Unusual form of AV nodal Wenckebach block.

A 73-year-old man had a fast atrioventricular (AV) nodal pathway accidentally ablated 4 years before, while attempting to ablate a septally located concealed accessory pathway (AP). After initiation of treatment with beta-blockers, because of systemic arterial hypertension, the patient presented to the emergency room complaining of a markedly diminished exercise tolerance. The 12 lead ECG showed an interesting AV nodal Wenckebach sequence, interrupted by P waves retrogradely conducted through the AP. The mechanisms explaining the ECG are discussed.     

经房室结双径路1:2传导引起的一种新型室上性心动过速

目的 报告一种新型的室上性心动过速；方法 总结该心动过速的电生理特点及射频消融治疗方法；结果 该型室上速的发生机制是窦性激动连续经房室结1：2下传激动心室，导致心室率经常是心房率的两倍，心动过速呈无休止性发作，并引起心动过速性心肌病。结论 这种心动过速可以经心内电生理检查确诊并通过射频消融改良房室结而根治。     

Double ventricular response in dual AV nodal pathways mimicking supraventricular as well as ventricular tachycardia

Supraventricular tachycardias confined to the AV junction areusually thought to be due to reentry using a slow and a fastconducting pathway. In the case presented, a marked differenceof conduction velocity in dual AV nodal pathways and retrogradeblock in the slow conducting pathway caused a ventricular doubleresponse to a single atrial depolarization. At a critical heartrate this phenomenon occurred in a bigeminal fashion, mimickingsupraventricular as well as ventricular tachycardia.     

Characterizing dual atrioventricular nodal physiology in pediatric patients with atrioventricular nodal reentrant tachycardia

INTRODUCTION: Dual atrioventricular (AV) nodal physiology, defined as an AH jump > or =50 msec with a 10 msec decrease in A1A2, is the substrate for atrioventricular nodal reentrant tachycardia (AVNRT) and yet it is present in a minority of pediatric patients with AVNRT. Our objective was to characterize dual AV nodal physiology as it pertains to a pediatric population. METHODS/RESULTS: We retrospectively reviewed invasive electrophysiology studies in 92 patients with AVNRT (age12.1 +/- 3.7 yrs) and in 46 controls without AVNRT (age 13.3 +/- 3.7 yrs). Diagnoses in controls: syncope (N = 31), palpitations (N = 6), atrial flutter (N = 3), history of atrial tachycardia with no inducible arrhythmia (N = 3), and ventricular tachycardia (N = 3). General anesthesia was used in 49% of AVNRT and 52% of controls, P = 0.86. There were no differences in PR, AH, HV, or AV block cycle length. With A1A2 atrial stimulation, AVNRT patients had a significantly longer maximum AH achieved (324 +/- 104 msec vs 255 +/- 67 msec, P = 0.001), and a shorter AVNERP (276 +/- 49 msec vs 313 +/- 68 msec P = 0.0005). An AH jump > or =50 msec was found in 42% of AVNRT versus 30% of controls (P = 0.2). Using a ROC graph we found that an AH jump of any size is a poor predictor of AVNRT. With atrial overdrive pacing, PR > or = RR was seen more commonly in AVNRT versus controls, (55/91(60%) vs 6/46 (13%) P = 0.000). CONCLUSIONS: Neither the common definition of dual AV nodes or redefining an AH jump as some value <50 msec are reliable methods to define dual AV nodes or to predict AVNRT in pediatric patients. PR > or = RR is a relatively good predictor of AVNRT.     

Unusual Wenckebach phenomenon due to an atrial tachycardia arising from the apex of Koch’s triangle in the presence of dual AV nodal physiology

A case of a patient with narrow QRS tachycardia and without structural heart disease is presented. The electrophysiologic study revealed an atrial tachycardia in the presence of dual atrioventricular (AV) nodal physiology and AV block at suprahisian level, the latter two leading to an unusual Wenckebach periodicity. The entire septal area was mapped as was the coronary sinus (CS) os and the earliest atrial activation was found at the apex of Koch’s triangle in close vicinity to the His bundle (HB). Cryomapping at that point reproducibly terminated the tachycardia without impairing AV conduction. Cryoablation rendered the tachycardia non-inducible. Discontinuous AV conduction persisted but AV nodal reentrant tachycardia (AVNRT) was not inducible. Six months later the patient is arrhythmia-free.     

Simplified "ATP test" for noninvasive diagnosis of dual AV nodal physiology and assessment of results of slow pathway ablation in patients with AV nodal reentrant tachycardia

INTRODUCTION: We recently reported that administration of adenosine triphosphate (ATP) during sinus rhythm identifies dual AV nodal physiology (DAVNP) in 76% of patients with inducible sustained AV nodal reentrant tachycardia (AVNRT) at electrophysiologic (EP) study. In that report, however, the ATP test was considered positive for DAVNP only when the results were reproducible at a given dose of ATP. The aim of the present study was to assess the value of a simplified ATP test for noninvasive diagnosis of DAVNP and abolition or modification of the slow pathway (SP) after radiofrequency ablation (RFA) in patients with inducible sustained AVNRT. METHODS AND RESULTS: The value of a single dose of ATP was studied in 105 patients with inducible sustained AVNRT and in 31 control patients before placement of EP catheters in the cardiac chambers. ATP (10 to 60 mg, in 10-mg increments) was injected during sinus rhythm until ECG signs of DAVNP (> or = 50 msec increase or decrease in PR interval in two consecutive beats, or occurrence of > or = 1 AV nodal echo beat) or > or = second-degree AV block was observed. DAVNP was observed in only 1 (3.2%) control patient. The test could be completed in 96 study patients. DAVNP was found by ATP test in 72 (75%) patients, whereas it was diagnosed by EP criteria in 82 (85%) patients. DAVNP by ATP test disappeared in 27 (96%) of 28 patients who underwent SP abolition and in 18 (60%) of 30 patients who underwent SP modification. In the 12 patients with persistent DAVNP determined by ATP test after SP modification, the number of beats conducted over the SP was significantly reduced (from 6.3+/-3.3 to 2.5+/-2.2 beats; P = 0.002). CONCLUSION: A single administration of ATP during sinus rhythm (at a given dose) enables noninvasive diagnosis of DAVNP in a high percentage of patients with inducible AVNRT and reliably confirms the results of RFA of the SP.     

射频消融房室结改良消融前后心脏电生理变化的探讨

目的比较房室结双径路伴房室结内折返性心动过速(AVNRT)患者,射频消融(RFCA)慢径路改良术,消融前、后心脏各部分腔内电生理改变。方法在相同条件下,于消融前、后分别进行腔内电生理检查。记录消融前、后:希氏束电图(HIS),心房有效不应期(A—ERP),功能不应期(A—FRP),心室有效不应期(V—ERP),功能不应期(V—FRP),房室结前传有效不应期(AVN—ERP),前传文氏点(AVN—WKB),房室结逆传有效不应期(VAN—ERP),逆传文氏点(VAN—WKB),将消融前、后心脏各部分电生理参数进行配对,经SPSS统计分析软件进行T检验分析。结果消融前、后:HIS电图,A—ERP,A—FRP,V—ERP,V—FRP,AVN—ERP,及VAN—WKB均无显著差异(P>0.05)。AVN—WKB,VAN—ERP有显著差异(P<0.05)。讨论射频消融房结改良对房室结双径路AVNRT疗效肯定。在消融前、后(急性期)房室结前、逆传电生理均有一定改变。这与消融改变了房室结的部分结构,如大部分病列慢径路消失有关。不同消融部位对房室结传导电理改变产生不同的结果。没有证据表明消融后,45岁以上年龄组房室结传导改变大于45岁以下年龄组。男女不同性别组之间亦无差异。     

Transesophageal electrophysiology study in the diagnosis of dual atrioventricular nodal nonreentrant tachycardia

“Double fire” is generally characterized by 1:2 atrioventricular conduction of sinus beats traveling down fast and slow pathways that result in double ventricular response. When this phenomenon repeats rapidly, dual atrioventricular nodal nonreentrant tachycardia (DAVNNT) occurs. We report a case of an irregular tachycardia with a comprehensive record that includes an electrocardiogram, a transesophageal electrophysiology study, and an intracardiac electrophysiology study. This is the first report of transesophageal electrophysiology study in the diagnosis of DAVNNT. A diagnosis of DAVNNT was deduced, and the patient was successfully treated with radiofrequency ablation of the slow pathway.     

Delineation of AV Conduction Pathways by Selective Surgical Transection: Effects on Antegrade and Retrograde Transmission

Introduction: The role for transitional cells as determinants of AH and HA conduction was examined in the superfused rabbit AV junction.Methods: Bipolar electrodes and microelectrodes were used to record antegrade A-H and retrograde H-A activation, before and after transection of the transitional cell input to the compact AV node.Results: During pacing from the high right atrium, inferior to the coronary sinus os, beneath the fossa ovalis, or on the anterior limbus, AV Wenckebach block (WB) was mediated by identical transitional cells grouped in close apposition to the compact AV node. Paced WB cycle lengths were shorter from the high right atrium (196 ± 12 msec) and inferior to the coronary sinus os (195 ± 8 msec) versus the fossa ovalis (217 ± 9 msec) or anterior limbus (206 ± 11 msec). With His bundle pacing, retrograde HA WB (211 ± 17 msec) was observed within the N cell region within the compact AV node. After transection of posterior and superior transitional cell input to the compact AV node, the antegrade AH WB cycle length was prolonged (245 ± 18 msec), with an increased WB incidence within the NH region (compact AV node)(5% to 41%; p = 0.014). The incidence of retrograde HA WB determined within the NH region was increased (30% to 88%), with a decrease in the stimulus-fast pathway conduction time (98 ± 7 to 49 ± 6 msec; p < 0.01).Conclusions: The data demonstrate (1) a common transitional cell population determining AH WB, independent of atrial stimulation site, and (2) a plasticity of transitional cell-compact AV node connections, with rapid AH and HA conduction favored by removal of posterior/superior AV nodal input.Supported by a grant from the American Heart Association, Oklahoma Affiliate.     

Concealed accessory pathway and dual AV conduction: drug-dependent reentrant tachycardia.

Electrophysiological studies were performed in a patient with paroxysmal supraventricular tachycardia and a normal surface ECG at the time of the study. Premature atrial stimulation revealed dual AV conduction and an echo zone during AV conduction over the fast and the slow pathway. The prolongation of the AV conduction time by a calcium antagonist, Ro 11-1781, permitted the induction of tachycardias via both pathways. Premature ventricular stimulation yielded constant VA conduction times with activation of the low right atrium before the high right atrium before the left atrium. During the tachycardia, premature right ventricular beats conducted to the atrium at a time when the AV node and the His bundle would be refractory. The study suggests the simultaneous occurrence of an occult accessory bundle connecting the right ventricle to the right atrium and dual AV conduction.     

Manifest and concealed AV nodal reentry in wenckebach type of AV conduction with AV junctional escape rhythm

An electrocardiogram was obtained that was characterized by sinus rhythm with progressive prolongation of the PR interval not followed by a blocked sinus impulse. After a critically long PR interval, the QRS complex was followed by a premature P′ wave, representing an echo beat, a manifest reentry in the atrioventricular (AV) node. The pause, occasioned by the premature P′ wave, was at times interrupted by an AV junctional escape beat, occurring with an escape interval of 1.21–1.24 seconds. On other occasions, however, the escape beat did not manifest on schedule, even though the pause was markedly longer than the escape cycle. This suggested that the manifest reentry was followed by a further concealed reentry, resulting in inapparent discharge of the AV junctional escape pacemaker, whose firing was postponed, thereby allowing the sinus impulse to capture the ventricles.     

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.     

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.     

Effect of site, summation and asynchronism of inputs on atrioventricular nodal conduction and refractoriness

The impulses coming from the sinus node synchronically penetratethe A V node via the crista terminalis and inter-atrial septum.Studies in superfused rabbit AV preparations suggest that thecrista terminalis is a more effective input than the inter-atrialseptum, and that the summation of both inputs facilitates AVnodal conduction. The aim of this study was to verify the hypothesisin a more physiological model, such as the whole rabbit heartperfused by a Langendorff system. Fifteen rabbit hearts were studied in a Langendorff perfusionsystem with six bipolar extracellular electrodes: two for stimulating(crista terminalis and inter-atrial septum) and four for recording(crista terminalis, inter-atrial septum, His bundle electrogramand right ventricle). Seven hearts (Group I) were consecutivelypaced at the crista terminalis, inter-atrial septum and bothsites simultaneously, to determine the AV nodal Wenckebach cyclelength and effective refractory period under basal conditionsand after acetylcholine (0.75 x 10^–6 M). In eight heartsunder 0.75 x 10^–6 M acetylcholine (Group II), the cristaterminalis and inter-atrial septum were simultaneously (delay= 0 ms) or sequentially (delay = 2,4, 6,8,10,12,14,and 16 ms)stimulated to calculate the AV nodal effective refractory periodand the AH interval at an atrial coupling interval 5 ms longerthan the AV nodal effective refractory period, for each delaytested. There were no basal differences in AV nodal parameters duringcrista terminalis pacing, inter-atrial septum pacing or simultaneousstimulation in both sites in Group I; after acetylcholine, theAV nodal Wenckebach cycle length and effective refractory periodtended to be shorter during crista terminalis pacing (cristaterminalis = 188 ±33 and 147±34; inter-atrialseptum = 195±35 and 158±35; both sites = 195±34and 154±36; values expressed in cycle length of pacing-ms),although the differences did not reach statistical significance.In Group II, the AH interval tended to prolong slightly on increasingthe delay between crista terminalis and inter-atrial septumstimulation (delay 0 = 119±31, 2 = 125±29, 4 =129±33,6 = 129±29,8 = 128±30,10 = 134±34,12= 132±35,14 = 129±32,and 16 = 131 ±31 ms),butagain the differences did not reach statistical significance;the A V nodal effective refractory period did not change whenthe delay was varied. Conclusions: (1) Neither the input site nor the synchronoussummation of inputs plays an important role in A V nodal conduction.(2) These results suggest that A Vnodal response during atrialtachyarrythymias depends more on atrial rate than on shiftingsin site and time coupling of inputs.     

Manifest Fast and Slow Pathway Conduction Patterns and Reentry in a Patient with Dual AV Nodal Physiology

Manifest Fast and Slow AV Nodal Conduction Patterns and Reentry. A 52-year-old woman with paroxysmal supraventricular tachycardias (PST) showed short and long PR intervals during sinus rhythm. Repetitive episodes of PST due to simultaneous anterograde conduction through fast and slow conduction pathways (one P-two QRS) were recorded. A self-limited episode of non-paroxysmal AV nodal reentry with anterograde slow and retrograde fast pathway conduction was initiated by a single atrial premature beat. Each pathway depicted distinct refractory periods, conduction velocities, unidirectional block, and Wenckebach-type block suggesting the possibility of a well-defined anatomical substratum.     

Irregular atrial activation during atrioventricular nodal reentrant tachycardia: evidence of an upper common pathway

Controversy continues regarding the precise nature of the reentrant circuit of AV nodal reentrant tachycardia, especially the existence of an upper common pathway. In this case report, we show that marked variation and irregularity in atrial activation (maximum AA interval variation of 80 msec) can exist with fixed and constant activation of the His bundle and ventricles during AV nodal reentrant tachycardia in a 45-year-old female patient. We propose that irregular atrial activation is due to variable and inconsistent conduction from the AV node to the atria through the perinodal transitional cell envelope extrinsic to the reentrant circuit. Our observations support the concept of an upper common pathway, at least in some patients with AV nodal reentrant tachycardia.     

Role of compact node and posterior extension in direction-dependent changes in atrioventricular nodal function in rabbit

INTRODUCTION: AV nodal conduction properties differ in the anterograde versus the retrograde direction. The underlying substrate remains unclear. We propose that direction-dependent changes in AV nodal function are the net result of those occurring in the slow and fast pathways. METHODS AND RESULTS: Anterograde and retrograde AV nodal properties were determined with a premature protocol before and after posterior extension (slow pathway) ablation, and before and after upper compact node (fast pathway) ablation. Each ablation was performed in a different group of six rabbit heart preparations. In control, nodal minimum conduction time (NCTmin) and effective refractory period (ERPN) typically were longer, and maximum conduction time (NCTmax) was shorter in the retrograde compared to the anterograde direction. Posterior extension ablation prolonged anterograde ERPN from 91 +/- 10 ms to 141 +/- 15 ms (P < 0.01) and shortened NCTmax from 150 +/- 13 ms to 82 +/- 7 ms (P < 0.01) but did not affect retrograde conduction. Thus, the posterior extension normally contributes to the anterograde but not retrograde recovery curve. Compact node ablation prolonged anterograde conduction (NCTmin increased from 57 +/- 2 ms to 73 +/- 7 ms, P < 0.01) but did not alter ERPN and NCTmax. This ablation abolished retrograde conduction in two preparations and resulted in retrograde slow pathway conduction in four, the latter being interrupted by posterior extension ablation. Thus, the compact node accounts for the baseline of the recovery curve in both directions. Ablation of the compact node results in anterograde slow pathway conduction over the entire cycle length range and may result in retrograde slow pathway conduction. CONCLUSION: Direction-dependent properties of the AV node arise from those of the compact node-based fast pathway and posterior extension-based slow pathway. Normal AV node has bidirectional dual pathways.     

What is the Atrioventricular Node? Some Clues in Sorting out its Structure‐Function Relationship

The anatomic and functional substrate underlying AV nodal rate-dependent and dual pathway properties remains highly controversial. This article focuses on some factors that impair the understanding of the AV nodal structure-function relationship and some clues toward sorting it out. A definition of the AV node that applies to both anatomic and functional studies, an orthogonal topographic representation of nodal structures, and the integration of rate-dependent and dual pathway behavior of the AV node are proposed as primary steps toward a better understanding of the AV nodal structure-function relationship. Further fact-based information is the key to the sorting out of this puzzle.     

Role of the compact node and its posterior extension in normal atrioventricular nodal conduction, refractory, and dual pathway properties

INTRODUCTION: The functional origin of AV nodal conduction, refractory, and dual pathway properties remains debated. The hypothesis that normal conduction and refractory properties of the compact node and its posterior nodal extension (PNE) play a critical role in the slow and the fast pathway, respectively, is tested with ablation lesions targeting these structures. METHODS AND RESULTS: A premature atrial stimulation protocol was performed before and after PNE ablation in six isolated rabbit heart preparations. Discrete (approximately 300 microm) histologically controlled PNE lesions amputated the AV nodal recovery curve from its left steep portion reflecting slow pathway conduction and prevented reentry without affecting the right smooth fast pathway portion of the curve. The ablation shortened A2H2max from 159 +/- 16 ms to 123 +/- 11 msec (P < 0.01) and prolonged the effective refractory period from 104 +/- 6 msec to 119 +/- 11 msec (P < 0.01) without affecting A2H2min (55 +/- 9 msec vs 55 +/- 8 msec; P = NS) and functional refractory period (174 +/- 7 msec vs 175 +/- 6 msec; P = NS). These results did not vary with the input reference used. In six other preparations, lesions applied to the compact node after PNE ablation shifted the fast pathway portion of the recovery curve to longer conduction times and prolonged the functional refractory period, suggesting a compact node involvement in the fast pathway. CONCLUSION: The normal AV nodal conduction and refractory properties reflect the net result of the interaction between a slow and a fast pathway, which primarily arise from the asymmetric properties of the PNE and compact node, respectively.     

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.