Anterograde Conduction Research Articles

Unmasking of Retrograde Conduction by Isoproterenol in a Concealed Accessory Pathway

A 52-year-old female with no structural heart disease presented with a right bundle branch block (RBBB)/right axis deviation tachycardia with a cycle length of 300 msec. P waves were not discernible on the surface ECG. Baseline electrophysiology study in the drug-free state revealed no evidence for anterograde or retrograde conducting accessory pathways (APs) or for dual AV node physiology. Retrograde VA block with AV dissociation was present at a ventricular paced cycle length of 600 msec (sinus cycle length of 635-700 msec). AV nodal Wenckebach occurred during decremental atrial pacing at a cycle length of 300 msec. During isoproterenol administration, a left lateral AP with retrograde only conduction became manifest with 1:1 VA conduction to 380 msec. No anterograde AP conduction was present. Orthodromic reciprocating tachycardia with a cycle length of 285-315 msec was easily induced. We conclude that total functional conduction block can exist in APs, and unmasking of total conduction block can be accomplished with isoproterenol. All patients with undiagnosed tachycardias should have full repeat stimulation studies during adrenergic stimulation if the initial baseline evaluation is nondiagnostic.

976-10 Fast-slow (Uncommon) Form of Atrioventricular Nodal Reentrant Tachycardia (AVNRT): New Classification Based on the Site of the Retrograde Slow AV Nodal Pathway

During fast-slow (uncommon) form of AVNRT. anterograde conduction occurs over the fast pathway (located at the anterior septum) and retrograde conduction occurs over the slow pathway (located at the posterior septum). Thus, in this variety of AVNRT retrograde atrial activation occurs first at or near the orifice of the coronary sinus (CSOS), then at the low septal right atrium (LSRA) in the His bundle recording site. However, retrograde slow pathway may possibly be located at the anterior septum; in such a case. activation of the LSRA would be earlier than that of the CSOS. To investigate the retrograde atrial activation, 12 pts with fast-slow AVNRT (cycle length; 305535 ms)were studied while recording the electrograms of the CSOS and the LSRA.ln addition, to investigate the location of the anterograde fast pathway, programmed atrial stimulation was done from the CSOS (or proximal CS) and the anterior high right atrium (HRA) during AVNRT. In all pts reentry using concealed accessory pathways with long conduction times was excluded. In 6/12 pts CSOS activation during AVNRT preceded the LSRA activation by ≥ 10 ms (posterior type). in 3/12 pts LSRA activation preceded the CSOS by ≥ 0 ms (anterior type); in the remaining 3 pts (middle type) those two sites were activated simultaneously (time difference ≥ 5 ms). In pts with posterior and middle type AVNRT. HRA stimulation during tachycardia preexcited the His bundle and the ventricle via the fast pathway without capturing the CSOS (i.e., inter-atrial dissociation) but the dissociation was not elucidated with CSOS stimulation. indicating that the anterogradely conducting fast pathway is anterior to the retrograde slow pathway. In pts with anterior AVNRT, CSOS stimulation (but not HRA stimulation) demonstrated the inter-atrial dissociation. establishing that the anterograde fast pathway is posterior to the retrograde slow pathway. In 6/6 pts with posterior and 3/3 pts with middle type AVNRT, P waves in inferior leads were deeply negative, but in 2/3 pts with anterior type AVNRT, P waves were biphasic or shallow. Fast-slow AVNRT could be divided into 3 types based on the slow pathway location (posterior, middle Or anterior). In anterior type fastslow AVNRT, radiofrequency ablation using a posterior approach may fail to eliminate the slow pathway.

1025-100 Patients with WPW Syndrome and Paroxysmal Atrial Fibrillation Shows Prolonged Atrial Conduction Time by Signal-Averaged P-Wave Electrocardiogram

The purpose of this study was to establish a relationship between the atrial activation assessed by signal-averaged P wave ECG (SAPW) and episodes of paroxysmal atrial fibrillation (PAF) in patients (pts) with WPW syndrome (WPWS). fourteen pts with documented episodes of PAF, without underlying heart disease were selected (12 men: age = 35.2 ± 11.1 years) from a total of 70 consecutives pts successfully submitted to radiofrequency catheter ablation of accessory pathway (AP). All pts with anterograde conduction over the AP. left side AP in 9 pts and right side AP in 5 pts. The SAPW were recorded with the Corazonix Predictor II system from the X, Y, Z leads (40–250 Hz, least Square filter, final noise < 0.3 μV). The total filter P wave duration (PWD) was obtained manually from the vector-magnitude in ms. Recordings were performed between 7 th and 14 th day after the ablation. No pts showed left atrial larger than 4.0 cm on the echocardiogram. The results were compared with a control group of 12 pts matched in age (5 men; age = 33.0 ± 10.2 years) without heart disease. Values were given as mean and 1SO and compared using non-paired Student t test (significance < 0.05). Control Group In = 12): PWD ranged from 115.0 to 129.5 ms with a mean of 124.4 ± 4.4 ms. WPWS with PAF (n = 14): PWD ranged from 130.0 to 171.0 ms with a mean of 142.9 ± 1 0.1 ms (p < 0.000). Eleven pts (78.5%) showed PWD > 135.0 ms. There were no differences between PWD and AP location. Recurrent PAF after ablation was noted in 3 pts (21% – PWD: 171.0, 1505 and 139.0 ms for each patient). With a cutoff < 135.0 ms for a normal PWD, the sensitivity was 78.5%, the specificity was 100%; the positive predictive value was 100% and the negative was 75% for SAPW to identify pts with WPWS and PAF. In the current study, pts with WPWS and PAF showed prolonged intra-atrial conduction time when compared with a control group. This may contribute to the development of PAF.

Localization and radiofrequency catheter ablation of left-sided accessory pathways during atrial fibrillation Feasibility and electrogram criteria for identification of appropriate target sites

Objectives. The purpose of the present study was to assess the feasibility of and electrophysiologic criteria for successful radio-frequency catheter ablation of left-sided accessory pathways during atrial fibrillation in patients with Wolff-Parkinson-White syndrome.Background. The onset of recurrent or sustained atrial fibrillation can complicate or significantly prolong accessory pathway catheter ablation procedures.Methods. We studied 19 consecutive patients (mean age [±SD] 44 ± 16 years) with Wolff-Parkinson-White syndrome who had ongoing atrial fibrillation with rapid anterograde conduction over the accessory pathway (mean ventricular rate [±SD] 173 ± 26 beats/min, range 130 to 220) at the beginning of the localization procedure during radiofrequency catheter ablation. Localization and ablation of the accessory pathway were performed with a 7F deflectable catheter (4-mm tip) that was placed underneath the mitral valve annulus. The electrophysiologic criteria from unipolar and bipolar local electrograms were compared for successful (n = 18) and unseccessful (n = 39) sites.Results. The accessory pathways were localized in the left posteroseptal (n = 6), posterior (n = 1), posterolateral (n = 7) and lateral (n = 5) regions and successfully ablated during atrial fibrillation in 18 (95%) of 19 patients with a mean of 3 ± 2 radiofrequency pulses (range 1 to 8, median 2). Presence of an accessory pathway potential (94% vs. 44%), early activation time of the ventricular electrogram (−3.2 ± 9.2 vs.−15.3 ± 12.6 ms) and recording of atrial activation (88% vs. 61%) from the ablation catheter were helpful in identifying successful sites (p < 0.001, p < 0.001 and p < 0.05, respectively, compared with unsuccessful sites). In addition, the ventricular activation time in relation to the intrinsic deflection of the unipolar electrogram was significantly earlier at successful than unsuccessful sites (18.1 ± 4.8 vs. 24.4 ± 6.6 ms, p < 0.01). A QS complex on the unipolar electrogram was observed at 96% of successful sites and at 94% of unsuccessful sites (p = 0.74). Multivariate logistic regression analysis revealed that the presence of an accessory pathway potential (p < 0.002) and early ventricular activation time in relation to the onset of the QRS complex (p < 0.001) were independent predictors of ablation success.Conclusions. Localization and radiofrequency catheter ablation of left-sided accessory pathways is possible in patients with sustained atrial fibrillation and rapid anterograde conduction over the accessory pathway during the ablation procedure. The electrophysiologic criteria described here can be used to reliably identify successful sites for radiofrequency ablation.

Catheter Ablation of the Left Bundle Branch for the Treatment of Sustained Bundle Branch Reentrant Ventricular Tachycardia

Sustained Bundle Branch Reentrant VT. Radiofrequency catheter ablation of the left bundle branch (LBB) was attempted in a patient with sustained bundle branch reentry. During sinus rhythm, the QRS had a complete LBB block pattern, and the LBB was activated retrogradely (transseptal). Ablation of the LBB eliminated inducibility of the tachycardia, while the QRS complex and the duration of the HV interval (70 msec) remained unchanged. Successful ablation of the LBB eliminated bundle branch reentry and yet maintained the anterograde conduction properties of the His-Purkinje system, obviating implantation of a permanent pacemaker.

Radiofrequency Ablation Therapy in Concealed Left Free Wall Accessory Pathway With Decrementai Conduction

An electrophysiologic study followed by transcatheter radiofrequency ablation therapy was performed in two adult patients with a permanent form of junctional tachycardia. Both patients had no structural heart disease and exhibited a normal resting ECG. The P wave during tachycardia was negative in leads 1, 3, and aVF, biphasic over V6, and positive in V1 and aVL in both patients, while the P-R/R-P interval ratio during tachycardia was 0.82 and 0.36, respectively, in both patients. Both patients displayed an eccentric atrial activation sequence with the earliest atrial activation occurring at the distal coronary sinus and a decremental retrograde conduction property during incremental ventricular pacing, suggesting the presence of a concealed slowly conducting left free wall accessory pathway. The tachycardia used the normal atrioventricular pathway for anterograde conduction and the concealed show left accessory pathway for retrograde conduction. It was terminated following adenosine administration in both patients; termination of tachycardia was due to a block in the retrograde accessory pathway in one patient and due to a block in the atrioventricular node in the other patient. Radiofrequency ablation was performed by the retrograde transaortic approach. The radiofrequency f4p4ent was delivered to the site of the earliest atrial activation during tachycardia at the ventricular aspect of the mitral annulus. The successful ablation site had a ventriculoatrial (VA) interval of 120 and 130 ms, respectively, and was located at the posterolateral and lateral aspects of the mitral annulus. Following ablation, there was no VA conduction; however, conduction through the normal atrioventricular pathway was noted during isoproterenol infusion in both patients. There was no induction of tachycardia. This study demonstrates that the permanent form of junctional tachycardia in adults can incorporate a concealed left free wall accessory pathway with a decremental property. Radiofrequency ablation therapy is effective and safe in this form of arrhythmia.

Differential effect of esmolol on the fast and slow AV nodal pathways in patients with AV nodal reentrant tachycardia.

AV nodal reentrant tachycardia (AVNRT) usually involves anterograde conduction over a slowly conducting ("slow") pathway and retrograde conduction over a rapidly conducting ("fast") pathway. A variety of drugs, such as beta blockers, digitalis, and calcium channel blockers, have been reported to prolong AV nodal refractoriness in both the anterograde and retrograde limbs of the circuit. However, few data are available that address whether the fast and slow pathways respond in a quantitatively different manner to drugs such as beta-adrenergic antagonists. In addition, it is not known whether the effects of these agents on refractoriness parallel the effects on conduction in the fast and slow pathways. The present study was performed to measure the effect of the intravenous beta-adrenergic agent, esmolol, on refractoriness and conduction in both the fast and slow AV nodal pathways in patients with AVNRT. Thirteen patients with discontinuous AV nodal conduction properties and typical AVNRT were studied. Anterograde and retrograde AV nodal functional assessment was performed at baseline and following steady-state drug infusion of intravenous esmolol at a dose of 500 micrograms/kg for 1 minute, 150 micrograms/kg per minute for the next 4 minutes, followed by a continuous maintenance infusion of 50 to 100 micrograms/kg per minute. The anterograde effective refractory period of the fast pathway increased from 381 +/- 75 msec at baseline to 453 +/- 92 msec during the infusion of esmolol (P = 0.003). The anterograde effective refractory period of the slow pathway was also prolonged by esmolol, from 289 +/- 26 msec to 310 +/- 17 msec (P = 0.005). However, the absolute magnitude of the change in the anterograde effective refractory period of the fast pathway (+72 +/- 59 msec) was significantly greater than the change in anterograde effective refractory period of the slow pathway (+21 +/- 16 msec, P = 0.01). The mean retrograde effective refractory period of the fast pathway increased from 276 +/- 46 msec to 376 +/- 61 msec during esmolol infusion (P = 0.03). Retrograde slow pathway conduction that could not be demonstrated at baseline became manifest in three patients during esmolol infusion. In contrast to the effects of esmolol on refractoriness, the AH interval during anterograde slow pathway conduction prolonged to a far greater extent (+84 msec) than the HA interval associated with retrograde fast pathway conduction (+5 msec, P = 0.04). The beta-adrenergic antagonist, esmolol, has a quantitatively greater effect on anterograde refractoriness of the fast than the slow AV nodal pathway. However, the effects on conduction intervals during AVNRT are greater in the anterograde slow pathway than in the retrograde fast pathway. These observations suggest that the fast and slow pathways may have differential sensitivities to autonomic influences. This difference in the response to beta-adrenergic antagonists may be exploited as a clinically useful method for demonstrating slow pathway conduction in some individuals with AVNRT.

Radiofrequency ablation therapy in atypical or multiple atrioventricular node reentry tachycardias

Electrophysiologic study and radiofrequency ablation therapy were performed in 23 patients with atypical (8 patients) or multiple (15) atrioventricular node reentry tachycardias. Dual pathways with anterograde fast and slow pathway conductions were demonstrated in 16 patients. Studies on retrograde conduction revealed the presence of three different pathways, including fast (15 patients), intermediate (17), and slow (16). The radiofrequency current was applied to the inferior aspect, one-third anterior two-thirds posterior between the His bundle and the ostium of the coronary sinus, of Koch's triangle along the tricuspid annulus in all patients. Application of the current resulted in selective ablation or modification of both retrograde intermediate and slow pathway conductions in 20 patients. In two patients retrograde fast pathway conduction was also modified. Complete atrioventricular block occurred in the remaining patient. Sixteen patients had no induction of tachycardia or echo, 4 had induction of a single echo, and 2 had induction of the slow-fast form tachycardia; one of those 2 patients underwent a second trial and was successful. A median application of 2 was delivered at a power of 25 ± 5 W and a duration of 18 ± 4 sec. The total fluoroscopic time was 25 ± 21 minutes. The anterograde fast pathway conduction was unaffected; the shortest atrial paced cycle length that sustained 1:1 fast pathway conduction was 329 ± 65 msec and 330 ± 68 msec before and after ablation, respectively. A follow-up electrophysiologic study was performed in 16 patients 60 ± 15 days after ablation. Eleven had no induction of tachycardia or echo, and five had induction of <3 echoes. This study demonstrated that radiofrequency ablation with the inferior approach is effective and safe in atypical or multiple atrioventricular node reenty tachycardias. It resulted in ablation of the slow pathway and retrograde intermediate pathway conduction with preserved atrioventricular conduction.

The Differential Diagnosis of a Regular Tachycardia with a Wide QRS Complex on the 12‐Lead ECG: Ventricular Tachycardia, Supraventricular Tachycardia with Aberrant Intraventricular Conduction, and Supraventricular Tachycardia with Anterograde Conduction Over an Accessory Pathway

Pacing and Clinical ElectrophysiologyVolume 17, Issue 9 p. 1515-1524 The Differential Diagnosis of a Regular Tachycardia with a Wide QRS Complex on the 12-Lead ECG: Ventricular Tachycardia, Supraventricular Tachycardia with Aberrant Intraventricular Conduction, and Supraventricular Tachycardia with Anterograde Conduction Over an Accessory Pathway EDUARDO ANTUNES, EDUARDO ANTUNES Cardiovascular Research and Teaching Institute Aalst, Cardiovascular Center, O.L.V. Hospital, Aalst, BelgiumSearch for more papers by this authorJOSEP BRUGADA, JOSEP BRUGADA Arrhythmia Unit, Hospital Clinic, Barcelona, SpainSearch for more papers by this authorGUNTER STEURER, GUNTER STEURER Cardiovascular Research and Teaching Institute Aalst, Cardiovascular Center, O.L.V. Hospital, Aalst, BelgiumSearch for more papers by this authorERIK ANDRIES, ERIK ANDRIES Cardiovascular Research and Teaching Institute Aalst, Cardiovascular Center, O.L.V. Hospital, Aalst, BelgiumSearch for more papers by this authorPEDRO BRUGADA, Corresponding Author PEDRO BRUGADA Cardiovascular Research and Teaching Institute Aalst, Cardiovascular Center, O.L.V. Hospital, Aalst, BelgiumAddress for reprints: Pedro Brugada, M.D., Professor of Cardiology, Cardiovascular Research and Teaching Institute Aalst, Cardiovascular Center, O.L.V. Hospital, Moorselbaan, 164. B-9300 Aalst, Belgium. Fax; 011-32-53-724587.Search for more papers by this author EDUARDO ANTUNES, EDUARDO ANTUNES Cardiovascular Research and Teaching Institute Aalst, Cardiovascular Center, O.L.V. Hospital, Aalst, BelgiumSearch for more papers by this authorJOSEP BRUGADA, JOSEP BRUGADA Arrhythmia Unit, Hospital Clinic, Barcelona, SpainSearch for more papers by this authorGUNTER STEURER, GUNTER STEURER Cardiovascular Research and Teaching Institute Aalst, Cardiovascular Center, O.L.V. Hospital, Aalst, BelgiumSearch for more papers by this authorERIK ANDRIES, ERIK ANDRIES Cardiovascular Research and Teaching Institute Aalst, Cardiovascular Center, O.L.V. Hospital, Aalst, BelgiumSearch for more papers by this authorPEDRO BRUGADA, Corresponding Author PEDRO BRUGADA Cardiovascular Research and Teaching Institute Aalst, Cardiovascular Center, O.L.V. Hospital, Aalst, BelgiumAddress for reprints: Pedro Brugada, M.D., Professor of Cardiology, Cardiovascular Research and Teaching Institute Aalst, Cardiovascular Center, O.L.V. Hospital, Moorselbaan, 164. B-9300 Aalst, Belgium. Fax; 011-32-53-724587.Search for more papers by this author First published: September 1994 https://doi.org/10.1111/j.1540-8159.1994.tb01517.xCitations: 48AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Citing Literature Volume17, Issue9September 1994Pages 1515-1524 RelatedInformation

Independent Ablation of Retrograde and Anterograde Accessory Connection Conduction at the Atrial and Ventricular Insertion Sites:

The impedance mismatch hypothesis has been proposed as one of the mechanisms responsible for accessory connection conduction block. We describe a case in which retrograde conduction across a posteroseptal accessory connection was ablated at the atrial insertion site in the coronary sinus os, whereas anterograde conduction was ablated at the ventricular insertion site in the left ventricle. The evidence supports the impedance mismatch concept as the cause of unidirectional conduction block and shows that the distal junction between the accessory connection and the myocardium is more vulnerable to ablation.

Effect of adenosine or adenosine triphosphate on antidromic tachycardia

Objectives. This study was designed to determine the effect of adenosine or adenosine triphosphate (ATP) on antidromic tachycardia.Background. Adenosine and adenosine triphosphate are useful for differential diagnosis of wide QRS tachycardia. It has been believed that tachycardia termination caused by these agents is due to the preferential depressive effect on the atrioventricular (AV) node, whereas their effect on accessory pathways is minimal. Methods. We studied the effect of adenosine or ATP on the termination pattern of antidromic tachycardia in 17 patients (10 men, 7 women; mean age [±SD] 32 ± 11 years) with one or more accessory pathways. Adenosine (6 to 12 mg [n = 10]) or ATP (8 to 20 mg [n = 7]) was injected rapidly through a central venous line and followed by 10 ml of saline flush after induction of sustained antidromic tachycardia.Results. Tachycardia was terminated in < 2 min in 14 patients (82%) after the injection and remained unchanged in 3 (18%). Tachycardia termination was due to conduction block in the accessory pathway (anterograde limb) in seven patients (50%) and in the AV node (retrograde limb) in another seven. Adenosine or ATP caused accessory pathway block in seven (88%) of the eight patients lacking retrograde accessory pathway conduction and in none of the nine patients having retrograde accessory pathway conduction (p < 0.01). All five ptients with an atriofascicular accessory pathway and unidirectional anterograde conduction had tachycardia termination due to anterograde accessory pathway block after injection of adenosine or ATP.Conclusions. 1) Adenosine or ATP effectively terminates antidromic tachycardia; 2) the termination is related to block in either the accessory pathway or the AV node; 3) accessory pathway block occurs in patients with a unidirectional, anterogradely conducting accessory pathway, especially an atriofascicular accessory pathway.

The differential diagnosis on the electrocardiogram between ventricular tachycardia and preexcited tachycardia.

The 12-lead surface electrocardiogram is a simple and useful tool for the differential diagnosis of regular wide QRS complex tachycardia. However, criteria do not as yet exist to discriminate between ventricular tachycardia and supraventricular tachycardia with anterograde conduction over an accessory pathway (preexcited tachycardia). Therefore, we designed a new stepwise approach with three criteria for the electrocardiographic differential diagnosis between ventricular tachycardia and preexcited tachycardia and prospectively studied 267 regular tachycardias with electrophysiologically proven mechanism and a wide QRS complex (> or = 0.12 s): 149 consecutive ventricular tachycardias and 118 consecutive preexcited regular tachycardias. Underlying heart disease was old myocardial infarction in 133 of 149 (89%) ventricular tachycardias. The patients presenting with preexcited tachycardia had no additional structural heart disease. Atrial fibrillation with preexcited QRS complex was not included. The criteria favoring ventricular tachycardia were: (1) presence of predominantly negative QRS complexes in the precordial leads V4 to V6, (2) presence of a QR complex in one or more of the precordial leads V2 to V6, and (3) AV relation different from 1:1 (more QRS complexes than P waves). The final sensitivity and specificity of these three consecutive steps to diagnose ventricular tachycardia were 0.75 and 1.00, respectively. This new stepwise approach is sensitive and highly specific for the differential diagnosis between ventricular tachycardia in coronary artery disease and preexcited regular tachycardia.

Dynamics of circus movement re-entry across canine Purkinje fibre-muscle junctions.

1. To determine the cellular electrophysiological mechanisms for unidirectional conduction block and re-entrant excitation, single cycles of circus movement re-entry were induced in canine Purkinje fibre-papillary muscle preparations containing two Purkinje fibre-muscle junctions (PMJs). The preparations were mounted in a partitioned tissue bath that permitted independent superfusion of each PMJ. The pre-existing dispersion of refractoriness between PMJs was accentuated by superfusing PMJ1 with normal Tyrode solution or Tyrode solution containing 6-8 mM KCl and superfusing PMJ2 with Tyrode solution containing 0.5 mM heptanol and 4-10 mM KCl. 2. Premature stimuli delivered to the Purkinje fibre induced unidirectional anterograde conduction block at PMJ2. Conduction proceeded from Purkinje cells to papillary muscle at PMJ1 and from papillary muscle retrogradely across the previously blocked PMJ2. 3. The difference in refractory periods between the two PMJs defined a range of premature coupling intervals within which re-entry was inducible. Conduction block at the PMJ occurred in papillary muscle at short coupling intervals and in the Purkinje fibre at longer intervals. 4. Once initiated, re-entry could be reset or annihilated by properly timed subthreshold current pulses delivered to cells at the PMJ. 5. To define better the mechanisms for conduction block and re-entry, an analytical model was developed using non-linear regression analysis to derive equations from the experimental results. Varying parameters within the constraints of the model reproduced the key features of the rate-dependent conduction block observed experimentally. Critical elements of the model included the induction of significant activation delays at short diastolic intervals and a reduction in the rate of action potential duration restitution after exposure to heptanol. 6. These results help to establish the conditions necessary for induction of one-dimensional circus movement re-entry and to define the roles of non-linearities of activation delay and excitability in the dynamics of conduction block at the PMJ.

Atypical forms of supraventricular tachycardia due to atrioventricular node reentry in children after radiofrequency modification of slow pathway conduction

Objectives. This study was performed to investigate the prevalence, mechanisms and clinical significance of supraventricular tachycardias inducible in children or adolescents after radiofrequency modification of slow pathway conduction for the treatment of atrioventricular (AV) node reentrant tachycardia.Background. Limited data have been reported with regard to the physiology of AV node reentrant tachycardia in young patients. Radiofrequency catheter ablation allows evaluation of the effects of selective modification of the different pathways involved in AV node reentrant tachycardia.Methods. Selective modification of slow pathway conduction was performed in 18 young patients (12.9 ± 3.4 years old) with typical (anterograde slow-retrograde fast) AV node reentrant tachycardia. Radiofrequency energy was applied across the posteromedial or midseptal tricuspid annulus, guided by slow pathway potentials and anatomic position. Programmed stimulation was performed after modification of slow pathway conduction defined as noninducibility of typical AV node reentrant tachycardia.Results. Modification of slow pathway conduction was achieved in each patient, with a median of four applications of radiofrequency energy. However, atypical forms of supraventricular tachycardia were inducible in 9 of 18 young patients after slow pathway modification: AV node reentrant tachycardia with 2 to 1 AV block (seven patients; anterograde fast-retrograde slow AV node reentrant tachycardia (five patients); and sustained accelerated junctional tachycardia (two patients). In comparison, atypical forms of tachycardia were inducible in only 2 of 59 adult patients with AV node reentrant tachycardia undergoing slow pathway modification in the same laboratory (p = 0.01). Additional applications of radiofrequency energy to the posteromedial tricuspid annulus rendered AV node reentrant tachycardia with 2 to 1 block and the fast-slow form of AV node reentrant tachycardia noninducible. Junctional tachycardia terminated spontaneously in both patients. During 9.8 ± 3 months of follow-up, slow-fast AV node reentrant tachycardia has recurred in one patient, whereas fast-slow AV node reentrant tachycardia has occurred in two patients, both with inducible fast-slow tachycardia after the initial modification of slow pathway conduction.Conclusions. Initial applications of radiofrequency energy may selectively modify the anterograde conduction of slow pathway fibers in young patients with AV node reentrant tachycardia. This may result in AV node reentrant tachycardia with 2 to 1 AV block or a reversal of the reentrant circuit (fast-slow tachycardia). Induction of these tachyarrhythmias indicates that further applications of radiofrequency energy are required for the successful modification of slow pathway conduction in young patients. The increased prevalence of inducible atypical arrhythmias among young patients suggests differences in the anatomic or electrophysiologic substrate of AV node reentrant tachycardia that may evolve as a function of age.

Differentiating SVT from VT--a personal viewpoint.

There are two situations in which it may be difficult to differentiate supraventricular tachycardia from ventricular tachycardia via the surface 12 lead electrocardiogram: (1) when supraventricular tachycardia is conducted to the ventricles with aberration, and (2) when ventricular preexcitation is present. In both cases, the physician in faced with a tachycardia with wide (> = 0.12 s) QRS complexes. In order to avoid improper or delayed therapy the physician should keep in mind simple facts. Ventricular tachycardia is far more common than supraventricular with aberrant conduction, as it accounts for more than 80% of tachycardia with wide QRS complexes. The first step is to determine the tolerance of the tachycardia and therefore whether prompt termination is required. If the tachycardia is associated with syncope, cardiac arrest, severe hypotension or angina, DC cardioversion is necessary. Diagnosis should be delayed until after termination of the tachycardia. If tachycardia is well tolerated, the bedside diagnosis should take into account the clinical context: age of the patient, history or presence of heart disease and patient medications. In an adult patient with a history of myocardial infarction, the most likely diagnosis is ventricular tachycardia. The second step is to exclude or ascertain the presence of preexcitation. If this is suspected in young adults or children an ECG in sinus rhythm should indicate overt preexcitation. The physician should be aware of the various mechanisms of tachycardia with preexcited QRS complexes, all of which have a common denominator: anterograde conduction through the accessory pathway.(ABSTRACT TRUNCATED AT 250 WORDS)

Radiofrequency catheter ablation of accessory pathways during entrainment of AV reentrant tachycardia.

Radiofrequency ablation of accessory pathways must sometimes be done during orthodromic atrioventricular reentrant tachycardia when manifest anterograde accessory pathway conduction is absent or retrograde fusion obscures accessory pathway location during ventricular pacing. Unfortunately, abrupt heart rate slowing upon radiofrequency induced termination of atrioventricular reentrant tachycardia often causes catheter dislodgment. We report our experience in circumventing this problem during radiofrequency ablation by using entrainment of atrioventricular reentrant tachycardia. The latter maintains retrograde activation pattern over the accessory pathway while preventing abrupt ventricular rate change. Eight patients (4 men and 4 women, mean age 37.3 +/- 17.9) with eleven left-sided accessory pathways were included. Ablation during entrainment was used as the first approach in three patients with concealed accessory pathways and one patient with a bidirectional accessory pathway. In another four patients, ablation during entrainment was used after technical difficulties in ablating during tachycardia. Only 1-3 radiofrequency applications were required to eliminate the accessory pathway using the entrainment technique. The catheter remained stable when accessory pathway conduction was interrupted by radiofrequency current. In conclusion, entrainment of atrioventricular reentrant tachycardia during radiofrequency application is useful for maintaining catheter position for accessory pathway ablation during atrioventricular reentrant tachycardia.

Limitations of adenosine in assessing the efficacy of radiofrequency catheter ablation of accessory pathways

Adenosine has been shown to reliably confirm the success of accessory pathway catheter ablation by producing transient atrioventricular (AV) block during atrial and ventricular pacing. This is due to the insensitivity of accessory pathway conduction to adenosine (with the rare exception of accessory pathways with decremental conduction properties). However, 4 of 204 consecutive patients who underwent successful accessory pathway ablation (as shown by adenosine-induced transient AV block) had recurrent AV reciprocating tachycardia involving a second, previously nonmanifest accessory pathway. In each case, the second accessory pathway was localized to a site disparate from the original pathway. No pathway showed decremental anterograde or retrograde conduction properties. In 2 patients, adenosine initially did not show the presence of the second concealed accessory pathway, because the refractory period of the accessory pathway was longer than the pacing cycle length used to assess ventriculoatrial conduction. Only when the refractory period of this second accessory pathway was shortened by infusion of isoproterenol did adenosine reveal the presence of the pathway during follow-up electrophysiologic study. In another patient, a non-decremental accessory pathway was shown to be sensitive to adenosine. In the remaining patient, the second accessory pathway may have been transiently injured during the initial study, thereby simulating adenosine sensitivity. Therefore, it is concluded that (1) adenosine is a highly, but not completely, effective method for immediately assessing the efficacy of accessory pathway catheter ablation; (2) concomitant infusion of isoproterenol during adenosine administration is necessary to recognize the presence of accessory pathways with prolonged refractory periods; and (3) assessment of the presence of accessory pathway conduction with adenosine after ablation should preferably be performed at the longest possible, paced cycle length.

Predictors of recurrent atrioventricular nodal reentry after selective slow pathway ablation

Although radiofrequency catheter ablation of the slow atrioventricular (AV) nodal pathway is highly effective for the management of AV nodal reentrant tachycardia (AVNRT), this arrhythmia may recur in some patients after an ablation procedure that initially renders AVNRT noninducible. A retrospective study examined the factors that are associated with the recurrence of AVNRT after selective radiofrequency catheter ablation of the slow pathway. Patients were included in the study if they had initially inducible, typical slow-fast AVNRT that was noninducible at the end of the ablation session. Selective ablation of the slow pathway was performed using radiofrequency energy applied along the tricuspid annulus near the coronary sinus ostium. AVNRT recurred after initially successful slow pathway ablation in 10 of 136 patients (7.4%) over a mean follow-up period of 20.1 ± 5.0 months; the time to recurrence ranged from 1 to 411 days. Despite the absence of inducible AVNRT, dual anterograde AV nodal conduction properties persisted after slow pathway ablation in 10 patients AVNRT recurred in 4 of 10 patients who had evidence of residual slow pathway conduction compared with only 6 of 126 who had no residual slow pathway conduction (p = 0.003). All patients with persistent slow pathway conduction and recurrent AVNRT also had residual AV nodal echo beats. AVNRT recurred in 3 of 6 patients without accelerated junctional tachycardia during radiofrequency application compared with only 7 of 109 with accelerated junctional tachycardia (p = 0.003). Thus, AVNRT infrequently recurs after successful selective radiofrequency ablation of the slow pathway. The presence of residual slow pathway conduction and AV nodal echo beats after ablation is associated with an increased risk of recurrent AVNRT.

Posterior (“atypical”) atrioventricular junctional reentrant tachycardia

The aim of this study was to characterize a relatively rare type of atrioventricular (AV) junctional reentrant tachycardia (AVJRT). Posterior AVJRT is a type of AV nodal tachycardia in which the site of earliest atrial activation is posterior to the AV node near the coronary sinus orifice. The mechanism of this tachycardia is not well understood. The characteristics of posterior AVJRT (n = 15) were compared with those of anterior (“common”) AVJRT (n =146) and supraventricular tachycardia using single posterior septal accessory pathways (n = 13). During posterior AVJRT, the AH interval was longer than the, retrograde conduction time (His to earliest atrial activity) in 11 cases (73%), indicating that these tachycardias were not fast-slow types of AVJRT. The mean ventriculoatrial (VA) interval in posterior AVJRT (93 ± 41 ms) was longer than in anterior AVJRT (11 ± 20 ms; p <0.005), but was similar to that in tachycardias using accessory pathways (106 ± 16 ms; p = NS). The site of earliest atrial activation during posterior AVJRT was similar to that in tachycardias using accessory pathways. In all cases of accessory pathway-friediated tachycardia, atrial activation could be advanced by ventricular extrastimuli delivered coincident with the His deflection, but atrial activation was not advanced in any case of posterior AVJRT unless the extrastimulus was delivered >80 ms before the His deflection. Anterograde conduction was similar in the posted or and anterior AVJRT groups. During ventricular pacing, the VA interval was longer in patients with posterior AVJRT (287 ± 113 ms) than in those with anterior AVJRT (199 ± 48 ms; p <0.005) or accessory pathways (133 ± 43 ms; p <0.005), and closely coupled ventricular extrastimuli caused greater increases in the VA interval (172 ± 114 vs 102 ± 31 and 60 ± 60 ms, respectively; both p <0.01). In 73% of cases, posterior AVJRT used a slow pathway for anterograde conduction and a different “slow” pathway for retrograde conduction, and thus was not an antidromic form of “common” AV nodal reentry. The retrograde limb of the circuit did not have the characteristics of an accessory pathway.

Catheter ablation of accessory pathways in children

The efficacy and safety of catheter ablation of accessory pathways (AP) was studied in 79 children (age, 4-16 years), using DC shocks (n = 25) or radiofrequency energy (n = 54). All patients had documented arrhythmias including ventricular fibrillation in four. Organic heart disease was present in four patients. AP locations were left lateral (n = 36), posteroseptal (n = 36), right lateral (n = 8), Mahaim fibres (n = 2) and right anteroseptal (n = 6). Seven patients had multiple AP. One patient had a preexcitation which appeared secondary to an atrio-infundibular connection (Fontan procedure). The ablation site of concealed or overt AP was identified by retrograde or anterograde conduction mapping, respectively. A mean of 2.6 +/- 1 cathodal shocks (80-160 J) was delivered to 25 patients over 29 sessions, resulting in initial AP ablation in all. Fulguration was uncomplicated in all except in one patient (4%) who developed a secondary complete AV block post-ablation. During a follow-up period of 30-69 months, intermittent preexcitation recurred in two asymptomatic patients, but no significant tachycardia was inducible at late electrophysiological study, including under isoproterenol infusion. Radiofrequency energy was applied to 54 patients during 62 sessions, using 20-40 watts for 30-60 s. AP ablation was initially achieved in all patients using a median of three impulses, without significant immediate side-effects. Two patients (4%) developed a short episode of blurred vision possibly due to a microembolism. After discharge, the follow-up period was 10 +/- 5 months (range 1 to 24). All patients but one (98%) were asymptomatic without any drug therapy.(ABSTRACT TRUNCATED AT 250 WORDS)