Atrioventricular Nodal Conduction Rather than Automaticity Determines the Ventricular Rate During Atrial Fibrillation and Atrial Flutter

AV Nodal Conduction During Atrial Fibrillation and Flutter . Introduction: Recent clinical studies have advanced the hypothesis that the atrioventricular (AV) node does not conduct cardiac impulses, but functions as a pacemaker whose discharge rate and rhythm are modulated electrotonically by atrial impulses. Major support for the hypothesis comes from the observation that the short ventricular cycles during atrial fibrillation can be totally eliminated by ventricular pacing at relatively long ventricular cycle lengths. Methods and Results: The hypothesis was tested in ten anesthetized open chest mongrel dogs with sustained atrial fibrillation or atrial flutter (AF). Large differences (> 120 msec) between the ventricular pacing cycle length that achieved > 95% ventricular capture and the shortest spontaneous RR cycle during AF were considered to be consistent with the modulated AV nodal pacemaker hypothesis, while values ≤ 120 msec were not. The results showed that the ventricular pacing cycle length capturing > 95% of ventricular complexes during AF depended on the spontaneous ventricular rate during AF. Short spontaneous RR cycles during AF required short ventricular pacing cycle lengths to achieve > 95% capture, and the difference between the ventricular pacing cycle length and the shortest spontaneous RR cycle length was narrow, i.e., ≤ 120 msec. Slower ventricular rates could be captured at longer ventricular pacing cycle lengths, and the difference between the ventricular pacing cycle length capturing > 95% of the ventricular complexes and the shortest spontaneous RR interval during AF was large, i.e., > 120 msec. A continuum existed, and values ≤ 120 msec could be transformed to values > 120 msec by increasing vagal intensity to slow the ventricular response. We also found in five dogs that we could not achieve overdrive suppression of automaticity of the putative AV nodal pacemaker focus by ventricular pacing at various cycle lengths and durations during atrial fibrillation. Conclusion: In conclusion, data from this study fail to support the modulated AV nodal pacemaker hypothesis and are more consistent with conventional concepts of AV nodal conduction.     

基础起搏周长对心房和房室传导系统不应期的影响

目的 探讨不同心房基础起搏周长(BCL)对心房、房室传导系统和旁道前向传导不应期的影响.方法 对30例患者行食管心房调搏检查,测定三个不同心房BCL下心房、房室传导系统功能和有效不应期,以及静脉注射普罗帕酮后起搏周长对不应期的影响.结果 随着心房BCL的缩短,心房有效不应期(AERP)、和旁道前向传导有效不应期及房室传导功能不应期(AVFRP)逐渐缩短(P<0.05和0.001),房室传导时间和有效不应期延长(P<0.05),房室结快、慢径路有效不应期无改变.注射普罗帕酮后心房BCL的改变对AERP和AVFRP无明显影响(P>0.05).结论 心房BCL可影响房室传导系统的不应期和传导性,这一作用与交感神经兴奋时的改变不同,应用抗心律失常药物后房室传导系统不应期不受心房BCL的影响.     

房室顺传和逆传对窦房结功能低下动物模型心房电生理学特性的影响

探讨房室顺传和逆传对窦房结功能障碍时心房电生理特性的影响。选择 6 0只健康新西兰大耳白家兔 ,开胸打开心包膜 ,于上腔静脉与右心耳交界处消融 ,有 5 0只成功建立单纯窦房结功能低下动物模型 ,随机分为心房起搏 (1∶1房室顺传 )组 ,心室起搏组 (又分 1∶1房室逆传组以及非 1∶1房室逆传组 )。观察房室顺传及房室逆传 1,2 ,4h以及 7d后 ,心房有效不应期 (AERP)、心房激动时间 (A2 )和心肌波长指数 (WLI)发生的变化。结果 :心室起搏 ,若存在 1∶1房室逆传 ,AERP缩短 ,A2 延长 ,WLI减小 ;若无 1∶1房室逆传 ,则AERP逐渐延长 ,A2 无明显变化 ,WLI增大。比较 1∶1房室逆传组与非 1∶1房室逆传组发现 ,同时段两组间AERP ,A2 和WLI存在显著性差异。同时发现 ,心房起搏 ,窦房结功能低下模型的AERP延长 ,A2 缩短 ,WLI增大。结论 :房室逆传能增加单纯窦房结功能低下动物模型电不稳定性 ,房室顺传则能抑制单纯窦房结功能低下动物模型心房电紊乱。     

国产美托洛尔静脉制剂控制阵发性心房颤动时快速心室反应的疗效评价

目的：研究国产美托洛尔静脉制剂用于控制阵发性心房颤动时快速心室率的效果。方法：３３例阵发性心房颤动患者分别接受了静脉美托洛尔（美托洛尔组，１６例）和毛花甙Ｃ（毛花甙Ｃ组，１７例）治疗。结果：１６例接受静脉美托洛尔５ｍｇ治疗的患者用药３０分钟后心室率从１２８±２１次／分降至９０±１８次／分（Ｐ＜０００１）；接受静脉毛花甙Ｃ０．４ｍｇ至０．６ｍｇ治疗者用药３０分钟后的心室率从１３４±１７次／分降至１０８±１７次／分（Ｐ＜００１）；用药３０分钟后美托洛尔组心率明显慢于毛花甙Ｃ组（Ｐ＜００１），而与毛花甙Ｃ组６小时后的心室率相当（８４±１８次／分，Ｐ＞００５）。两组患者用药前后的血压无明显变化。所有患者都没有因为药物副作用而终止试验。结论：国产美托洛尔静脉制剂能迅速有效和安全地控制阵发性心房颤动时快速心室反应     

Chronic Augmentation of the Parasympathetic Tone to the Atrioventricular Node: A Nonthoracotomy Neurostimulation Technique for Ventricular Rate Control During Atrial Fibrillation

Long‐Term Cardiac Neurostimulation. Introduction: The right inferior ganglionated plexus (RIGP) selectively innervates the atrioventricular node. Temporary electrical stimulation of this plexus reduces the ventricular rate during atrial fibrillation (AF). We sought to assess the feasibility of chronic parasympathetic stimulation for ventricular rate control during AF with a nonthoracotomy intracardiac neurostimulation approach. Methods and Results: In 9 mongrel dogs, the small endocardial area inside the right atrium, which overlies the RIGP, was identified by 20 Hz stimulation over a guiding catheter with integrated electrodes. Once identified, an active‐fixation lead was implanted. The lead was connected to a subcutaneous neurostimulator. An additional dual‐chamber pacemaker was implanted for AF induction by rapid atrial pacing and ventricular rate monitoring. Continuous neurostimulation was delivered for 1–2 years to decrease the ventricular rate during AF to a range of 100–140 bpm. Implantation of a neurostimulation lead was achieved within 37 ± 12 min. The latency of the negative dromotropic response after on/offset or modulation of neurostimulation was <1 s. Continuous neurostimulation was effective and well tolerated during a 1–2 year follow‐up with a stimulation voltage <5 V. The neurostimulation effect displayed a chronaxie‐rheobase behavior (chronaxie time of 0.07 ± 0.02 ms for a 50% decrease of the ventricular rate during AF). Conclusion: Chronic parasympathetic stimulation can be achieved via a cardiac neurostimulator. The approach is safe, effective, and well tolerated in the long term. The atrioventricular nodal selectivity and the opportunity to adjust the negative dromotropic effect within seconds may represent an advantage over pharmacological rate control. (J Cardiovasc Electrophysiol, Vol. 21, pp. 193‐199, February 2010)     

Slowing of the Atrial Flutter Rate During 1:1 Atrioventricular Conduction in Humans and Dogs: An Effect Mediated Through Atrial Pressure and Volume

Atrial Flutter Rate and Atrial Pressure . Introduction: During atrial flutter the effects of 1:1 atrioventricular (AV) conduction on the rate of atrial flutter was studied in 12 patients and 14 dogs. Methods and Results: (A) In all patients, the development of 1:1 AV conduction was associated with a significant increase in flutter cycle length (261.7 ± 9.9 to 281.8 ± 12.1 msec, mean increase 20.3 ± 3.2 msec, P < 0.001). The flutter cycle length returned to control values when 1:1 AV conduction ceased. In four patients in whom atrial pressure was monitored, the prolongation of the atrial flutter cycle interval during 1:1 AV conduction was associated with an immediate rise in atrial pressure (4.0 ± 0.4 to 6.5 ±0.7 mmHg, P < 0.003). (B) In order to examine the mechanism of this phenomenon, similar studies were carried out in dogs with experimentally induced atrial flutter. 1:1 AV conduction consistently lengthened the flutter cycle length during control conditions or following vagotomy and during the administration of isoproterenol. This was always associated with a rise in atrial filling pressure. Inferior vena cava occlusion consistently shortened the flutter cycle length and this was also independent of vagotomy and isoproterenol administration. The atrial filling pressure fell during inferior vena cava occlusion. During 1:1 AV conduction, the prolonged flutter cycle length was shortened by inferior vena cava occlusion to values prior to 1:1 AV conduction. Conclusion: The rate of atrial flutter is accelerated by reductions in atrial pressure, and slowed by increased atrial pressure. These effects are independent of the vagus nerve or an adrenergic agonist. Changes in atrial pressure and volume affect characteristics of the atrial flutter circuit, and thus can modulate the rate of atrial flutter.     

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?     

预激综合征合并心房颤动与房室旁道位置分布的关系

为探讨预激综合征合并心房颤动（简称房颤）的临床特点和机制以及与房室旁道位置分布的关系，对经导管射频消融（连续治疗）成功的２９８例预激综合征患者进行了分析，其中２６例患者既往心电图证实有房颤发作。结果表明：显性旁道合并房颤（２２／１７４，１３％）多于隐匿性旁道（４／１２４，３％），Ｐ＜０．００５；右侧旁道（１７／１０５，１６％）多于左侧旁道（９／１９３，５％），Ｐ＜０．０５；右侧显性旁道（１６／９０，１８％）多于左侧显性旁道（６／８４，７％），Ｐ＜０．０１。即显性旁道尤其是右侧显性旁道合并房颤较多。支持显性旁道患者心室收缩提前（右侧旁道心室激动发生得更早）导致心房内压升高及电不稳定是预激综合征患者房颤发生机制的论点     

Rhythm versus Rate Control Trials in Atrial Fibrillation

The recent completion of five trials comparing the strategy of rhythm control versus the strategy of rate control in the management of recurrent atrial fibrillation has advanced considerably our understanding of the treatment of this common clinical problem. The background to this research question is outlined, followed by an overview of the five trials and their results. Data on important clinical events from four of the trials are pooled and presented. The aggregate results of the trials do not demonstrate any clear advantage of the rhythm control approach. The findings elevate rate control to the position of an acceptable primary therapy in the types of patients studied and underline the concept that the primary goal of antiarrhythmic therapy for atrial fibrillation at this time is control of symptoms. Under these circumstances, a "safety first" approach is prudent and monitoring for adverse drug effects is mandatory. The results underscore the importance of continuous anticoagulation in patients with stroke risk factors. Finally, the results from these trials help to set the agenda for future research on rhythm management in atrial fibrillation. (J Cardiovasc Electrophysiol, Vol. 14, pp. S35-S39, September 2003, Suppl.)     

Left Atrial Conduction Along the Coronary Sinus During Ectopic Atrial Tachycardia and Atrial Fibrillation:

Introduction: Correlation function analysis was applied to endocardial electrograms to investigate conduction patterns along the coronary sinus (CS) during sinus rhythm (SR) and atrial tachycardias.
Methods and Results: Eighteen recordings were obtained from 14 patients with supraventricular tachycardias. Five atrial fibrillation (AF) recordings were compared to 10 SR recordings and 3 ectopic atrial tachycardia (EAT) recordings. The maximum correlation coefficient was used to assess similarity between signals, i.e., if they originate from the same wavefront. The cumulative time delay, calculated as pairwise summation of interelectrode time delays, was used as an indicator of activation sequence along the CS. Method validation using SR showed right-to-left conduction with high correlations in 8 of 10 recordings indicating one single wavefront. EAT recordings showed consistent left-to-right conduction with left atrial foci and right-to-left with right atrial focus and lower correlations than SR. All 5 AF recordings showed predominantly left-to-right conduction direction, also with correlations lower than SR.
Conclusion: (1) Correlation function analysis can be used to assess agreement between signals and direction of activation spread. (2) Due to the position of CS, the results can be used to derive mechanisms of interatrial conduction. (3) Consistency in electrical activity propagation along CS is common in AF. (J Cardiovasc Electrophysiol, Vol. 14, pp. S148-S153, October 2003, Suppl.)     

室房逆传对窦房结功能及心房肌电活动影响及其意义的实验研究

目的:探讨室房逆传(VAC)对兔窦房结功能低下动物模型窦房结功能及心房肌电活动的影响.方法:选用40只健康新西兰大耳白家兔,其中32只成功制作窦房结功能低下动物模型,以200次/分的起搏频率起搏右心室,将家兔分为1:1VAC组(22只)、非1:1VAC组(10只).观察心室起搏1 h,2 h,4 h,7 d后窦房结功能低下家兔模型右心房压、心房有效不应期、心房激动时间、心肌波长指数、校正窦房结恢复时间的变化,并比较两组上述指标的差别.结果:①1:1VAC组心室起搏1 h后右心房压明显升高(P＜0.01),心房有效不应期、心房激动时间、心肌波长指数、校正窦房结恢复时间无明显变化(P＞0.05);2 h后右心房压继续升高(P＜0.01),校正窦房结恢复时间、心房激动时间延长(P＜0.01),心房有效不应期缩短(P＜0.01),心肌波长指数减小(P＜0.01);4 h后上述指标变化更明显(P＜0.01);7 d后右心房压恢复至原来水平(P＞0.05),心房有效不应期、心房激动时间、心肌波长指数、校正窦房结恢复时间变化更明显(P＜0.01).②非1:1VAC组心室起搏1 h后右心房压明显升高(P＜0.01),校正窦房结恢复时间、心房有效不应期、心房激动时间、心肌波长指数无明显变化(P＞0.05);2 h、4 h后右心房压进一步升高(P＜0.01),校正窦房结恢复时间、心房有效不应期、心房激动时间、心肌波长指数无明显变化(P＞0.05);7 d后右心房压恢复至原来水平(P＞0.05),心房有效不应期、心房激动时间缩小(P＜0.05),校正窦房结恢复时间、心肌波长指数无明显变化(P＞0.05).③1:1VAC组与非1:1VAC组比较:1 h时两组间右心房压、校正窦房结恢复时间、心房有效不应期无明显变化(P＞0.05),但1:1VAC组心房激动时间延长(P＜0.05)、心肌波长指数减小(P＜0.05);2 h时右心房压、心房有效不应期无明显变化(P＞0.05),1:1VAC组校正窦房结恢复时间、心房激动时间明显延长(P＜0.01),心肌波长指数明显减少(P＜0.01);心室起搏4 h,7 d后右心房压无明显变化(P＞0.05),但1:1VAC组心房有效不应期、校正窦房结恢复时间、心房激动时间、心肌波长指数变化更明显(P＜0.01).结论:VAC对窦房结功能及心房肌电活动能产生不良影响.病态窦房结综合征患者应尽量避免使用VVI起搏器,最好安装生理性起搏器.     

房室结消融及起搏器治疗改善心房颤动患者心功能和生活质量的研究

探讨房室结消融 +VVIR起搏器 (ABL +PM)治疗对永久性心房颤动 (简称房颤 )患者生活质量、心功能的改善及评估该治疗的安全性。选择 30例永久性房颤患者 ,14行例ABL +PM治疗 ,16例行药物治疗。治疗前及治疗后 12个月所有患者均做GWB和CSS生活质量评分 ,心脏超声测左室内径及射血分数值 ,活动平板测运动耐力 ,用Holter记录最快、最慢心率。并观察治疗后临床事件的发生。结果 :永久性房颤患者ABL +PM或药物治疗前、后组内比较 ,患者心室率、心功能、运动耐力及生活质量均得到改善 (P <0 .0 5 ) ;但ABL +PM组左室内径缩小 (P <0 .0 5 ) ,药物治疗组无改变 (P >0 .0 5 )。ABL +PM或药物治疗后 12个月组间比较 ,ABL +PM组心室率控制、左室内径、心功能、运动耐力及生活质量改善优于药物组 (P <0 .0 5 )。再次住院人次ABL +PM组较药物组减少 (P <0 .0 5 ) ,死亡、恶性室性心律失常和血栓栓塞事件两组无差异 (P >0 .0 5 )。结论 :ABL +PM或药物治疗均能改善永久性房颤患者心功能、运动耐力及生活质量 ,但ABL +PM优于药物治疗。ABL +PM是一种简单易行安全的治疗方法。     

The Relation Between Hypertrophied Myocardium and Ventricular Fibrillation Threshold in Spontaneously Hypertensive Rats

Objectives To investigate the relation between hypertrophied myocardium and ventricular fibrillation threshold in spontaneously hypertensive rats (SHR). Methods 20 male SHR were randomly divided into two groups; 10 week group (n = 10) and 18 week group (n=10). 10 week male Wistar rats were controlled group (n=10). The systolic blood pressure (SBP), heart mass index (HMI), ventricular effective refractory period (VERP) and ventricular fibrillation threshold(VFT) were measured respectively. Results①The SBP and HMI of SHR were significantly higher than those of Wistar rats(P < 0.001). The VFT of SHR were significantly lower than that of Wistar rats (P < 0.001).②In SHR, the SBP and HMI of 18 week SHR were significantly higher than those of 10 week SHR (P< 0.001). The VFT of 18 week SHR were significantly lower than that of 10 week SHR (P < 0.001).③There were no significant difference of VERP among 10 week SHR, 18 week SHR and Wistar rats(P > 0.05).④There was no relationship between HMI and VFT or SBP in Wistar rats. There was significant relationship between HMI and VFT or SBP in different age spontaneously hypertensive rats.⑤HMI, age and species of animal were the major influent factors of VFT. Conclusions The VFT of hypertrophied myocardium decreased. The higher the degree of hypertrophy of myocardium and the higher the systolic blood pressure were, the lower the ventricular fibrillation threshold was.     

肾素血管紧张素系统和心房颤动

肾素 血管紧张素系统 (RAS)是机体重要的神经内分泌系统之一 ,对机体血压和体液、电解质平衡起重要调节作用。近年来的研究表明 ,RAS和心房颤动有关。在房颤动物模型和房颤患者都发现了RAS激活证据 ,RAS激活后通过多种机制影响心房结构和电生理特性 ,从而影响房颤的发生和维持 ,采取不同措施干预RAS已取得了有益作用 ,本文将对上述内容做一综述。     

孤立性心房颤动患者心率变异与 P 波离散度的相关性研究

目的:探讨孤立性心房颤动患者心率变异性(HRV)与P波离散度(Pd)的关系.方法:在动态心电图上分析30例孤立性心房颤动患者(房颤组)的心率变异性指标,包括孤立性心房颤动发作前、后5分钟的时域、频域指标:RR间期的标准差、低频段功率、高频段功率以及低频段功率/高频段功率和24小时时域指标:全部RR间期的标准差、每5分钟平均RR间期的标准差、相邻RR间期差值的均方根和相邻RR间期差值大于50ms的心搏数占总心搏数的百分比,并计算P波最大宽度与P波离散度,再与30例正常对照组进行比较.结果:①对孤立性心房颤动患者发作前、后5分钟的时域、频域指标进行比较,可见孤立性心房颤动患者发作前5分钟RR间期的标准差、高频段功率较发作后5分钟增高(P＜0.05),而低频段功率/高频段功率降低(P＜0.05),差异有统计学意义,低频段功率无明显变化(P＞0.05).②24小时时域分析显示房颤组的全部RR间期的标准差、每5分钟平均RR间期的标准差、相邻RR间期差值的均方根和相邻RR间期差值大于50ms的心搏数占总心搏数的百分比高于正常对照组(P＜0.01),差异有统计学意义.③房颤组的P波最大宽度、P波离散度高于正常对照组(P＜0.01),差异有统计学意义.④房颤组的全部RR间期标准差、每5分钟平均RR间期的标准差、相邻RR间期差值的均方根和相邻RR间期差值大于50ms的心搏数占总心搏数的百分比与P波最大宽度、P波离散度呈正相关(P＜0.01),差异有统计学意义.结论:孤立性心房颤动患者迷走神经张力增高,特别在发作前迷走神经张力有明显增强,并且其P波最大宽度、P波离散度显著增高,两者之间有一定的相关性,可能是孤立性心房颤动的发病机制之一.     

Refractoriness and Conduction Interaction During Modulation of Non-Ischemic Ventricular Fibrillation by Flecainide

Purpose: To study refractoriness and conduction interaction during modulation of non-ischemic ventricular fibrillation (VF) by flecainide. Methods: Isolated feline and rabbit hearts were used. (a) In the feline hearts (n = 8), electrophysiological parameters were measured before and after flecainide administration (0.6, 1.2 × 10^–6 M). During pacing the parameters were: epicardial conduction time, refractoriness and 1:1 pacing/response capture. During 8 min of electrically-induced tachyarrhythmias they included heart rate and normalized entropy reflecting the degree of organization. (b) In rabbit hearts (n = 4), three-dimensional mapping was performed before and after flecainide administration (2 × 10^–6 M). To follow changes in organization, local RR-intervals and differences in activation time between adjacent epicardial electrodes were measured immediately and 80 sec after VF induction. Results: In feline hearts with flecainide, fibrillation was more difficult to induce, more frequently terminated spontaneously and was slower and more organized; conduction time was markedly lengthened, and refractoriness less than 1:1 capture, was moderately prolonged. An inverse correlation was observed between arrhythmia properties, rate and organization, and changes in refractoriness and conduction time. In rabbit, the number of wave fronts was reduced, RR-intervals were prolonged but at the same time activation time differences between adjacent electrodes were smaller following flecainide administration. Conclusions: It is suggested that flecainide modulation of VF properties is associated with conduction suppression and refractoriness prolongation, which act in a synergistic, additive way.     

粉防己碱抗豚鼠再灌注早期心室颤动及其机制

目的：探讨粉防己碱抗豚鼠再灌注早期心室颤动作用及其机制。方法：利用心肌缺血再灌注损伤模型，研究粉防己碱对再灌注早期心脏去甲肾上腺素（ＮＡ）释放及心室颤动发生的影响。结果：①粉防己碱使心脏流出液中ＮＡ含量从每克心脏组织３．７２±０．９６ｐｍｏｌ／ｍｉｎ减低为０．７８±０．３６ｐｍｏｌ／ｍｉｎ（ｎ＝７，Ｐ＜０．００１）。②粉防己碱可明显降低再灌注早期心室颤动的发生（Ｐ＜０．０５）。结论：粉防己碱可明显减少再灌注早期心交感神经递质ＮＡ的释放，同时可明显减少心室颤动发生。该减少再灌注早期心交感神经递质ＮＡ释放的作用应是抗再灌注性心律失常—心室颤动作用机制之一。     

房室折返性心动过速合并阵发性心房颤动的射频导管消融策略

目的探讨房室折返性心动过速（AVRT）合并阵发性心房颤动的射频导管消融（下称消融）策略。方法对经电生理检查证实的AVRT患者15例行旁道消融术,其中男性9例,女性6例,并对术后心房颤动的转归进行12～36个月的随访,观察心房颤动发生、持续时间、有无心律失常等情况。结果13例未再发生心房颤动,2例有严重器质性心脏病的患者仍有阵发性心房颤动复发,但发作次数明显减少,口服胺碘酮可控制症状。1例动态心电图示频发房性期前收缩。结论AVRT与阵发性心房颤动发生率增高密切相关,AVRT是心房颤动的触发因素。旁道消融后,阵发性心房颤动可明显改善,未改善者与心房扩大等心房基质未改善有关。