Patient with atrioventricular node reentrant tachycardia with eccentric retrograde left-sided activation: treatment with radiofrequency catheter ablation

We describe a patient with supraventricular tachycardia with triple atrioventricular (AV) node pathway physiology. A discontinuous curve was present in the antegrade AV nodal function curves. During right ventricular pacing, the earliest retrograde atrial activation was recorded at the left-sided coronary sinus electrode. The retrograde ventricular-atrial interval was long and had decremental conduction. We induced a slow-slow AV node reentrant tachycardia (AVNRT) with eccentric retrograde left-sided activation. After slow pathway ablation, dual AV nodal pathway physiology was present. AVNRT with eccentric retrograde left-sided activation is relatively rare, and our findings suggest that eccentric retrograde left-sided atrial inputs consist partially of a slow pathway and disappear with slow pathway ablation.     

Slow-fast form of atrioventricular nodal reentrant tachycardia with eccentric retrograde left-sided activation

A case of atypical AV nodal reentrant tachycardia (AVNRT) with eccentric retrograde left-sided activation, masquerading as tachycardia using a left-sided accessory pathway, is reported. Initially, it appeared that the tachycardia was a typical slow-fast form of AVNRT. The earliest retrograde activation, however, was registered at a site approximately 3 cm from the coronary sinus orifice (left atrial free wall), indicating atypical AVNRT. Atrial tachycardia and orthodromic AV reciprocating tachycardia using an accessory AV pathway were excluded. Slow pathway ablation at the posteroseptal right atrium eliminated the tachycardia. It was suggested that the anterograde limb of the tachycardia circuit was a slow AV nodal pathway with typical posteroseptal location, whereas the retrograde limb was a long atrionodal pathway connecting the compact AV node and the left atrial free wall near the mid-coronary sinus.     

Electrophysiological mechanisms of conversion of typical to atypical atrioventricular nodal reentrant tachycardia occurring after radiofrequency catheter ablation of the slow pathway

This report presents an adult patient with conversion of typical to atypical atrioventricular nodal reentrant tachycardia (AVNRT) after slow pathway ablation. Application of radiofrequency energy (3 times) in the posteroseptal region changed the pattern of the atrioventricular (AV) node conduction curve from discontinuous to continuous, but did not change the continuous retrograde conduction curve. After ablation of the slow pathway, atrial extrastimulation induced atypical AVNRT. During tachycardia, the earliest atrial activation site changed from the His bundle region to the coronary sinus ostium. One additional radiofrequency current applied 5 mm upward from the initial ablation site made atypical AVNRT noninducible. These findings suggest that the mechanism of atypical AVNRT after slow pathway ablation is antegrade fast pathway conduction along with retrograde conduction through another slow pathway connected with the ablated antegrade slow pathway at a distal site. The loss of concealed conduction over the antegrade slow pathway may play an important role in the initiation of atypical AVNRT after slow pathway ablation.     

Unique electrophysiologic characteristics of atrioventricular nodal reentrant tachycardia with different ventriculoatrial block patterns: Effects of slow pathway ablation and insights into the location of the reentrant circuit

BACKGROUND: The electrophysiologic mechanisms of different ventriculoatrial (VA) block patterns during atrioventricular nodal reentrant tachycardia (AVNRT) are poorly understood. OBJECTIVES: The purpose of this study was to characterize AVNRTs with different VA block patterns and to assess the effects of slow pathway ablation. METHODS: Electrophysiologic data from six AVNRT patients with different VA block patterns were reviewed. RESULTS: All AVNRTs were induced after a sudden AH "jump-up" with the earliest retrograde atrial activation at the right superoparaseptum. Different VA block patterns comprised Wenckebach His-atrial (HA) block (n = 4), 2:1 HA block (n = 1), and variable HA conduction times during fixed AVNRT cycle length (CL) (n = 1). Wenckebach HA block during AVNRT was preceded by gradual HA interval prolongation with fixed His-His (HH) interval and unchanged atrial activation sequence. AVNRT with 2:1 HA block was induced after slow pathway ablation for slow-slow AVNRT with 1:1 HA conduction, and earliest atrial activation shifted from right inferoparaseptum to superoparaseptum without change in AVNRT CL. The presence of a lower common pathway was suggested by a longer HA interval during ventricular pacing at AVNRT CL than during AVNRT (n = 5) or Wenckebach HA block during ventricular pacing at AVNRT CL (n = 1). In four patients, HA interval during ventricular pacing at AVNRT CL was unusually long (188 +/- 30 ms). Ablations at the right inferoparaseptum rendered AVNRT noninducible in 5 (83%) of 6 patients. CONCLUSION: Most AVNRTs with different VA block patterns were amenable to classic slow pathway ablation. The reentrant circuit could be contained within a functionally protected region around the AV node and posterior nodal extensions, and different VA block patterns resulted from variable conduction at tissues extrinsic to the reentrant circuit.     

PR/RR Interval Ratio During Rapid Atrial Pacing:

Method for Confirming Slow Pathway Conduction. Introduction: Although the AV conduction curve in patients with AV nodal reentrant tachycardia (AVNRT) is usually discontinuous, many patients with this arrhythmia do not demonstrate criteria for dual AV nodal pathways. During rapid atrial pacing, the PR interval often exceeds the pacing cycle length when there is anterograde conduction over the slow pathway and AVNRT is induced. The purpose of this prospective study was to determine the diagnostic value of the ratio of the PR interval to the RR interval during rapid atrial pacing as an indicator of anterograde slow pathway conduction in patients undergoing electrophysioiogic testing. Methods and Results: The PR and RR intervals were measured during rapid atrial pacing at the maximum rate with consistent 1:1 AV conduction in four study groups: (1) patients with inducible AV nodal reentry and the classical criterion for dual AV nodal pathways during atrial extrastimulus testing (AVNRT Group 1); (2) patients with inducible AV nodal reentry without dual AV nodal pathways (AVNRT Group 2); (3) control subjects ≤ 60 years of age without inducible AV nodal reentry; and (4) control subjects > 60 years of age without inducible AV nodal reentry. For both groups of patients with inducible AV nodal reentry, AV conduction was assessed before and after radiofrequency ablation of the slow AV nodal pathway. Before slow pathway ablation, the PR/RR ratio exceeded 1.0 in 12 of 13 AVNRT Group 1 patients (mean 1.27 ± 0.21) and 16 of 17 AVNRT Group 2 patients (mean 1.18 ± 0.15, P = NS Group 1 vs Group 2). After slow pathway ablation, the maximum PR/RR ratio was < 1.0 in all AVNRT patients (Group 1 = 0.59 ± 0.08, P < 0. 00001 vs before ablation: Group 2 = 0.67 ± 0.11; P < 0.00001 vs before ablation). Among both groups of control subjects, the PR/RR ratio was > 1.0 in only 3 of 27 patients with no relation to patient age. Conclusion: The ratio of the PR interval to the RR interval during rapid atrial pacing at the maximum rate with consistent 1:1 AV conduction provides a simple and clinically useful method for determining the presence of slow AV nodal pathway conduction. This finding may be particularly useful in patients with inducible AV nodal reentry without dual AV nodal physiology on atrial extrastimulus testing.     

Paroxysmal supraventricular tachycardia with persistent ventriculoatrial block

We report the case of a 64-year-old patient with paroxysmal supraventricular tachycardia and persistent VA block. Induction and maintenance of tachycardia occurred without apparent activation of the atria. Diagnostic characteristics were most compatible with AV nodal reentrant tachycardia (AVNRT). Automatic junctional tachycardia and orthodromic nodoventricular or nodofascicular reentry tachycardia were considered in the differential diagnosis. Upper common pathway block during AVNRT may be explained by either intra-atrial conduction block or purely intranodal confined AVNRT. The arrhythmia was cured by a typical posteroseptal ablation approach guided by slow pathway potentials.     

Electrophysiologic Spectrum of Atrioventricular Nodal Behavior in Patients with Atrioventricular Nodal Reentrant Tachycardia Undergoing Selective Fast or Slow Pathway Ablation

AV Nodal Behavior After Ablation. Introduction; The objective of this report is to delineate the atrioventricular (AV) nodal electrophysiologic behavior in patients undergoing fast or slow pathway ablation for control of their AV nodal reentrant tachycardia (AVNRT).
Methods and Results: One hundred sixteen consecutive patients with symptomatic AVNRT were included. Twenty-two patients underwent fast pathway ablation with complete abolition of AVNRT in all and development of complete AV block in five patients. Of 17 patients with intact AV conduction postablation, 12 had demonstrated antegrade dual pathway physiology during baseline study, which was maintained in three and lost in nine patients postablation. Two patients with successful fast pathway ablation developed uncommon AVNRT necessitating a slow pathway ablation. Twenty-one patients demonstrated both common and uncommon forms of AV nodal reentry during baseline study. The earliest site of atrial activation was close to the His-bundle recording site (anterior interatrial septum) during common variety and the coronary sinus ostium (posterior interatrial septum) during the uncommon AV nodal reentry in all 21 patients. Ninety-six patients underwent successful slow pathway ablation. Among these, the antegrade dual pathway physiology demonstrable during baseline study (60 patients) was maintained in 25 and lost in 35 patients postablation.
Conclusion: These data suggest that: (1) dual pathway physiology may persist after successful ablation, which might be a reflection of multiple reentrant pathways in patients with AVNRT: and (2) the retrograde pathways during common and uncommon AVNRT have anatomically separate atrial breakthroughs. These findings have important electrophysiologic implications regarding the prevailing concept of the AV nodal physiology in patients with AVNRT.     

快慢型房室结折返性心动过速的电生理特点

目的分析快慢型房室结折返性心动过速（AVNRT）患者的临床特征、心电网和电生理检查特点、射频消融治疗特点,旨在为临床长RP。心动过速鉴别提供帮助。方法11例经心内电生理检查证实为慢快型房室结折返性心动过速的患者,回顾性分析其临床特征、心电图特点及电生理检查特点及射频消融治疗。结果心动过速表现为窄QRs波心动过速,RP’〉P’R,P。在Ⅱ、Ⅲ、aVF导联倒置,RP’间期为350±25ms,心率为1664-30bpm。11例患者中有3例出现室房逆传跳跃现象。心房程序刺激无明显跳跃现象,11例均可由心房StS：刺激诱发心动过速发作,且容易诱发,容易终止。心动过速发作时,5例CS9．10A波最早,6例HiS的A波最早,其中1例静推ATP心动过速终止。11例患者中9例经房室结改良消融传统慢径获得成功,2例在冠状静脉窦内消融成功,术后随访3个月以上均未再发作心动过速。结论长RP’心动过速的诊断和鉴别诊断有一定困难,如能排除慢旁道和房速,应考虑快慢型房室结折返性心动过速。     

Adenosine-Sensitive Atrial Reentrant Tachycardia Originating from the Atrioventricular Nodal Transitional Area

Adenosine-Sensitive AT from AVN Area. Introduction : Atrial tachycardia shows wide variations in its electrophysiologic properties and sites of origin. We report an atrial tachycardia with ECG manifestations and electrophysiologic characteristics similar to an atypical form of AV nodal reentrant tachycardia (AVNRT).
Methods and Results : This supraventricular tachycardia was observed in 11 patients. It was initiated by atrial extrastimulation with an inverse relationship between the coupling interval of an extrastimulus and the postextrastimulus interval. Its induction was not related to a jump in the AH interval, and its perpetuation was independent of conduction block in the AV node. Ventricular pacing during tachycardia demonstrated AV dissociation without affecting the atrial cycle length. A very small dose of adenosine triphosphate (mean 3.9 ± 1.2 mg) could terminate the tachycardia. The earliest atrial activation during tachycardia was recorded at the low anteroseptal right atrium with a different intra-atrial activation sequence from that recorded during ventricular pacing, where the tachycardia was successfully ablated in 9 of 10 attempted patients. Bidirectional AV nodal conduction remained unatttched after successful ablation.
Conclusion : There may he an entity of adenosine-sensitive atrial tachycardia probably due to focal reentry within the AV node or its transitional tissues without involvement of the AV nodal pathways. This tachycardia can he ablated without disturbing AV nodal conduction from the right atrial septum.     

Role of invasive electrophysiologic testing in the evaluation and management of adult patients with focal junctional tachycardia

Focal junctional tachycardia (FJT) is characterized by a rapid often irregular narrow complex tachycardia with episodes of atrioventricular (AV) dissociation. This uncommon arrhythmia is most likely due to abnormal automaticity or triggered activity. The patients are often quite symptomatic and if left untreated may develop heart failure particularly if their tachycardia is incessant. In patients refractory to medical management, the role of radiofrequency ablation involves either (1) selective ablation of the tachycardia focus while preserving AV conduction or as a last resort (2) AV junction ablation followed by pacemaker implantation. The clinician should first assess whether ventriculoatrial (VA) conduction is present or absent during tachycardia. If present, radiofrequency ablation should be applied at the site of earliest retrograde atrial activation. In the absence of VA conduction and hence an atrial target site, sequential lesions should be applied in the posterior septum (slow pathway region) followed by lesions applied in midseptum and anteroseptum respectively if tachycardia persists. To further minimize the risk of AV nodal block, some authors delivered radiofrequency energy during atrial overdrive pacing to assess AV conduction during ablation. Others recommended mapping the perinodal region and applying radiofrequency ablation at the site where catheter manipulation resulted in tachycardia termination. Using this ablative approach, the risk of AV block is around 5–10%.     

Characterization of subforms of AV nodal reentrant tachycardia.

BACKGROUND: Different subforms of AV nodal reentrant tachycardia (AVNRT) have been described ("Slow/Fast", "Slow/Slow" and "Fast/Slow"). Our aim is to improve definition of these subforms, based on systematic evaluation, in a large cohort of patients, of the site of earliest atrial activation, timing intervals, and evidence for the presence or absence of a lower common pathway (LCP). METHODS AND RESULTS: In 344 patients, AVNRT using a slow pathway (SP) for antegrade conduction and earliest atrial activation at the superior septum (i.e. retrograde fast pathway) was present in 81.4% (Slow/Fast). AVNRT using an SP for antegrade conduction and earliest atrial activation at the inferior septum or proximal coronary sinus (i.e. retrograde slow pathway; Slow/Slow) was present in 13.7%. AVNRT with a short A-H interval and retrograde SP conduction (Fast/Slow) was present in 4.9%. All timing intervals during tachycardia are dependent on autonomic tone. H-A intervals during tachycardia (H-A(t)) overlap in Slow/Slow and Slow/Fast AVNRT: Slow/Slow therefore may mimic Slow/Fast AVNRT. The H-A interval during pacing at the tachycardia cycle length (H-A(p)) better discriminates both subforms. The difference between H-A(p) and H-A(t) (Delta H-A) was significantly longer in Slow/Slow compared with Slow/Fast AVNRT (isoprenaline 0.5 microg/min: 27+/-18 ms vs. 1+/-9 ms; p<0.001). Delta H-A>15 ms had a specificity and sensitivity for Slow/Slow of 94% and 64%, respectively. A Delta H-A>15 ms, combined with other data, pointed to the presence of a long LCP in 36 of 43 evaluable Slow/Slow (84%) and all Fast/Slow, but in only 10% of Slow/Fast (p<0.001). Retrograde conduction during ventricular pacing at the tachycardia cycle length was present in only 6% of Fast/Slow. CONCLUSIONS: AVNRT subforms can be distinguished based on a systematic evaluation of atrial activation sequence, timing intervals and evidence for the presence of an LCP.     

Change in the retrograde atrial activation sequence following radiofrequency modification of the atrioventricular node: implications for the electrophysiologic circuit of a variant of atrioventricular nodal reentrant tachycardia

INTRODUCTION: Despite the great success in treating AV nodal reentrant tachycardia (AVNRT) with radiofrequency modification of the AV node, the dimensions of the electrophysiologic circuit of this arrhythmia remain unclear, and simple models fail to explain all tachycardia-related phenomena. METHODS AND RESULTS: We describe three unusual cases of supraventricular tachycardia (SVT). In all three cases, retrograde atrial activation during ventricular pacing or during SVT manifested local left atrial electrograms recorded from the coronary sinus preceding the septal atrial electrograms (eccentric activation), with earliest atrial activity at the lateral or posterolateral mitral annulus. Electrophysiologic maneuvers and observations were consistent with AVNRT as the mechanism in each case. In all cases, radiofrequency modification of the AV node eliminated inducible SVT and abolished dual pathway AV nodal physiology. The retrograde atrial activation sequence during ventricular pacing changed after ablation in each case, with septal atrial electrograms preceding left atrial electrograms recorded from the coronary sinus (concentric activation). CONCLUSION: The observations in these cases cannot be explained by the traditional model of slow, fast, and intermediate AV nodal pathways. A model incorporating a circuit close to the AV node with left atrial and coronary sinus connections is proposed.     

Unusual induction of slow-fast atrioventricular nodal reentrant tachycardia. Report of two cases

INTRODUCTION: Generally, the induction of typical atrioventricular nodal reentrant tachycardia (AVNRT) occurs with a premature atrial stimulus that blocks in the fast pathway and proceeds down the slow pathway slowly enough to allow the refractory fast pathway time to recover. We describe two cases in which a typical AVNRT was induced in an unusual fashion. RESULTS: The first case is a 41-year-old man with paroxysmal supraventricular tachycardia. During the electrophysiology study, the atrial extrastimulus inducing the typical AVNRT was conducted simultaneously over the fast (AH) and the slow pathway (AH'). A successful ablation of the slow pathway was performed. During the follow-up no recurrence was noted. The second case is a 52-year-old woman with a Wolff-Parkinson-White syndrome due to a left posterior accessory pathway. After 5 minutes of atrioventricular reentrant tachycardia (AVRT) induced by a ventricular extrastimulus, a variability of the antegrade conduction was noted in presence of the same VA conduction. In fact, a short AH interval (fast pathway) alternated with a more prolonged AH intervals (slow pathway) that progressively lengthened until a typical AVNRT was induced. The ablation of the accessory pathway eliminated both tachycardias. DISCUSSION: A rare manifestation of dual atrioventricular nodal pathways is a double ventricular response to an atrial impulse that may cause a tachycardia with an atrioventricular conduction of 1:2. In our first case, an atrial extrastimulus was simultaneously conducted over the fast and the slow pathway inducing an AVNRT. This nodal reentry implies two different mechanisms: 1) a retrograde block on the slow pathway impeding the activation of the slow pathway from the impulse coming down the fast pathway, and 2) a critical slowing of conduction in the slow pathway to allow the recovery of excitability of the fast pathway. Interestingly, in the second case, during an AVRT the atrial impulse suddenly proceeded alternately over the fast and the slow pathway. The progressive slowing of conduction over the slow pathway until a certain point which allows the recovery of excitability of the fast pathway determines the AVNRT. This is a case of "tachycardia-induced tachycardia" as confirmed by the fact that the ablation of the accessory pathway eliminated both tachycardias.     

Successful elimination of concealed accessory pathway-mediated tachycardia by ablation of AV nodal slow pathway

We report a case of atrioventricular reentrant tachycardia (AVRT) using a concealed para-Hisian accessory pathway for retrograde conduction, which also required anterograde conduction over the AV nodal slow pathway to maintain the tachycardia. The shortest VA interval during AVRT (70 ms) was noted at a site with His bundle electrogram amplitude of 0.25 mV. The AVRT was cured by radiofrequency ablation of the AV nodal slow pathway without affecting accessory pathway conduction. The patient has not reported any sustained palpitations at 2 years after ablation while receiving no medications. The case presented in this report illustrates a para-Hisian AVRT that was successfully eliminated by an unconventional approach of ablation of the atrial inputs to the AV nodal slow pathway.     

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.     

"Left-variant" atypical atrioventricular nodal reentrant tachycardia: electrophysiological characteristics and effect of slow pathway ablation within coronary sinus

Introduction: Recent anatomical and electrophysiological studies have demonstrated the presence of leftward posterior nodal extension (LPNE); however, its role in the genesis of atrioventricular nodal reentrant tachycardia (AVNRT) is poorly understood. This study was performed to characterize successful slow pathway (SP) ablation site and to elucidate the role of LPNE in genesis of atypical AVNRT with eccentric activation patterns within the coronary sinus (CS).
Methods and Results: Among 45 patients with atypical AVNRT (slow-slow/fast-slow/both = 20/22/3 patients) with concentric (n = 37, 82%) or eccentric CS activation (n = 8, 18%), successful ablation site was evaluated. Among 35/37 patients (95%) with concentric CS activation, ablation at the conventional SP region outside CS eliminated both retrograde SP conduction and AVNRT inducibility. Among eight patients with eccentric CS activation, the earliest retrograde atrial activation was found at proximal CS 16 ± 4 mm distal to the ostium during AVNRT. The earliest retrograde activation site was located at inferior to inferoseptal mitral annulus, consistent with the presumed location of LPNE. Ablation at the conventional SP region with electroanatomical approach only rendered AVNRT nonsustained without elimination of retrograde SP conduction in seven of eight patients (88%). Ablation targeted to the earliest retrograde atrial activation site within proximal CS (15 ± 4 mm distal to the ostium); however, eliminated retrograde SP conduction and rendered AVNRT noninducible in six of eight patients (75%).
Conclusion: In 75% of "left-variant" atypical AVNRT, ablation within proximal CS was required to eliminate eccentric retrograde SP conduction and render AVNRT noninducible, suggesting LPNE formed retrograde limb of reentrant circuit.     

多型房室结折返性心动过速的机制和射频导管消融

目的分析多型房室结折返性心动过速（AVNRT）并存的电生理机制和射频导管消融结果。方法18例经电生理检查后行射频导管消融的多型AVNRT患者。慢快型和慢慢型AVNRT的消融方法为首选消融前传慢径（房室结右侧后延伸）,快慢型AVNRT的消融方法为消融最早慢径逆传心房激动部位。消融成功的标准为消除1：1前传慢径,消除快慢型AVNRT的逆传慢径,不能诱发任何类型AVNRT。结果11例在消融前的电生理检查中诱发出2种类型AVNRT,均在三尖瓣环与冠状静脉窦口之间（房室结右侧后延伸）成功消融。7例在电生理检查中诱发出1种类型,消融此型后又诱发出另外1种类型,其中4例在房室结右侧后延伸进一步消融成功,另3例均经左侧后延伸进一步消融成功。消融术后随访6个月至8年,18例均无复发。结论对于大多数多型AVNRT,房室结右侧后延伸可能为其折返环的主要基质,消融可成功治愈多型AVNRT。在少部分多型AVNRT中,左侧后延伸与右侧后延伸可能分别作为不Ⅻ类型AVNRT折返环的主要基质,需要分别消融才能成功治愈。     

程控刺激不能诱发的房室结折返性心动过速慢径消融的临床疗效评估

目的　评价程控刺激不能诱发的房室结折返性心动过速 (AVNRT)射频消融慢径的临床疗效。方法　 6 1例有心动过速病史且心电图疑诊为AVNRT的病人 ,电生理检查有房室结双径(DAVNP)但不能诱发AVNRT ,随机分为两组。A组 30例不消融而进行临床随访 ,当心动过速复发且经心电图证实为窄QRS心动过速者接受射频消融阻断慢径。B组 31例接受射频消融以阻断慢径 ,术后临床随访。结果　A、B两组分别有 2 4例和 2 7例病人完成随访。A组 2 4例随访中分别在 1年内发作心动过速 ,再次接受消融阻断慢径后随访 (12 .1± 12 .2 )个月 ,仅 1例复发心动过速 (4.2 % ) ,与消融前比较差异有显著性 (P <0 .0 0 0 1)。B组 2 7例平均随访 (2 4 .2± 17.6 )个月 ,1例复发心动过速 (3.7% ) ,与A组病人消融前相比差异有显著性 (P <0 .0 0 0 1) ,而与其消融后比较差异无显著性 (P >0 .0 5 )。结论　有阵发性心动过速病史且心电图疑诊为AVNRT的病人 ,电生理检查有DAVNP而不能诱发心动过速者 ,射频消融阻断慢径具有良好的临床疗效。     

Radiofrequency Ablation of a Concealed Nodoventricular Mahaim Fiber Guided by a Discrete Potential

INTRODUCTION: We present the case of a 17-year-old woman who underwent an electrophysiological study and radiofrequency (RF) ablation of supraventricular tachycardia refractory to medical treatment. Two right-sided, concealed, nondecremental atrioventricular accessory pathways (AV-APs) involved in orthodromic circus movement tachycardias were identified. After RF ablation of both AV-APs, evidence of bidirectional dual AV nodal conduction was demonstrated and regular narrow complex tachycardia was induced. METHODS AND RESULTS: During the tachycardia, retrograde slow and fast AV nodal pathway conduction with second-degree ventriculoatrial (VA) block and VA dissociation were observed. During the tachycardia with second-degree VA block, ventricular extrastimuli elicited during His-bundle refractoriness advanced the next His potential or terminated the tachycardia. Mapping the right atrial mid-septal region, a distinct high-frequency activation P potential was recorded in a discrete area, two thirds of the way from the His bundle toward the os of the coronary sinus. Detailed electrophysiologic testing with the recordable P potential demonstrated that the tachycardia utilized a concealed nodoventricular AP arising from the proximal slow AV nodal pathway. CONCLUSION: The tachycardia with slow 1:1 VA conduction could be reset by ventricular extrastimuli elicited during His-bundle refractoriness advancing the subsequent activation P potential and atrial activation. RF ablation guided by recording of the activation P potential resulted in elimination of both the slow AV nodal pathway and the nodoventricular connection with preservation of the normal AV conduction system.     

Elimination of AV Nodal Reentrant Tachycardia with 2:1 VA Block by Posteroseptal Ablation

AV Nodal Reentrant Tachycardia. AV nodal reentry capable of VA block during tachycardia was successfully eliminated using a posteroseptal ablation pulse delivered well away from the site of earliest atrial activation during tachycardia. A possible explanation is that the arrhythmia represented typical AV nodal reentrant tachycardia with transient intra atrial conduction block during tachycardia.