Retrograde Supernormal Conduction in Concealed Accessory Atrioventricular Pathway Following Catheter Ablation

Supernormal Conduction in Concealed Kent Following Ablation. A case is presented of a 63-year-old woman with a concealed accessory pathway that exhibited retrograde supernormal conduction after radiofrequency catheter ablation. Although ventricular pacing at a slow rate revealed no retrograde conduction over the accessory pathway following ablation, the tachycardia recurred 15 months later. During ventricular pacing there was retrograde 1:1 conduction over the accessory pathway at a fast rate while there was intermittent VA dissociation with rare retrograde conduction at the slower rate. Ventricular extrastimulus testing demonstrated a supernormal conduction zone of the coupling interval. Thus, accessory pathways may exhibit supernormal conduction after catheter ablation. Pacing should be performed at both slow and fast rates to confirm the presence of conduction block following ablation.     

预激综合征旁道传导的裂隙现象

通过分析1例预激综合征旁道传导发生的裂隙现象,探讨了旁道裂隙现象可能的发生机理,并就其诊断及临床意义等问题进行了讨论。就作者所知,在国内外文献中,本文首次证实旁道也可发生裂隙现象。     

Clinical and Experimental Evidence of Supernormal Excitability and Conduction

True supernormality of excitability and conduction has been demonstrated in normal Purkinje fibers in in vitro studies. In the clinical setting, supernormality of conduction is manifested better than expected. This phenomenon is much more common than previously thought, particularly in the presence of certain clinical conditions. If a careful scanning of the cardiac cycle is performed on all patients with intermittent bundle branch block and second degree or advanced infranodal AV block, accessory pathways and mulfunctioning pacemakers, it is anticipated that a much larger amount of supernormal excitability and conduction will be unmasked.     

Impulse Formation and Conduction of Excitation in the Atrioventricular Node

AV Nodal Conduction. Meijler et al. have recently challenged the classical concept of AV nodal conduction (the conduction hypothesis) and suggest that the AV node might he controlling ventricular rhythmicity through its automaticity electrotonically modulated In atrial excitation (the modulated pacemaker hypothesis). This article critically evaluates the three major arguments of Meijler: (1) the absence of convincing evidence for conduction of excitation in the AV node; (2) the prevalence of disproportionately short AV intervals in larger animals; and (3) elimination of KR intervals shorter than the cycle length of ventricular pacing during atrial fibrillation, to judge which of these two hypotheses would more satisfactorily explain various experimental and clinical findings accumulated in the past. Previous observations including microelectrode mapping of the rabbit AV junction during regular sinus rhythm as well as second–degree AV block, clinical and experimental studies on concealed conduction, and studies on the ventricular response to atrial fibrillation appear to he compatible with the conduction hypothesis, whereas clearcut evidence for automatic impulse formation in the AV node has not been presented, except in a small number of hearts showing spontaneous AV junctional rhythms. In view of these observations and theoretical considerations based on comparative anatomy of the AV node–His–Purkinje system and on the latest experimental study on the equine AV node, the authors conclude that the conduction hypothesis appears to better explain all the available data, except perhaps in a few cases with second–degree intra–AV nodal block.     

心房超常传导与房性心律失常相关性探讨

目的：探讨心房超常传导（ＳＮＣ）与房性心律失常发生之间的关系。方法：按常规行心内电生理检查，观察有无ＳＮＣ发生及心房超常传导带与传导时间最大减少值。结果：有自发或诱发房性心律失常者（Ⅰ、Ⅱ组），ＳＮＣ检出率较无自发或无诱发房性心律失常者（Ⅲ组）明显增加（Ｐ＜０．０５）；３６例有ＳＮＣ者中２０例（５５．５６％）有自发或诱发的房性心律失常，而３９例无ＳＮＣ者中仅８例（２０．５１％）有自发或诱发的房性心律失常，两者比较相差非常显著（Ｐ＜０．００５）。结论：ＳＮＣ与房性心律失常的发生密切相关。     

Decremental Conduction in the Posterior and Anterior AV Nodal Inputs

The role for fiber orientation as a determinant of conduction and block in the posterior (slow pathway, SP) and anterior (fast pathway, FP) AV nodal inputs was examined using multiple extracellular bipolar and intracellular microelectrode recordings in the superfused canine AV junction (N = 14). Results: In both inputs, antegrade longitudinal conduction velocity decremented in association with decreased action potential amplitude and dV/dt _max. A similar decrement was also present in the SP transverse to fiber orientation. SP conduction block occurred preferentially near its insertion into the compact AV node with very slow conduction (0.05 ± 0.01 M/sec) preceding conduction block. Distal antegrade FP conduction block occurred before conduction block occurred at more proximal FP sites. Conduction in the distal FP was maintained at a higher velocity (0.11 ± 0.01 M/sec, p < 0.05 vs. SP) before 2:1 conduction block was observed. Conduction velocity, action potential amplitude, and dV/dt _max were not different at any SP or FP site for paired activation transverse and longitudinal to fiber orientation. Conclusions: The data do not demonstrate a role for fiber orientation determining decremental conduction and block in transitional cell AV nodal inputs. Decremental conduction in both the SP and FP inputs is consistent with a proximal-to-distal gradient in resting membrane potential, action potential amplitude, dV/dt _max, and intracellular excitability in transitional cells during antegrade activation.     

Simultaneous dual fast and slow pathway conduction upon induction of typical atrioventricular nodal reentrant tachycardia: electrophysiologic characteristics in a series of patients

INTRODUCTION: Simultaneous dual atrioventricular nodal conduction (SDNC) through slow (SP) and fast pathway (FP) is a rare phenomenon observed upon the induction of atrioventricular nodal reciprocating tachycardia (AVNRT). The aim of this study is to report the electrophysiological features of patients showing typical AVNRT induced through SDNC. METHODS AND RESULTS: Among 461 consecutive patients with typical AVNRT submitted to radiofrequency catheter ablation (RFCA), seven patients (1.5%) with SDNC at tachycardia onset (group I: 6 female; age 60-72 years, mean 65.2 +/- 3.8 years) and 118 age-matched controls (group II: 60 female; age 60-88 years, mean 68.4 +/- 6.8 years) were considered. Controls were further subdivided into two subgroups according to age: subgroup A (94 patients, age 60-75 years) and subgroup B (24 patients, age >75 years). The value of the following parameters was significantly higher in group I than in group II and in subgroup A: A-H interval [113 +/- 26 vs. 89 +/- 27 (P < 0.01) vs. 84 +/- 19 (P < 0.001)], ventriculoatrial conduction effective refractory period [355 +/- 85 vs. 293 +/- 87 (P < 0.05) vs. 281 +/- 82 (P < 0.05)], SP conduction time upon AVNRT induction [444 +/- 104 vs. 350 +/- 72 (P < 0.01); vs. 345 +/- 67 (P < 0.001)], AVNRT cycle length [484 +/- 103 vs. 396 +/- 71 ms (P < 0.05); vs. 384 +/- 69 (P < 0.05)], and rate of AVNRT induction from ventricle [71% vs. 10% (P = 0.001); vs. 6% (P = 0.001)]. Differences were mostly not significant between group I and subgroup B. SP location and RFCA success rate were similar in all groups. CONCLUSION: In a population of AVNRT patients, SDNC at AVNRT induction is infrequent and it prevails beyond the fifth decade of life and in females. SDNC is associated with peculiar AVN conduction features, which resemble the age-related modifications of AVN conduction.     

房室传导不典型文氏现象的心电图特点及临床意义

目的探讨房室传导不典型文氏现象的心电图特点及临床意义。方法回顾性分析9例(其中男6例,女3例,年龄19～81岁)房室传导不典型文氏现象的临床资料。结果9例房室传导不典型文氏现象病例中,1例为单纯房室阻滞,1例交替性文氏传导,2例非交替性文氏传导,5例房室结双径路。其中4例为病理性阻滞伴严重器质性心脏病,其他为迷走高敏所致生理性阻滞。结论年轻患者不典型文氏型房室阻滞者以迷走高敏所致功能性阻滞多见,有器质性心脏病者发生不典型文氏现象时,心电图表现复杂并常与其他心律失常共存。     

Developmental Effects of d-Sotalol on Anterograde and Retrograde Atrioventricular Conduction in the Rabbit

Developmental Electrophysiology of d-Sotalol. Introduction : These experiments investigate the developmental effects of d-sotalol on standard electrophysiologic parameters of anterograde and retrograde AV conduction in the rabbit.
Methods and Results: Using bipolar electrograms and standard pacing techniques, the effects of graded concentrations of d-sotalol on anterograde and retrograde conduction in mature and immature perfused rabbit hearts were compared. Also, a quantitative assessment of the drug's effects on a rate-dependent property of anterograde AV node (AVN) conduction, termed the "recovery process," was compared in mature and immature rabbit hearts. The main developmental electrophysiologic findings of this investigation are: (1) in both the mature and immature rabbit heart, d-sotalol increases the anterograde conduction time and prolongs refractoriness of the AVN, yet the minimal concentrations of d-sotalol that produce these changes are lower in the neonate; (2) d-sotalol increases the anterograde refractory period of the His-Purkinje system in both age groups, but increases anterograde infra-Hisian conduction only in the neonate; (3) 1 × 10⁻⁴ M d-sotalol significantly changes the time constant of the AVN recovery process in the neonate, hut not in the adult; (4) for retrograde conduction, slow conduction through the AVN (HA_max) and infra-Hisian region (VH_max) are increased by d-sotalol in the neonate, but not in the adult.
Conclusions: The findings of this study illustrate that d-sotalol has different effects on parameters of the developing AV conduction system. This implies that there may he maturational changes in the ionic currents that are responsible for anterograde and retrograde AVN and His-Purkinje conduction.     

The Long QT Syndrome with Impaired Atrioventricular Conduction: A Malignant Variant in Infants

Distal Conduction Disease in the Long QT Syndrome. Introduction : The long QT syndrome (LQTS) is occasionally complicated by impaired AV conduction, mostly 2:1 AV block. This form of LQTS can manifest before birth or during neonatal life, and it is more sporadic than familial. It is usually an isolated disorder, although it can be accompanied by a variety of cardiovascular and other anomalies. In spite of different treatment modes, mortality is high.
Methods and Results : The reported case presented not only with 2:1 AV conduction, but also with Wenckebach episodes with impaired right and left bundle branch conduction, and decremental conduction in the His-Purkinje axis. We also observed sinus pauses and accelerated AV junctional escape beats.
Conclusion : Our findings, and similar observations by others., suggest involvement of the sinus node and the distal conduction system in this form of the LQTS. Several histologic studies have documented abnormalities within the conduction system, including apoptosis. Because of the rare occurrence and poor prognosis of the LQTS with impaired AV conduction, international guidelines for diagnosis and treatment are needed. Development of an internal cardiac defibrillator for this young age group is necessary.     

Progressive Atrioventricular Conduction Block in a Mouse Myotonic Dystrophy Model

Introduction: Myotonic dystrophy is caused by expansion of a CTG trinucleotide repeat on human chromosome 19, and leads to progressive skeletal myopathy and atrioventricular conduction disturbances. A murine model of myotonic dystrophy has been designed by targeted disruption of the myotonic dystrophy protein kinase (DMPK) gene. The DMPK-deficient mice display abnormalities in A-V conduction characteristics, similar to the human cardiac phenotype. The purpose of this study was to determine whether age-related progression of A-V block occurs in a mouse model of DMPK-deficiency.Methods and Results: Surface ECGs and intracardiac electrophysiology (EP) studies were performed in 60 immature and 90 adult homozygous (DMPK), heterozygous (DMPK), and wild-type (WT) DMPK control mice. Complete studies were obtained on 141 of 150 mice. The RR, PR, QRS, and QT intervals were measured on ECG. Sinus node recovery time, AV refractory periods, paced AV Wenckebach and 2:1 block cycle lengths, atrial and ventricular effective refractory periods were compared between genotypes and age groups. There were no differences in ECG intervals or EP findings in the young mutant mice, but progressive PR prolongation in older mice. The A-V conduction defects are also sensitive to DMPK gene dosage. Adult DMPK mice develop 1°, 2° and 3° A-V block, whereas DMPK mice develop only 1° heart block.Conclusion: These data demonstrate that both age and DMPK dose are important factors regulating cardiac conduction in myotonic dystrophy. This mouse model of DM is remarkably similar to the human phenotype, with age-related progression in atrioventricular conduction defects.     

经食管调搏诱发左侧旁道并房室结加速传导心动过速

探讨左侧旁道 (LAP)并房室结加速传导 (EAVNC)心动过速 (TA)经食管诱发方式的影响 ,对 5 9例突发突止TA患者作食管心房调搏和心内电生理检查。结果有 18例具有房室结加速传导 ,SR间期轻度延长 ,诱发室上性心动过速 (SVT)的方法与无EAVNC患者具有不同的刺激模式。结论 :当心房起搏频率≥ 2 0 0次 /分 ,房室传导是 1∶1,需更强的S1S2 S3 或Burst法才能诱发SVT ,这样可避免遗漏左侧隐匿性旁道的诊断 ,前向 1∶1传导的AH间期是决定LAP并EAVNC顺向型房室折返性心动过速频率的重要因素。     

射频消融阻断房室旁路后室房逆传的特点

以射频电流阻断90例预激综合征患者的房室旁路.62例(68.9%)于旁路消融后呈室房分离,28例(31.1%)呈室房递减性传导.室房分离与患者年龄、性别及旁路传导特性无关,但左或右游离壁旁路阻断 后室房分离者多于递减传导者,而间隔旁路阻断后差别不显著.3例复发均为室房递减传导者.本研究提示,心房激动长期经旁路下传致房室结功能废用性退化可能为室房分离的原因,旁路阻断后室房递减传导者应仔细检测以除外潜在的旁路逆传.     

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.     

Dynamic Behavior of the Atrioventricular Node:

AV Nodal Memory. The wide variety of delays that the atrioventricular node can generate in response to an increased rate are explained by dynamic interactions between the three intrinsic properties of recovery, facilitation, and fatigue. The functional model presented suggests that any deviation of nodal conduction time from its minimum basal value represents, at any given time, the net sum of the effects produced by these properties. When a constant fast atrial rate is suddenly initiated, the node first "sees" a shortening in recovery time and responds by an increase in conduction time. This increase further shortens the recovery time of the ensuing beat, which is accordingly further delayed, and so on until a steady state is reached or a block occurs. However, these events do not occur alone. The second heat al the fast rate is conducted with a shorter conduction time than expected from the recovery time alone, and is therefore facilitated. These facilitatory effects develop within one short cycle and dissipate within one long cycle. They affect increasingly the conduction time of beats occurring with shorter cycle lengths. While steady-state effects of recovery and facilitation occur within seconds, nodal conduction time continues to increase slowly over several minutes when a rapid rate is maintained. This effect is attributed to fatigue, which develops and dissipates with a slow, symmetric time course. The dynamics of these properties can now be directly studied with selective stimulation protocols, and have many implications for the understanding of nodal behavior in the context of supraventricular tachyarrhythmias.     

Use of Only a Regular Diagnostic His-Bundle Catheter for Both Fast and Reproducible "Para-Hisian Pacing" and Stable Right Ventricular Pacing

Pacing from the Diagnostic His-Bundle Catheter. Introduction : Para-Hisian pacing, i.e., pacing the anteroseptal right ventricle (RV) with or without direct capture of the His bundle (HB), allows the differentiation of VA conduction over the AV node from conduction over an accessory pathway. Classically, it is performed by maneuvering a separate pacing catheter around the HB catheter, which may be difficult and time-consuming.
Methods and Results : This study prospectively evaluated the use of a single standard octapolar HB catheter with 2-mm interelectrode spacing for simultaneous (para-Hisian) pacing from the distal bipole and recording from the three proximal bipoles in 148 consecutive patients. Para-Hisian pacing was successful in 146 of 148 patients, performed within a median of only 10 seconds, and easily repeated several times during the course of an electrophysiologic study. Retrograde HB activation could he recorded in 132 of 146 patients; a clearly different surface ECG configuration confirmed the presence or absence of HB capture in all other patients. Interestingly, stable RV pacing could he performed from the HB catheter for the rest of the electrophysiologic study in 138 of 142 patients in whom this was tried. RV pacing from this site also led to better interpretation of retrograde conduction, due to clear visualization of retrograde HB activation.
Conclusion : Pacing from the distal dipole of a regular diagnostic HB catheter provides a fast and reliable way to perform para-Hisian pacing. Therefore, it may be advocated as a routine diagnostic protocol during electrophysiologic procedures. Moreover, pacing from this site obviates the need for a separate RV pacing catheter in most patients.     

Observations on variability of atrioventricular nodal conduction in man and the dual-pathway response

A study was made of nodal conduction times of atrial stimuliwith fixed coupling intervals, in 23 patients divided into twogroups according to their atrial stimulus test response: GroupI (continuous AV node function curve; 17 cases) and Gruop II(dual AV node pathway; six cases). The stimulation protocolinvolved the delivery of 75 stimuli with a fixed coupling interval20 ms greater than the effective refractory period (ERP) ofthe AV node (Group I) or fast pathway (Group II). The atrialcoupling intervals (A1A2) and node conduction times (A2H2) weremeasured. An evaluation was made of the dispersion of intervalswith range (R) and of the distribution of A2H2 times (² test). In both Groups, R (A2H2) was greater than R(A1A2) (P<0.05):R(A2H2) in Group II was greater than R(A2H2) in Group I (P <0.001). In Group I the distribution of A2H2 was non-normal infour cases and bimodal in five; in Group II the distributionwas non-normal and bimodal in all cases. It is concluded that: (1) the AV node generates a dispersionin its conduction times in the vicinity of its ERP, althoughthe nodal conduction curve is continuous: and (2) the so-calleddual pathway may constitute an exaggeration of AV node responseinhomogeneity.