Mechanisms of regular,wide QRS tachycardia in infants and children

A regular, wide QRS tachycardia was electrocardiographically documented in 32 patients aged 1 month to 18 years. The mechanisms of the tachycardia were evaluated using standard multicatheter electrophysiologic techniques. These mechanisms included (1) orthodromic reciprocating tachycardia with bundle branch aberration (seven patients), (2) antidromic reciprocating tachycardia using single (three patients), or multiple (three patients) atrioventricular connections (Kent bundles), (3) atrial flutter with ventricular preexcitation over accessory connections (eight patients), (4) reciprocating tachycardia using a nodoventricular connection (Mahaim fiber) (five patients), and (5) ventricular tachycardia (six patients). Regular, wide QRS tachycardias are not rare in pediatric patients. Their mechanisms can be quite complex, and electrocardiographic analysis with respect to QRS configuration, heart rate, or the presence or absence of ventriculoatrial dissociation is not sufficient for diagnostic purposes. Our results show that considerable understanding of the mechanism of regular, wide QRS tachycardias can be obtained by multicatheter electrophysiologic study. Understanding the mechanism is essential in order to make rational use of available therapeutic options.     

One to one atrioventricular conduction during atrial pacing at rates of 300/minute in absence of wolff-parkinson-white syndrome

One to one atrioventricular (A-V) or atrio-His bundle (A-H) conduction occurred during right atrial pacing at rates of 300/min in two patients with short P-R (and A-H) intervals, narrow QRS complexes and recurrent supraventricular tachyarrhythmias. Patient 1 had episodes of reciprocating A-V tachycardia and of atrial fibrillation with very fast rates (270 to 290/min) that were slowed to 100 to 135/min after administration of intravenous verapamil. Enhanced A-V (A-H) conduction was exposed only during stimulation from the high right atrium, but not from the low lateral right atrium or coronary sinus. Patient 2 had episodes of atrial flutter with 1:1 A-V conduction and rates of 290/min. The H-V interval was short (25 ms) during sinus rhythm and atrial pacing presumably because conduction occurred through an atrio-“distal” His bundle (atriofascicular) tract. In contrast, the H-V interval was normal (40 ms) in echo beats or when the “proximal” His bundle was stimulated.In these two patients, having as “common denominators” short P-R (and A-H) intervals, narrow QRS complexes and recurrent supraventricular tachyarrhythmias, enhanced A-V (A-H) conduction was (1) possibly due to different electrogenetic mechanisms; (2) pacing-site dependent; (3) manifested, during atrial fibrillation and atrial flutter, by extremely fast ventricular rates; and (4) unrelated to the rate of reciprocating A-V tachycardias because the latter was predominantly a function of anterograde conduction through the “slow” nodal pathway.     

Observations on the antidromic type of circus movement tachycardia in the Wolff-Parkinson-White syndrome

In the differential diagnosis of tachycardias showing a wide QRS complex and having a 1 to 1 relation between ventricular and atrial events, a supraventricular tachycardia with anterograde conduction over an accessory pathway and retrograde conduction by way of the specific conduction system must be considered. Five patients showing this type of circus movement tachycardia were studied by programmed electrical stimulation of the heart. Sudden changes in the tachycardia cycle length were observed in these patients that were based on changes in the VH interval. This finding suggested a change in the reentrant circuit with anterograde conduction over the accessory pathway but retrograde conduction sometimes occurring over the right bundle branch and at other times over one of the two divisions of the left bundle branch system. Characteristically, the tachycardia cycle length changed suddenly depending on the bundle branch used in retrograde direction. In one patient, an important difference was also observed between the anterograde effective refractory period of the accessory bypass (280 ms) and the shortest RR interval between preexcited QRS complexes during atrial fibrillation (measuring 190 ms). It is postulated that the short RR intervals during atrial fibrillation in the Wolff-Parkinson-White syndrome could result from bundle branch reentry after activation of the ventricles over the accessory pathway.     

Clinical and electrophysiologic observations in patients with concealed accessory atrioventricular bypass tracts

In 12 of 46 consecutive patients with paroxysmal supraventricular tachycardia or atrial flutter-fibrillation, without electrocardiographic evidence of ventricular preexcitation, electrophysiologic studies suggested the presence of accessory atrioventricular (A-V) pathways capable only of retrograde conduction (concealed Wolff-Parkinson-White syndrome). The ages of these patients ranged from 29 days to 71 years (mean 39.2 years). Most patients were clinically symptomatic with palpitations, dizziness, weakness or congestive heart failure. One patient had “cardiac dysrhythmia” described by an obstetrician during intrauterine life. Eleven patients manifested A-V reciprocating tachycardia involving the normal pathway for anterograde conduction and the accessory pathway for retrograde conduction. The remaining patient manifested recurrent paroxysms of atrial flutter-fibrillation as a result of rapid ventriculoatrial activation through the accessory pathway during the atrial vulnerable phase.

The electrophysiologic observations were analyzed with regard to clinical and electrocardiographic characteristics in these patients. The presence of concealed accessory pathways should be suspected in patients presenting with (1) an “incessant” form of tachycardia, (2) spontaneous onset of A-V reciprocal rhythms or reciprocating tachycardias after acceleration of the sinus rate without antecedent atrial extrasystoles or P-R interval prolongation, (3) slowing of the tachycardia rate consequent to the development of functional bundle branch block, (4) retrograde P waves (negative in leads II, III and aVF) discernible after the QRS complexes, with the R-P interval being shorter than the P-R interval during both A-V reciprocal rhythm and reciprocating tachycardia, and (5) oc-currence of atrial flutter-fibrillation in association with A-V reciprocal rhythms.

It is suggested that medical treatment in patients having concealed accessory pathways should be aimed at increasing the refractoriness of either the A-V node or the accessory pathway for reciprocating tachycardia, while increasing the refractoriness of the atrium and the accessory pathway in cases with atrial flutter-fibrillation. Pacemaker therapy and surgical intervention may be indicated in selected patients refractory to antiarrhythmic agents.     

Akuttherapie lebensbedrohlicher tachykarder Rhythmusstörungen

Life-threatening supraventricular tachyarrhythmias include atrial fibrillation, atrial flutter, AV-nodal reentrant tachycardia with rapid ventricular response and preexcitation syndromes combined with atrial fibrillation. Ventricular tachyarrhythmias still remain one of the leading causes of death; these arrhythmias include monomorphic and polymorphic ventricular tachycardia, torsade de pointes tachycardia, ventricular fibrillation and ventricular flutter. In all patients with tachycardias, an attempt should be made to differentiate between narrow (QRS duration < 0.12 s) or wide QRS complex (QRS duration ≥ 0.12 s) tachycardias. In the assessment of patients (pts) with supraventricular/ventricular tachyarrhythmias, attention should be given to identify whether the tachycardia is associated with worsening angina or low cardiac output. In pts with narrow QRS complex tachycardias or pts with atrial fibrillation and preexcitation syndromes immediate synchronized cardioversion should be performed if signs or symptoms of instability (hypotension, evidence of end-organ dysfunction, worsening angina) exist. In pts with a stable hemodynamic situation, vagal maneuvers, adenosine or calcium channel blockers can be used. Management of atrial flutter usually centers on cardioversion or rapid atrial pacing to normal sinus rhythm. In the treatment of patients with deemed unstable ventricular tachycardia (VT), electrical cardioversion is the treatment of choice. In more stable patients, ajmaline is the preferred agent after myocardial infarction and lidocaine if myocardial ischemia is present. In pts with torsade de pointes tachycardias aggressive steps must be taken to prevent degeneration of this rhythm to ventricular fibrillation (VF). Magnesium sulfate has recently been demonstrated efficacious and is currently considered first-line drug therapy. Transcutaneous overdrive pacing should be attempted if magnesium is unsuccessful. The pt with pulseless VT or VF demands early electrical countershock.     

Onset of atrial fibrillation during antidromic tachycardia: Association with sudden cardiac arrest and ventricular fibrillation in a patient with Wolff-Parkinson-White syndrome

Electrophysiologic evaluation in an 18 year old youth with the Wolff-Parkinson-White syndrome who had a sudden cardiac arrest while playing racquetball revealed two types of paroxysmal reciprocating tachycardia: (1) A normal QRS tachycardia with a short ventriculoatrial (V-A) interval fulfilled the criteria for reentry within the atrioventricular (A-V) node; and (2) a wide QRS tachycardia with a QRS configuration of maximal preexcitation was demonstrated to be the result of an antidromic mechanism.During laboratory study, the wide QRS tachycardia spontaneously degenerated into atrial fibrillation. In the basal state, the shortest R-R interval between preexcited QRS complexes was 270 ms, but after infusion of isoproterenol (1.6 μg/min intravenously), the shortest R-R interval became 180 ms. Consequently, this electrophysiologic study suggested that evolution of antidromic reciprocating tachycardia into atrial fibrillation with a rapid ventricular response during exercise-induced catecholamine release may have been the mechanism for ventricular fibrillation in this patient.     

Catheter ablation of left posteroseptal accessory pathways and of long RP' tachycardias with a right endocardial approach

Fifty-four patients with a posteroseptal accessory connection and symptomatic tachycardias underwent catheter ablation of the anomalous pathway. Eight had the permanent form of reciprocating tachycardias (long RP' tachycardia) and 46 had a left posteroseptal preexcitation marked by a prominent R wave in lead VI. In 14 of 19 patients, ventriculoatrial conduction time during tachycardia lengthened in conjunction with functional left bundle branch block; this behaviour was significantly different from a series of patients with right posteroseptal preexcitation in which functional left bundle branch block lengthened the ventriculoatrial time in only one of 12 patients. A quadripolar electrode catheter was left within the proximal coronary sinus in order to locate the earliest atrial or ventricular activation site. The appropriate bipole was used as the radiographic and electrophysiological reference of the insertion of the accessory pathway. A catheter was then positioned on the septal side of the right atrium, outside the coronary sinus, so that atrial activity during reciprocating tachycardia and ventricular activity during preexcitation were synchronous with or earlier than that recorded within the proximal coronary sinus. Accessory pathway potential was not recorded in any patient. Early ventricular potential occurring --1.5 +/- 8 ms relative to delta wave onset was present at that site. In 38 patients, including 5 with permanent junctional tachycardia, high current (14 mA) pacing yielded direct ventricular paced QRS complexes (no delay spike-QRS) with a morphology similar to left posteroseptal maximal preexcitation. Slight movements of catheter position yielded significantly different pace-maps. One to eight 160 J cathodal shocks (510 +/- 213 J cumulative per patient) were delivered at this site in 61 sessions. Following fulguration, tachycardia recurred without drugs in only one patient over a follow-up period of 20 +/- 13 months. Asymptomatic intermittent preexcitation recurred in two patients. In all patients with long RP' tachycardia, the ablation procedure was successful without the need for drugs or permanent cardiac pacing. A long-term follow-up electrophysiological study in 18 patients demonstrated that conduction through the anomalous pathway was absent in 16 and deeply altered in the two patients with intermittent preexcitation; no tachycardia was inducible in any patient. In conclusion, catheter ablation of left posteroseptal accessory pathways is a feasible procedure using a right atrial approach outside the coronary sinus. This technique is also effective for the treatment of the permanent form of reciprocating tachycardia.     

Quintuple pathways participating in three distinct types of atrioventricular reciprocating tachycardia in a patient with Wolff-Parkinson-White syndrome

Electrophysiologic studies were performed in a patient with recurrent supraventricular tachyarrhythmias. Sinus and paced atrial beats had QRS complexes characteristic of atrioventricular (A-V) conduction through a manifest left lateral accessory pathway (Wolff-Parkinson-White syndrome, type A). Three distinct types of A-V reciprocating tachycardia and three different modes of retrograde atrial activation were demonstrated. Type 1 tachycardia involved the slow A-V nodal pathway and a second (left lateral or left paraseptal) accessory A-V pathway capable of retrograde conduction only. Type 2 tachycardia was of the slow-fast A-V nodal pathway type. Type 3 tachycardia involved a heretofore undescribed circuit in that retrograde conduction occurred through an accessory A-V pathway with long retrograde conduction times and anterograde conduction through both the manifest left lateral accessory A-V pathway and fast A-V nodal pathway. Premature ventricular beats delivered late in the cycle of this tachycardia advanced (but did not change) the retrograde atrial activity without affecting the timing of the corresponding anterograde H deflection. In summary, this patient had five (three accessory and two intranodal) pathways participating in three different types of A-V reciprocating tachycardia; the recurrence of these were prevented with oral amiodarone therapy.     

Investigation of the preexcitation syndromes

Assessment of the localization and function of accessory atrioventricular pathways may be undertaken with noninvasive and invasive examination techniques. Noninvasive methods, however, such as electrocardiography, vectorcardiography, precordial mapping, echocardiography and scintigraphy do not enable exact delineation of the site of the accessory pathway since, in general, their use requires maximal preexcitation; moreover, they are of less value in the presence of septal bundles, multiple accessory pathways or intraventricular conduction disturbances. Accordingly, localization of accessory atrioventricular pathways is based on data obtained from intracardiac electrography such as the interval between stimulus and delta wave during atrial pacing, retrograde atrial sequence, VA conduction time at onset of right or left bundle branch block as well as responses to programmed ventricular stimulation during orthodromic reciprocating tachycardia. The most exact method for determination of the localization of the Kent bundle employs intraoperative endocardial and epicardial mapping with analysis of VA and AV conduction times during reciprocating tachycardia, ventricular stimulation and atrial pacing. The conduction properties of the accessory atrioventricular bundle may be estimated noninvasively based on the persistence of a delta wave as a function of the heart rate, the influence of antiarrhythmic agents on the anterograde conduction via the normal pathway as well as the shortest interval between two consecutive QRS complexes with delta waves during atrial fibrillation. Functional assessment is carried out invasively through recording the anterograde and retrograde refractory periods of the Kent bundle as well as observations during programmed atrial and ventricular stimulation or induced atrial fibrillation.     

The electrophysiologic basis and management of symptomatic recurrent tachycardia in patients with ebstein's anomaly of the tricuspid valve

Twenty-two patients with Ebstein's anomaly were evaluated because of recurrent tachycardia. A total of 30 accessory pathways were present in 21 of the 22 patients. Twenty-six accessory pathways were of the atrioventricular (A-V) type while four were Mahaim fibers. Multiple accessory pathways were present in eight patients. Twenty-five of the 26 accessory A-V pathways were right-sided, either in the posterior septum (12 pathways) or the posterolateral free wall (13 pathways); one patient with corrected transposition of the great arteries had a left-sided accessory A-V pathway in a lateral free wall location. Patients with accessory A-V pathways had a long minimal ventriculoatrial (V-A) conduction time during reciprocating tachycardia (192 ± 47 ms) and usually showed a persistent complete or incomplete right bundle branch block morphology.At surgery, preexcitation was invariably localized to the atrialized ventricle. The long V-A conduction time during reciprocating tachycardia appeared to consist of late activation of the local ventricle in the region of the accessory pathway with a further delay occurring before excitation of adjacent atrium presumably due to conduction over the accessory pathway. Accessory A-V pathways were successfully sectioned with no deaths in 13 of 15 patients.On the basis of these data, certain electrocardiographic findings encountered in the study of patients with recurrent tachycardia should point to the possibility of associated Ebstein's anomaly: morphology of the surface electrocardiogram suggesting preexcitation of the right posterior septum or right posterolateral free wall as well as the combination during reciprocating tachycardia of a long V-A interval and right bundle branch block.     

Radiofrequency catheter ablation of accessory pathway in a patient with Ebstein's anomaly and atrial septal defect--a case report

The authors report the case of a 57-year-old woman with Ebstein's anomaly and atrial septal defect. She was referred to their hospital for treatment of refractory paroxysmal wide QRS tachycardia. Her 12-leads ECG in sinus rhythm showed ventricular preexcitation of type B Wolff-Parkinson-White syndrome. In a baseline electrophysiological study, a wide QRS tachycardia with right bundle branch block configurations was induced. This tachycardia was orthodromic atrioventricular reciprocating tachycardia with a right inferior accessory pathway. Radiofrequency current was successfully delivered at the inferior site of the atrialized right ventricle. Radiofrequency catheter ablation seems to be useful for supraventricular tachycardia in patients with Ebstein's anomaly and atrial septal defect.     

Wolff-Parkinson-White Syndrome Presenting as the Permanent Form of Junctional Reciprocating Tachycardia

Permanent Reciprocating Tachycardia and Preexcitation. The substrate of the permanent form of junctional reciprocating tachycardia is an accessory pathway with no spontaneous anterograde conduction, usually located in the posteroseptal area. We report a case of this type of tachycardia with overt anterograde ventricular preexcitation. Electrophysiologic study confirmed that tachycardia was due to an accessory pathway with long retrograde conduction time; electrophysiologic findings suggested longitudinal dissociation of the accessory pathway. Radiofrequency application at the coronary sinus os resulted in disappearance of preexcitation and cure of the tachycardia.     

Functional bundle branch block and orthodromic reciprocating tachycardia cycle length: do not bet on accessory pathway location.

AIMS: To show 2 examples in which the analysis of the effect of bundle branch block on orthodromic reciprocating tachycardia cycle length was misleading. METHODS AND RESULTS: We performed an electrophysiological study in two patients with orthodromic reciprocating tachycardia showing a transition from wide to narrow QRS during tachycardia. Our two cases of left bundle branch block during reciprocating tachycardia using infero-septal pathways show that ventricular to atrial conduction time prolongation may be larger than 30 ms and may be concealed by a shortening of atrial to ventricular conduction time. In the 2 cases, the atrial insertion of the accessory pathway could be successfully ablated from the right atria at the ostium of the coronary sinus. CONCLUSIONS: The observation of the association between left bundle branch block and cycle length prolongation during reciprocating tachycardia may be associated with a successful ablation at the ostium of the coronary sinus.     

Clinical,electrocardiographic and electrophysiologic observations in patients with paroxysmal supraventricular tachycardia

Seventy-nine patients without ventricular preexcitation but with documented paroxysmal supraventricular tachycardia were analyzed. Electrophysiologic studies suggested atrioventricular (A-V) nodal reentrance in 50 patients, reentrance utilizing a concealed extranodal pathway in 9, sinus or atrial reentrance in 7 and ectopic automatic tachycardia in 3. A definite mechanism of tachycardia could not be defined In 10 patients (including 7 whose tachycardia was not inducible). The three largest groups with inducible tachycardias were compared in regard to age, presence of organic heart disease, rate of tachycardia, functional bundle branch block during tachycardia and relation of the P wave and QRS complex during tachycardia. A-V nodal reentrance was characterized by a narrow QRS complex and a P wave occurring simultaneously with the QRS complex during tachycardia. Reentrance utilizing a concealed extranodal pathway was characterized by young age, absence of organic heart disease, fast heart rate, presence of bundle branch block during tachycardia and a P wave following the QRS complex during tachycardia. Sinoatrial reentrance was characterized by frequent organic heart disease, a narrow QRS complex and a P wave in front of the QRS complex during tachycardia.In conclusion, a mechanism of paroxysmal supraventricular tachycardia could be defined in most patients. Observations of clinical and electrocardiographic features in these patients should allow prediction of the mechanism of the tachycardia.     

Mahaim纤维的电生理特征和导管射频消融

探讨Mahaim纤维的电生理特征和导管射频消融的可行性。 1996年 5月至 1999年 4月对 4例拟诊为Mahaim纤维引起的逆向型房室折返性心动过速的病人进行了电生理检查和射频导管消融。男 3例、女 1例 ,年龄 31± 19岁 ,心动过速发作史 15± 14年 ,频率 2 0 1± 17(180～ 2 2 0 )次 /分 ,发作时均有明显的心悸症状。 4例窦性心律时心电图除 1例轻微预激外均正常。心房程序电刺激可以诱发心动过速。心室起搏时从房室结逆传 ,静脉注射ATP 2 0mg室房分离。 4例Mahaim心动过速均只有前传并呈递减传导特性。 1例同时合并房室结折返性心动过速。 2例导管操作发生心房颤动并经过Mahaim纤维前传 ,1例持续发作、1例短暂发作。 4例分别在心房起搏、心动过速和心房颤动时三尖瓣心房侧标测和消融。心室预激较体表V1导联QRS波起始处提前 40± 6 (34～ 46 )ms处消融均获成功 ,1例靶点位于右前侧壁、3例位于右后侧壁。能量 35± 5W ,消融 5± 3次 ,X线透视时间 38± 2 1min。无手术相关的并发症。合并房室结折返性心动过速 1例同时作了慢径改良。分别随访 3个月～ 3年无 1例心动过速复发。临床研究证实 ,导管射频消融是治疗Mahaim介导的心动过速的有效、可行和安全的方法     

Termination of circus movement tachycardia utilizing an accessory atrioventricular pathway by retrograde concealed penetration of the atrioventricular node through the bundle branch system: A mechanism of tachycardia termination in Wolff-Parkinson-White syndrome

A 30 year old woman with Wolff-Parkinson-White syndrome underwent electrophysiologic study for investigation of circus movement tachycardia utilizing the accessory pathway for retrograde conduction. The accessory pathway was located on the right side. Episodes of circus movement tachycardia with left and right bundle branch block were induced. Some episodes of circus movement tachycardia with left bundle branch block terminated spontaneously. Two episodes of spontaneous termination at the level of the atrioventricular (A-V) node were preceded by prolongation of the H-V interval causing delay in atrial activation. This delayed atrial cycle was then followed paradoxically by spontaneous termination of the tachycardia in the A-V node. A similar phenomenon could be demonstrated reproducibly with single echo beats induced by coronary sinus extrastimuli. It appears that retrograde concealed penetration of the A-V node through the bundle branch system during anterograde left bundle branch block is the most likely mechanism for this phenomenon.     

Catheter ablation of Mahaim fibers with preservation of atrioventricular nodal conduction

Three patients with refractory preexcited tachycardia implicating Mahaim fibers underwent attempted catheter ablation of the accessory pathway. In the absence of demonstrable retrograde conduction in Mahaim fibers, we located the accessory pathway ventricular insertion site using the criteria of concordance between paced and spontaneous QRS morphologies during pace-mapping and earliest onset of local electrogram relative to surface preexcited QRS. At this site, a QS-like pattern of unfiltered unipolar electrograms with steep downstroke was recorded. The optimal site appeared radiologically at the right ventricular anterior wall or the adjacent septum, 2-4 cm from the tricuspid anulus. Three to six 160-J shocks were delivered at this site using an anterior chest wall plate as anode. After fulguration, conduction through the Mahaim tract was absent. A right bundle branch block persisted in two patients. All patients remained free of preexcited tachycardia during 12-16 months of follow-up. Postablation electrophysiological assessment showed no preexcitation in any patient. No reciprocating tachycardia was inducible, even during isoproterenol infusion. Atrioventricular nodal conduction parameters were unchanged from baseline study. Catheter ablation of Mahaim fibers is an effective alternative method for the treatment of tachycardias that include the accessory pathway in the circuit.     

Simultaneous anterograde fast-slow atrioventricular nodal pathway conduction after procainamide

Three patients with paroxysmal supraventricular tachycardia underwent electrophysiologic studies that included His bundle recordings, incremental atrial and ventricular pacing and extrastimulation before and after intravenous infusion of 500 mg of procainamide. In all three patients the tachycardia was induced during atrial pacing or premature atrial stimulation, or both. Two of the three patients had discontinuous atrioventricular (A-V) nodal curves with induction of a slow-fast tachycardia during failure in anterograde fast pathway conduction and one patient had a smooth A-V nodal curve with induction of a slow-fast tachycardia at critical A-H interval delays. After procainamide: (1) in all three patients atrial pacing induced A-V nodal Wenckebach periodicity (cycle length 300 to 400 ms) resulting in simultaneous anterograde fast and slow pathway conduction (one atrial beat resulting in two QRS complexes) and retrograde fast pathway conduction initiating an echo response or a slow-fast tachycardia, or both; (2) in all three patients there was enhanced conduction and shortening of refractoriness of the anterograde fast pathway and depressed conduction and lengthening of refractoriness of the retrograde fast pathway; and (3) in two patients there was inability to sustain tachycardia because of selective block within the retrograde fast pathway. In conclusion: (1) procainamide altered conduction and refractoriness of the anterograde fast and slow pathways so that simultaneous conduction could occur during atrial pacing, resulting in a double ventricular response and a slow-fast echo or tachycardia, or both; and (2) the differential effects of procainamide on anterograde fast and retrograde fast pathways suggests two functional A-V nodal fast pathways, one for anterograde and the other for retrograde conduction.     

Electrophysiologic characteristics and radiofrequency ablation of concealed nodofascicular and left anterograde atriofascicular pathways

INTRODUCTION: True nodoventricular or nodofascicular pathways and left-sided anterograde decremental accessory pathways (APs) are considered rare findings. METHODS AND RESULTS: Two unusual patients with paroxysmal supraventricular tachycardia were referred for radiofrequency (RF) ablation. Both patients had evidence of dual AV nodal conduction. In case 1, programmed atrial and ventricular stimulation induced regular tachycardia with a narrow QRS complex or episodes of right and left bundle branch block not altering the tachycardia cycle length and long concentric ventriculoatrial (VA) conduction. Ventricular extrastimuli elicited during His-bundle refractoriness resulted in tachycardia termination. During the tachycardia, both the ventricles and the distal right bundle were not part of the reentrant circuit. These findings were consistent with a concealed nodofascicular pathway. RF ablation in the right atrial mid-septal region with the earliest atrial activation preceded by a possible AP potential resulted in tachycardia termination and elimination of VA conduction. In case 2, antidromic reciprocating tachycardia of a right bundle branch block pattern was considered to involve an anterograde left posteroseptal atriofascicular pathway. For this pathway, decremental conduction properties as typically observed for right atriofascicular pathways could be demonstrated. During atrial stimulation and tachycardia, a discrete AP potential was recorded at the atrial and ventricular insertion sites and along the AP. Mechanical conduction block of the AP was reproducibly induced at the annular level and at the distal insertion site. Successful RF ablation was performed at the mitral annulus. CONCLUSION: This report describes two unusual cases consistent with concealed nodofascicular and left anterograde atriofascicular pathways, which were ablated successfully without impairing normal AV conduction system.     

Reciprocating tachycardia and anterograde conduction by a nodoventricular pathway

Two patients were investigated for paroxysmal regular tachycardia with left bundle branch block centrifugation. A right-sided nodo-ventricular accessory pathway was demonstrated in both cases at electrophysiological investigation with His bundle recording and atrial and ventricular programd pacing techniques. However, the function of this pathway was different in the two cases. In the first case, there were no signs of an accessory pathway on the surface ECG in sinus rhythm but it could be unmasked by simple right atrial pacing at the same rhythm (widening of the QRS and shortening of HV from 40 to 25 ms). The tachycardias could be only initiated by ventricular extrastimulus. They showed major pre-excitation with left sided delay and a 1/1 atrio-ventricular response. There was no His potential before the ventriculogramme which retained the same configuration throughout the attack. The investigations also suggested the presence of a dual nodal pathway with the accessory pathway connected to the slow pathway. In the second case, the presence of an accessory pathway could be suspected from the appearance of the QRS complex in sinus rhythms. Tachycardia was initiated by an atrial extrastimulus with initially a first complex showing slightly more marked pre-excitation and a distinct His potential before the QRS but with a shorter HV interval than in sinus rhythm. Then the reciprocating tachycardia had appearances of major pre-excitation, left-sided delay and a 1/1 atrio-ventricular response. However, in contrast to the first case, all ventricular complexes were preceded by a His potential and the degree of pre-excitation was variable with a HV interval ranging from 0 to 15 ms. These two cases merit attention because of: --their points in common: nodal duality and an accessory pathway which was not atrio-ventricular (decremental conduction) but nodo-right ventricular, conducting well in the anterograde direction but more or less masked in sinus rhythm; the presence of the accessory pathway was clearly visible during reciprocating tachycardia; --the differences: in the first case the nodo-ventricular pathway formed part of the circuit of the reciprocating tachycardia which was antidromic: descending limb, the slow nodal pathway and then the accessory nodo-ventricular pathway; ascending limb, the His bundle and then the rapid nodal pathway. In the second case, the reciprocating tachycardia was entirely intranodal, the accessory pathway not being involved in the circuit but connected to it in parallel with the normal Hisian pathway.