S2. The S1Sc interval was shortened in 2 msec steps. Summation was present if Sc plus S2 evoked a propagated response. Prevalence of summation increased along with an increase in current intensity of Sc (P less than 0.01). For pacing protocol #2 (7 dogs), current intensity of S1, S2 and Sc was equal (twice diastolic threshold, 5 or 10 mA). As the distance between site of Sc and that of S2 increased, prevalence of summation decreased (P less than 0.01). Summation did not occur when Sc was delivered at a site only 5 mm away from the site of S2. In conclusion, summation of excitation with a single conditioning stimulus was both time and strength dependent, and limited in development spatially.     

Electrophysiological differences between the epicardium and the endocardium of the left atrium

Background: Electrophysiological properties of the atrial endocardium compared to epicardium are not well understood. The purpose of this study was to compare the electrophysiological properties and vulnerability to arrhythmia induction from these regions. Methods and Results: Transseptal endocardial and percutaneous epicardial mapping were performed in a porcine model (n = 7). Two opposing 4‐mm electrophysiological catheters were positioned endocardially and epicardially. A circular mapping catheter (CMC) was positioned at the ostium of the common inferior pulmonary vein (CIPV) recording left atrial (LA)‐PV potentials. Endocardial and epicardial effective refractory periods (ERPs) at two basic cycle lengths (CLs) of 600 and 400 ms were recorded from four anatomic locations (CIPV, LA appendage, right superior PV, and LA posterior wall). Atrial repetitive response (ARR) induction was also tested from endocardial and epicardial sites. Overall, 254 ERP measurements (mean 36.3 per animal) and 84 induction attempts (mean 12 per animal) were performed. The ERP was significantly shorter in the epicardium compared to the endocardium at basic CL of 400 ms (P = 0.006) but not at CL of 600 ms (P = 0.2). In addition, only the epicardium demonstrated ERP shortening when the CL of the basic drive was shortened (P = 0.03). ARR could be induced more often from the epicardium (P = 0.002) and fibrillatory activity with epicardial/endocardial dissociation was recorded (n = 3). Also, the earliest PV activation site on the CMC was noted to be different in 16.5% of cases during epicardial and endocardial pacing. Conclusion: The electrophysiological characteristics of the atrial epicardium are different from the endocardium with a shorter ERP and more frequent ARR induction by programed stimulation. (PACE 2011; 37–46)