'Dual atrioventricular nodal pathways" in patients with Wolff-Parkinson-White syndrome.

'Dual atrioventricular nodal pathways" were found in five patients who also had the Wolff-Parkinson-White syndrome. All five patients had a re-entrant tachycardia that used the atrioventricular node for conduction in the anterograde direction and an accessory atrioventricular pathway for conduction in the retrograde direction. One of the patients also had a re-entrant tachycardia that originated within the atrium or the atrioventricular node. Dual atrioventricular nodal pathways were identified in three of the five patients during their first electrophysiological study because the effective refractory period of the accessory atrioventricular pathway in the anterograde direction was longer than the effective refractory period of the fast atrioventricular nodal pathway. In the other two patients the dual atrioventricular nodal pathways were found only after operative division of an accessory atrioventricular pathway. Re-entrant tachycardia that uses an accessory pathway may be cured by operative division of the accessory pathway. Tachycardia resulting from re-entry within the atrioventricular node cannot be cured by an operation unless the normal conduction system is divided and a permanent pacemaker implanted. These five patients indicate the importance of determining the aetiology of tachycardia by studying the tachycardia itself and not only the type of atrioventricular conduction present.     

从慢径消融发生的交界区心律试探房室结双径的本质

７６例慢－快型房室结折返性心动过速（ＡＶＮＲＴ）患者接受房室结慢径消融术。６５例慢径阻断、９例双径存在但ＡＶＮＲＴ不能诱发、２例快径阻断。慢径阻断后，除快径的前传有效不应期（ＥＲＰ）缩短（２８７．０±７９．０ｍｓｖｓ３４４．０±８７．０ｍｓ，Ｐ＜０．０１）外，房室传导的文氏点、２１阻滞点、室房传导的１１点、快径逆传ＥＲＰ、前传和逆传功能不应期均无明显改变。共放电８４１次，其中无交界区心律的３１７次放电，无一次消融成功。６５例慢径阻断者，交界区心律减少或消失。以上结果提示快径和慢径可能是两条各具电生理特性的传导纤维。     

心动过速RR间期交替的发生机制及导管射频消融治疗

目的　分析QRS心动过速伴RR间期长短交替的发生机制及导管射频消融情况。方法　对 6例心动过速伴RR间期长短交替患者 ,常规行动态心电图及食管电生理检查。心内电生理检查提示存在房室旁路或房性心动过速伴房室结双径路 ,先进行旁路或房性心动过速的消融 ,消融成功后再进行心内电生理检查 (包括应用异丙肾上腺素进行心动过速诱发 ) ,如不能诱发心动过速则终止手术。若提示存在房室结多径路 ,则进行慢路径改良术。结果　食管电生理检查提示 :4例患者存在房室旁路伴房室结双径路 ;2例患者存在房室结三径路。心内电生理检查及消融结果显示 :3例患者为房室旁路伴房室折返性心动过速 ,成功消融后不能诱发房室结折返性心动过速 ;1例患者同时存在房室及房室结折返性心动过速 ,成功消融房室旁路后再改良慢路径 ;2例患者为房室结三径路 ,经慢径路改良后房室结传导曲线连续 ,未诱发心动过速。 6例患者无并发症发生 ,随访期间无心动过速发作。结论　室上性心动过速伴RR间期交替发生率较低 ,且均与房室结传导不连续有关。心动过速伴RR间期交替发生机制较为复杂 ,除了与房室结纵向传导的不连续有关外 ,还与其不应期密切相关。食管电生理检查与心内电生理检查相比对揭示RR间期交替的发生机制具有较高的诊断价值。     

Electrophysiologic properties of cibenzoline in Wolff-Parkinson-White syndrome and atrioventricular nodal reentry tachycardia

The electrophysiologic effects of the new class-1 antiarrhythmic drug cibenzoline (1.5 mg/kg within 10 min, followed by an infusion of 0.5 mg for 30 min) were investigated in six patients with atrioventricular (av) nodal reentrant tachycardia and nine patients with atrioventricular tachycardia. Sinus cycle length, sinus node recovery time, effective refractory period (ERP) of the atrium and the ventricle as well as the ERP of the av node were not significantly affected by cibenzoline. Retrograde conduction via the av node was prevented by cibenzoline in 6/15 patients, retrograde ERP was increased in 4/15 patients and in 5/15 patients determination of the retrograde ERP of the AV node was impossible. Intranodal conduction time (AH-interval) and infranodal conduction time (HV-interval) was increased from 96 +/- 27 ms to 117 +/- 40 ms (p less than 0.01) and 36 +/- 12 ms to 62 +/- 12 ms (p less than 0.01), respectively. In four patients with antegrade conduction along the accessory pathway no antegrade conduction was seen after the application of cibenzoline. Retrograde ERP of the accessory pathway was increased in two patients, it was unchanged in three patients, and no retrograde conduction along the accessory pathway was seen in four patients. AV nodal reentrant tachycardia was not inducible, after cibenzoline in 4/6 patients and in 5/9 patients with AV reentrant tachycardia. If tachycardia remained inducible, an increase in tachycardia cycle length from 333 +/- 46 ms to 402 +/- 24 ms was observed (p less than 0.01). In conclusion the electrophysiologic effects of cibenzoline make it a suitable drug for the treatment of av nodal reentrant tachycardia and atrioventricular tachycardia.     

Incidence, determinants and significance of fixed retrograde conduction in the region of the atrioventricular node. Evidence for retrograde atrioventricular nodal bypass tracts.

Of 104 consecutive patients studied in our laboratory with His bundle electrograms, atrial and ventricular pacing and the atrial and ventricular extrastimulus techniques, 18 patients in whom the existence and utilization of ventriculoatrial (V-A) bypass tracts were excluded demonstrated evidence for fixed and rapid retrograde conduction in the region of the atrioventricular node (A-V) as suggested by the following: (1) short (36 +/- 2 msec [mean +/- standard error of mean]) and constant retrograde H2-A2 intervals during retrograde refractory period studies; (2) significantly (P less than 0.025) better V-A than A-V conduction; (3) significantly (P less than 0.025) shorter retrograde functional refractory period of the V-A conducting system than of the A-V conduction system; and (4) the retrograde effective refractory period of the A=V nodal region was not attainable in any of the 18 patients. Fourteen of the 18 patients (77 percent) had a history of palpitations and 10 (51 percent) had documented paroxysmal supraventricular tachycardia; in 13 (72 percent) single echoes or sustained reentrant supraventricular tachycardia, or both, could be induced during atrial pacing or atrial premature stimulation studies, or both. During tachycardia all these 13 patients had a short (37 +/- 2.4 msec) and constant conduction time in the retrograde limb (H-Ae interval) of the reentrant circuit that was identical to the H2-A2 interval. In conclusion, fixed and rapid retrograde conduction in the region of the A-V node (1) is seen in approximately 17 percent of patients, (2) is associated with a large incidence of reentrant paroxysmal supraventricular tachycardia, and (3) suggests the presence of A-V nodal bypass tracts (intranodal or extranodal functioning in retrograde manner).     

The electrophysiology of atrioventricular nodal reentry tachycardia following the Mustard or Senning procedure and its radiofrequency ablation

We describe the electrophysiological studies undertaken in four patients with atrioventricular nodal reentry tachycardia in the setting of concordant atrioventricular and discordant ventriculo-arterial connections (transposition). Radiofrequency ablation was attempted in three, all with success. Clear evidence of dual antegrade pathways through the atrioventricular node was present in only one of the four, but other characteristics of discrete fast and slow pathways into the atrioventricular node were present in all. Atrioventricular nodal reentry tachycardia was inducible in all. In the three patients in whom ablation was attempted, the application of radiofrequency energy to the low medial regions of the systemic venous atrium (morphologically left) consistently caused junctional accelerated rhythm, but these lesions were not successful in eliminating the tachycardia. Successful radiofrequency ablation required a retrograde approach to the region of the slow pathway in the pulmonary venous atrium (morphologically right).     

Determinants of tachycardia induction using ventricular stimulation in dual pathway atrioventricular nodal reentrant tachycardia

Factors determining tachycardia induction using ventricular stimulation in atrioventricular (AV) nodal reentrant tachycardia utilizing the slow pathway for anterograde and the fast pathway for retrograde conduction were analyzed in 53 patients. Sixteen patients had tachycardia induced by ventricular stimulation. In 15, tachycardia was inducible with incremental ventricular pacing. In 4 of these 15 patients, the tachycardia was also induced with V1V2 testing, while in 11 patients, the tachycardia was not induced with V1V2 testing. In 9 of the latter 11 patients, tachycardia could be induced with V1V2V3 testing, suggesting that the retrograde effective refractory period (ERP) of the right bundle (RB) or the relative refractory period of the His-Purkinje system (HPS) was the limiting factor for tachycardia induction during V1V2 testing. In the remaining one patient, tachycardia was induced with V1V2V3 testing, which provoked a premature ventricular beat, leading to tachycardia induction. Tachycardia was not induced by ventricular stimulation in 37 patients. Factors deterring tachycardia induction in these patients may be related to the retrograde ERP or functional refractory period (FRP) of the HPS, the retrograde ERP of the fast pathway, and an insufficient conduction delay of the circuit (retrograde fast and anterograde slow pathway) to allow anterograde conduction of the slow pathway. In conclusion, AV nodal reentrant tachycardia can be induced by ventricular stimulation in approximately 30% of patients with incremental ventricular pacing and/or ventricular extrastimulus testing. Induction of tachycardia with ventricular stimulation, nevertheless, is frequently limited by the retrograde FRP or ERP of the HPS, the retrograde ERP of the fast pathway, and possibly by an insufficient conduction delay of the circuit.     

Atrioventricular reciprocating tachycardia involving twin atrioventricular nodes in patients with complex congenital heart disease

INTRODUCTION: Histologic studies of autopsy specimens described the coexistence of two distinct AV nodes (so-called "Minckeberg sling" or "twin AV nodes") in specific congenital heart defects; however, the clinical electrophysiologic (EP) characteristics of twin AV nodes have not been characterized in detail. METHODS AND RESULTS: Since April 1993, a total of seven patients with complex congenital heart disease presented with AV reciprocating tachycardia suspected to be mediated by twin AV nodes. A common anatomic finding was AV discordance ([S,L,L] or [I,D,D]) with a malaligned complete AV canal defect in 5 of 7 patients. Intracardiac EP study was performed in five cases, and ablation was attempted in three patients with successful elimination of tachycardia inducibility by interruption or modification of 1 of the 2 AV nodes. Important EP characteristics included (1) the existence of two discrete nonpreexcited QRS morphologies, each with an associated His-bundle electrogram; (2) decremental as well as adenosine-sensitive anterograde and retrograde conduction; and (3) inducible AV reciprocating tachycardia with anterograde conduction over one AV nodal pathway and retrograde conduction over the alternate AV nodal pathway. The existence of two AV nodes was further supported in the group treated with radiofrequency ablation by the development of transient accelerated junctional rhythm during energy delivery with an identical QRS morphology to that generated by anterograde conduction over the targeted AV node. CONCLUSION: Reciprocating tachycardia mediated by twin AV nodes can be a source of recurrent supraventricular tachycardia in patients with specific forms of complex congenital heart disease. Successful treatment with catheter ablation is possible.     

Transcatheter modification of the atrioventricular node using radiofrequency energy.

120 consecutive patients with symptomatic atrioventricular nodal reentrant tachycardia (AVNRT) underwent catheter ablation using radiofrequency energy. Fast pathway ablation was attempted in the first 16 consecutive patients by application of radiofrequency current in the anterior and superior aspect of the tricuspid annulus. Successful results were accomplished in 13 patients, complete AV block occurred in three. The other 104 patients initially underwent ablation of the slow pathway in the posterior and inferior aspects of the tricuspid annulus which was successful in 98 patients. The remaining six patients subsequently underwent a fast pathway ablation with successful results in four and AV block in two. Therefore, 102 (98%) of the last 104 patients became free of AVNRT while maintaining intact AV conduction. This study demonstrates that both AV nodal conduction pathways can be selectively ablated. However, slow pathway ablation seems safer and should be considered as the first approach.     

射频电能消融术治疗房室结折返性心动过速的临床应用

应用射频电能房室连接区部分消融术治疗5例房室结折返性心动过速.术后5例之房室逆行传导均消失,4例房室结双径路不复存在,其中3例伴Ⅰ度房室结内传导阻滞,临床电生理复查5例之心动过速不能诱发.随访1.5～12.5月,所有患者均未再发心动过速,亦未服用任何抗心律失常药物.作者认为射频电能是改变房室传导较好的能源,具有比直流电安全、方便,损伤小,疗效高的特点.此外,本文对达到良好改变房室传导的射频消融部位,所用电能大小及释放时间等作了讨论.     

Conduction properties of the antegrade fast and slow AV nodal pathways associated with AV nodal reentrant tachycardia.

To elucidate differences in conduction properties among the normal atrioventricular (AV) node and the antegrade fast and slow dual AV nodal pathways (DAVNPW), AV nodal conduction curves were analyzed quantitatively in 38 patients. Eighteen patients had antegrade DAVNPW with AV nodal reentrant tachycardia (AVNRT) (dual pathways group) and the remaining 20 had smooth AV nodal conduction curves, without evidence of AV nodal dysfunction (control group). The effective refractory period (ERP) of the antegrade fast pathway was longer than that of the normal AV node (at both basic cycle lengths of 700 and 500 msec, p less than 0.01). Although the atrial premature beats were delayed by a longer ERP in the fast pathway, there was no significant difference in the degree of prolongation of AV nodal conduction time related to shortening of the coupling interval (i.e., ratio of A2H2 increment to A1A2 decrement) between these two pathways. On the other hand, the ERP of the antegrade slow pathway was similar to that of the normal AV node. The degree of prolongation of AV nodal conduction time (relative to the shortening of the coupling interval) was greater in the antegrade slow pathway than in the normal AV node. In conclusion, these findings suggest that in DAVNPW with AVNRT: (1) the antegrade fast pathway is similar to the AV node and its conduction properties are unlikely to be better than those of the normal AV node and (2) the antegrade slow pathway has quantitatively poorer conduction properties than the normal AV node, since it has a greater degree of decremental conduction.     

经导管射频消融改良房室结治疗房室结折返性心动过速

报道24例病人经射频消融(RFCA)慢径改良房室结治疗房室结折返性心动过速(AVNRT)的研究结果。RFCA后24例病人均不再诱发AVNRT(100％),其中23例慢径传导消失(95.8％),1例慢径传导明显减慢(4.2％)。认为RFCA改良慢径对房室和室房传导没有明显影响,其消融成功的可能预测指标为:X线影象消融电极位于房室结后下部、消融电极图A/V<0.4,放电出现交界性早搏或并行性交界性心律。     

Selective transcatheter ablation of the fast and slow pathways using radiofrequency energy in patients with atrioventricular nodal reentrant tachycardia.

BACKGROUND. The safety and efficacy of selective fast versus slow pathway ablation using radiofrequency energy and a transcatheter technique in patients with atrioventricular nodal reentrant tachycardia (AVNRT) were evaluated. METHODS AND RESULTS. Forty-nine consecutive patients with symptomatic AVNRT were included. There were 37 women and 12 men (mean age, 43 +/- 20 years). The first 16 patients underwent a fast pathway ablation with radiofrequency current applied in the anterior/superior aspect of the tricuspid annulus. The remaining 33 patients initially had their slow pathway targeted at the posterior/inferior aspect of the right interatrial septum. The fast pathway was successfully ablated in the initial 16 patients and in three additional patients after an unsuccessful slow pathway ablation. A mean of 10 +/- 8 radiofrequency pulses were delivered; the last (successful) pulse was at a power of 24 +/- 7 W for a duration of 22 +/- 15 seconds. Four of these 19 patients developed complete atrioventricular (AV) block. In the remaining 15 patients, the post-ablation atrio-His intervals prolonged from 89 +/- 30 to 138 +/- 43 msec (p less than 0.001), whereas the shortest 1:1 AV conduction and effective refractory period of the AV node remained unchanged. Ten patients lost their ventriculoatrial (VA) conduction, and the other five had a significant prolongation of the shortest cycle length of 1:1 VA conduction (280 +/- 35 versus 468 +/- 30 msec, p less than 0.0001). Slow pathway ablation was attempted initially in 33 patients and in another two who developed uncommon AVNRT after successful fast pathway ablation. Of these 35 patients, 32 had no AVNRT inducible after 6 +/- 4 radiofrequency pulses with the last (successful) pulse given at a power of 36 +/- 12 W for a duration of 35 +/- 15 seconds. After successful slow pathway ablation, the shortest cycle length of 1:1 AV conduction prolonged from 295 +/- 44 to 332 +/- 66 msec (p less than 0.0005), the AV nodal effective refractory period increased from 232 +/- 36 to 281 +/- 61 msec (p less than 0.0001), and the atrio-His interval as well as the shortest cycle length of 1:1 VA conduction remained unchanged. No patients developed AV block. Among the last 33 patients who underwent a slow pathway ablation as the initial attempt and a fast pathway ablation only when the former failed, 32 (97%) had successful AVNRT abolition with intact AV conduction. During a mean follow-up of 6.5 +/- 3.0 months, none of the 49 patients had recurrent tachycardia. Forty patients had repeat electrophysiological studies 4-8 weeks after their successful ablation, and AVNRT could not be induced in 39 patients. CONCLUSIONS. These data suggest that both fast and slow pathways can be selectively ablated for control of AVNRT. Slow pathway ablation, however, by obviating the risk of AV block, appears to be safer and should be considered as the first approach.     

Radiofrequency catheter ablation of Mahaim tachycardia by targeting Mahaim potentials at the tricuspid annulus.

BACKGROUND--Reentrant tachycardias associated with Mahaim pathways are rare but potentially troublesome. Various electrophysiological substrates have been postulated and catheter ablation at several sites has been described. OBJECTIVE--To assess the efficacy and feasibility of targeting discrete Mahaim potentials recorded on the tricuspid annulus for the delivery of radiofrequency energy in the treatment of Mahaim tachycardia. PATIENTS--21 patients out of a consecutive series of 579 patients referred to one of three tertiary centres for catheter ablation of accessory pathways causing tachycardia. All had symptoms and presented with tachycardia of left bundle branch block configuration or had this induced at electrophysiological study. In all cases, the tachycardia was antidromic with anterograde conduction over a Mahaim pathway. RESULTS--6 patients had additional tachycardia substrates (4 had accessory atrioventricular connections and 2 had dual atrioventricular nodal pathways and atrioventricular nodal reentry). After ablation of the additional pathways, Mahaim potentials were identified in 16 (76%) associated with early activation of the distal right bundle branch and radiofrequency energy at this site on the tricuspid annulus abolished Mahaim conduction in all 16 cases. In 2 patients there was early ventricular activation at the annulus without a Mahaim potential but radiofrequency energy abolished pre-excitation. In the remaining patients no potential could be found (1 patient), no tachycardia could be induced after ablation of an additional pathway (1 patient), or no Mahaim conduction was evident during the study (1 patient). During follow up (1-29 months (median 9 months)) all but 1 patient remained symptom free without medication. CONCLUSIONS--Additional accessory pathways seem to be common in patients with Mahaim tachycardias. The identification of Mahaim potentials at the tricuspid annulus confirms that most of these pathways are in the right free wall and permits their successful ablation and the abolition of associated tachycardia.     

Initiation of atrioventricular nodal reentrant tachycardia in patients with discontinuous anterograde atrioventricular nodal conduction curves with and without documented supraventricular tachycardia: Observations on the role of a discontinuous retrograde conduction curve

To evaluate factors playing a role in initiation of atrioventricular (AV) nodal reentrant tachycardia utilizing anterogradely a slow and retrogradely a fast conducting AV nodal pathway, 38 patients having no accessory pathways and showing discontinuous anterograde AV nodal conduction curves during atrial stimulation were studied. Twenty-two patients (group A) underwent an electrophysiologic investigation because of recurrent paroxysmal supraventricular tachycardia (SVT) that had been electrocardiographically documented before the study. Sixteen patients (group B) underwent the study because of a history of palpitations (15 patients) or recurrent ventricular tachycardia (one patient); in none of them had SVT ever been electrocardiographically documented before the investigation. Twenty-one of the 22 patients of group A demonstrated continuous retrograde conduction curves during ventricular stimulation. In 20 tachycardia was initiated by either a single atrial premature beat (18 patients) or by two atrial premature beats. Fifteen of the 16 patients of group B had discontinuous retrograde conduction curves during ventricular stimulation, with a long refractory period of their retrograde fast pathway. Tachycardia was initiated by multiple atrial premature beats in one patient. Thirteen out of the remaining 15 patients received atropine. Thereafter tachycardia could be initiated in three patients by a single atrial premature beat, by two atrial premature beats in one patient, and by incremental atrial pacing in another patient. In the remaining eight patients tachycardia could not be initiated. Our observations indicate that the pattern of ventriculoatrial conduction found during ventricular stimulation is a marker for ease of initiation of AV nodal tachycardia in patients with discontinuous anterograde AV nodal conduction curves.     

房室结改良术终点与复发率的关系

为探讨房室结改良术成功后不同电生理终点对复发率的影响，观察了８０例房室结改良术患者复发情况。其中双径现象消失（Ａ组）５１例；仍有双径现象，但无心房回波（Ｂ组）２１例；有双径现象，且有１个心房回波（Ｃ组）８例。消融成功后观察３０ｍｉｎ，急性复发４例（５．８％）；术后随访１４．７±５．６（６～３９）个月慢性复发３例（３．８％），共复发７例（８．８％）。７例中，Ａ组与Ｂ组各２例、Ｃ组３例，复发率分别为３．９％、９．５％、３７．５％。其中Ａ组与Ｃ组比较复发率差异非常显著（Ｐ＜０．０１），其余差异无显著性（Ｐ＞０．０５）。此结果表明，选用三种终点中的任何一种，术后大多数患者都未复发。而为了降低复发率，除了消融成功后至少应观察３０ｍｉｎ以消除急性复发外，在技术成熟的单位，可力争以双径现象消失为改良术终点。     

Attenuated nodal response. Apropos of 30 cases

In a population of 600 consecutive patients undergoing endocavitary electrophysiological study to assess nodal conduction, 40 had an atriohisian Wenckenbach point of over 200/mn. In 30 cases, vagal stimulation with ATP (10 to 40 mg IV) provoked an increase in atrioventricular conduction, with lengthening the AH interval by over 100 p. 100 or transient atrioventricular block. This increase allowed elimination of an accessory atriohisian pathway which could give similar high Wenckenbach points, but which do not show decremental conduction. In all our cases, the conduction passed through the artrioventricular node (AVN) whose response to rapid atrial stimulation was attenuated compared to normal. The parameter of this attenuated nodal response varied from case to case, but in general, the intervals were shorter than normal. The AH interval was less than 50 ms in 22 cases (N = 70 +/- 20 ms). The effective nodal refractory period was shorter than the functional atrial refractory period in 20 cases. The shortest atrial cycles transmitted 1/1 to the ventricles ranged from 230 to 300 ms (274 +/- 33 ms) (N = 375 +/- 40 ms). The functional structure of the AVN was studied by the lengthening of the AH interval with heart rate : 5 types were distinguished : 10 patients had progressive lengthening of AH interval greater than 100 ms (Type I) as in a normal AVN; 5 had progressive lengthening of AH interval of less than 50 ms (Type II), 5 had progressive lengthening of AH which then remained stable for a number of heart rates before lengthening again (Type III); 3 had an initial moderate lengthening of the AH interval which then became more rapid (Type IV) and 7 had no change in AH until 120/mn and then a progressive lengthening was observed (Type V). Two functional groups could also be identified depending on whether the lengthening was progressive, suggesting a single nodal pathway (Types I and II) or on whether differing increases were observed related to the atrial rate, suggesting two (Types IV and V) or even three (Type III) atrionodal or intranodal pathways with different refractory periods. Of these 30 patients, only 14 had documented supraventricular tachycardia, 13 being atrial fibrillation and the other a junctional tachycardia. Attenuated nodal behavior does not seem to be a direct cause of supraventricular arrhythmias but these arrhythmias were not tolerated as well because of the special properties of the atrioventricular node.     

Electrophysiologic effects and clinical efficacy of flecainide in children with recurrent paroxysmal supraventricular tachycardia

The electrophysiologic effects of intravenous flecainide were evaluated in 16 patients aged 9 +/- 4 years: 15 with recurrent paroxysmal supraventricular tachycardia (SVT) and 1 with overt accessory pathway and history of syncope. Eleven patients had an accessory pathway; it was concealed in 2, overt in 9 and in 10 of these patients an orthodromic atrioventricular reentrant tachycardia was induced. Five patients without accessory pathway had an atrioventricular nodal reentrant tachycardia. After intravenous flecainide (1.5 mg/kg) the effective refractory period of the atrium and ventricle increased significantly; the anterograde and retrograde effective refractory periods of the atrioventricular node did not. Flecainide blocked retrograde conduction in the accessory pathway in 4 patients (effective refractory period 245 +/- 41 ms) and anterograde conduction in 8 of 9 patients (effective refractory period 284 +/- 57 ms). The mean cycle length of orthodromic reciprocating tachycardia and atrioventricular nodal reentrant tachycardia increased significantly. After flecainide tachycardia was noninducible in 6 patients with orthodromic reciprocating tachycardia and in 1 with atrioventricular nodal reentrant tachycardia. It was inducible but nonsustained (less than or equal to 30 seconds) in 1 patient with orthodromic reciprocating tachycardia and in 3 with atrioventricular nodal reentrant tachycardia. Fifteen patients continued oral flecainide treatment for 19 +/- 11 months.(ABSTRACT TRUNCATED AT 250 WORDS)     

Mechanisms of junctional tachycardia showing ventricular pre-excitation.

Over a period of five years 12 patients underwent electrophysiological studies for the investigation of recurrent tachycardias which showed ventricular pre-excitation. Nine patients had a type B pattern and two a type A. One patient had episodes of both types. Dual atrioventricular nodal pathways were found in six of seven patients with atrioventricular nodal re-entrant tachycardia mechanisms. Single direct atrioventricular accessory pathways were present in four patients, single nodoventricular pathways in five, and multiple pathways in three. Twenty one tachycardias were induced, of which 13 showed ventricular pre-excitation. Five patients had nodoventricular pathway conduction during atrioventricular nodal tachycardia and one during atrioventricular re-entrant tachycardia. Only three patients had simple antidromic tachycardia and one additional atrioventricular nodal tachycardia with bystander atrioventricular accessory conduction. Three patients had three different tachycardias, three had two types, and six had one type. Thus junctional tachycardias showing ventricular pre-excitation are often associated with multiple mechanisms and complex anatomical and functional substrates. An accessory pathway was an essential component in only six of 13 tachycardias showing ventricular pre-excitation. Determination of the tachycardia mechanism requires detailed study and analysis.     

Catheter ablation of retrograde fast pathway in patients with atrioventricular nodal reentrant supraventricular tachycardia.

Atrioventricular (AV) nodal reentrant tachycardia is a common cause of supraventricular tachycardia. The present study describes catheter ablation of this form of tachycardia in 23 patients using direct current shocks. The aim of ablation was to abolish conduction through the retrograde pathway while preserving the anterograde conduction. All patients had symptomatic, drug resistant, slow-fast variety of dual atrioventricular nodal reentrant tachycardia. Using the retrograde atrial activation in the His bundle catheter as the reference, the optimal ablation site was selected by positioning an electrode catheter to obtain atrial activation synchronous with or earlier than the atrial activation at the reference electrode. Shocks of 100-300 joules were delivered at this site resulting in blockade of retrograde conduction in all patients. Ventriculo-atrial conduction studied 24 hours after the procedure was still absent in 16, modified in 2 and resumed in 3 patients. Two patients developed permanent complete heart block and were given pacemakers. At repeat electrophysiologic study performed after 2-4 months in 10 patients, the supraventricular tachycardia could not be induced. The AH interval was 67 +/- 10 msec during control study and to 115 +/- 39 msec at restudy (p < 0.001). The ventriculo-atrial conduction was absent in 7 cases and had been modified in 1 case. Over a follow up period of 1-30 months (mean 10.8 +/- 7.1 mo) 17 patients (73%) remained free of the arrhythmia without medication or pacemaker. Three other patients were easily controlled with digoxin. Thus, catheter modification of AV node results in permanent cure of the AV nodal tachycardia in majority of patients.