Anterograde Limb Research Articles

Simplification of resetting response in slow/fast atrioventricular nodal reentrant tachycardia: the 3 catheters approach

Abstract Background The resetting response is a maneuver that helps identify the anterograde limb of slow/fast atrioventricular nodal reentrant tachycardia (AVNRT). The actual described maneuver involved a 5 catheters approach, and the related complications are poorly described.(1) Purpose We describe a simplified approach with 3 catheters and the related complications of the maneuver. Methods A quadripolar catheter was placed in the His bundle region; a decapolar catheter in the coronary sinus (CS) and a 4 mm tip non irrigated or irrigated catheter was used for pacing and ablation. An 8.5 French Sl0 sheath was used to ensure contact and stability. In confirmed slow/fast AVNRT using the fast pathway as the retrograde limb (earliest retrograde atrial activity located in the parahisian region), a single decremental atrial extrastimulus was delivered at the lower part of the triangle of Koch and 2-3 cm inside the CS on the roof. Pacing maneuver was started near the end of the QRS complex and decremented by 10 ms per interval. The higher atrial signal with the best A/V ratio on the CS catheter was used as sense reference for resetting response. The end point of ablation was non inducibility. Results Ten patients were included in a 4-month period, comprising 2 redo procedures. The maneuver was not performed in 4 patients (40%) due to non-sustained tachycardia. Atrial fibrillation was induced in 2 patients (20%) during the maneuver systematically due to an atrial extrastimulus preceding the H potential (negative HA interval). In the 4 remaining patients with successful resetting response, the HA interval in successful ablation spot varies between 31 to 82 ms. The involved anterograde limb was the right extension in 3 (75%) and the left extension in 1 (25%). Conclusion Resetting response can be performed with a 3 catheters approach, the main limitation is non sustained tachycardia, and atrial fibrillation induced by short coupled extrastimulus.Resseting response in LIE and RIE

PO-05-226 ORTHODROMIC RECIPROCATING TACHYCARDIA RELYING ON ABERRANT CONDUCTION: NEED FOR A LAGER CIRCUIT

Aberrant conduction during orthodromic reciprocating tachycardia (ORT) can prolong the ventriculo-atrial conduction time, which is found essential for the reentry in certain situations. To investigate the prevalence and different mechanism of aberrancy-dependent ORT. ORT cases relying on aberrancy from 220 cases in our center were searched using the following criteria: (1) Multiple episodes of ORT with aberrant conduction in ECG ; (2) No baseline BBB during sinus rhythm; (3) Absence of narrow QRS form during tachycardia unless isoproterenol used; (4) Restoration of bundle branch conduction giving rise to tachycardia termination or circuit alteration. ECGs and intracardiac tracings during study were carefully examined. 3 patients from 220 patients (1.4%) with ORT showed the phenomenon of dependence on aberrancy. Clinical tachycardia episodes of the patients were short in time. All accessory pathways (APs) were located at anterolateral regions of atrioventricular annulus. None of them had baseline bundle branch block. Creating functional bundle branch block was necessary to induce the tachycardias. In the first patient with ORT and left bundle branch block (LBBB), a late-delivered premature ventricular contraction (PVC) was able to advance the next A and reset the tachycardia, which was diagnostic for ORT with aberrancy. Meanwhile, left bundle branch conduction was restored which narrowed the next QRS complex. Tachycardia was then terminated by the advanced wavefront reaching the ventricular insertion site of AP which was refractory. In the second case, termination of the tachycardia was always preceded by a spontaneous LBBB restoration, with the V and subsequent A at MA advanced, suggesting anterograde block in the AV node. In the other case was, induction required both right BBB and slow pathway conduction. When isoproterenol was given, fast pathway recovered followed by BBB restoration, which made anterograde limb again switched to slow pathway. All pathways were successfully ablated during the procedure. All patients have been free of arrhythmias for at least 6 months. Extra transseptal time caused by aberrancy can be an integral part of ORT, which can explain the infrequent or late onset and unsustainable episodes of ORT in certain patients and is useful in understanding the circuit and localizing the pathway.

Wide QRS complex supraventricular tachycardia with negative precordial concordance: Electrocardiographic clues for Mahaim pathway with Ebstein anomaly

Ebstein's anomaly is often accompanied by either Wolff-Parkinson-White syndrome or atriofascicular Mahaim. These bypass tracts give rise to antidromic atrioventricular (AV) re-entrant tachycardias, in which the bypass tract serves as the anterograde limb of the circuit and the AV node as the retrograde limb of the reentrant circuit. Since the antidromic AV reentrant tachycardia over a Mahaim fibre has a typically left bundle braunch block (LBBB) morphology, it is easy to make a misdiagnosis of supraventricular tachycardia with functional LBBB or even of ventricular tachycardia particularly in the presence of negative concordance. Some electrocardiographic clues might prevent misdiagnosis of ventricular tachycardia and inadvertent ICD implantation.

The double adenosine test: A simple and non-invasive tip to unmask unapparent pre-excitations at the emergency department

We describe a simple method to unmask unapparent pre-excitations at the emergency room. This method allows a non-invasive and definite diagnosis of accessory pathways capable of anterograde conduction. In patients presenting with paroxysmal SVT, close inspection of the electrocardiogram during sinus rhythm should look for a pre-excitation. Unfortunately, a pre-excitation can be completely unapparent during sinus rhythm despite the presence of an antegradely conducting accessory pathway. This is typically the case in the so-called Mahaim fibers. These bypass tracts give rise to antidromic atrioventricular reentrant tachycardias, in which the bypass tract serves as the anterograde limb of the circuit and the atrioventricular node as the retrograde limb of the reentrant circuit. In these patients, it is easy to make a misdiagnosis of supraventricular tachycardia with functional left bundle branch block. Indeed, due to the slow and decremental conduction properties of these bypass tracts, the baseline ECG is either normal or shows only subtle pre-excitation. Herein, we describe a simple tip, consisting of two successive administrations of adenosine (during ongoing tachycardia [upper panel] and during sinus rhythm [lower panel]), to make a non-invasive and definite diagnosis of this condition at the emergency department. By blocking the anterograde conduction over the atrioventricular node, adenosine infusion during sinus rhythm will indeed result in ventricular activation occurring exclusively over the accessory pathway. Importantly, the use of this simple method to unmask accessory pathways capable of anterograde conduction is not limited to the diagnosis of Mahaim fibers. Indeed, it can be used more generally in patients presenting with paroxysmal SVT whenever the ECG following tachycardia termination does not definitely rule out the presence of an accessory pathway ( Fig. 1 ).

Fast-Fast form of Atypical AV Nodal Reentrant Tachycardia: Incidence, Electrophysiological Characteristics and Results of Catheter Ablation

Background: Both typical and atypical AV nodal reentrant tachycardias (AVNRT) are usually amenable to slow pathway (SP) ablation at the inferoseptal areas. However, rare cases of unusual forms of AVNRT are resistant to SP ablation and their characteristics remain to be elucidated. Methods and Results: Total of 1252 AVNRTs induced in 950 cases were reviewed. Both anterograde and retrograde limbs of tachycardia circuit (TC) were classified into fast pathway (FP) or SP according to the A-H (AHI) and H-A intervals (HAI) during the tachycardia; the anterograde FP (AHI ⁄= 220 msec), and retrograde FP (HAI ⁄= 120 msec). Accordingly, the 1252 AVNRTs were classified into slow-fast (S/F: n=998), slow-slow (S/S: n=119), fast-slow (F/S: n=129) and fast-fast (F/F: n=6) forms. The F/F forms were induced by atrial or ventricular extrastimulation without associated jump-up in the AHI and HAI, and they were characterized by shorter tachycardia cycle length (260±55 msec), short AHI (153±39 msec) and HAI (107±19 msec) during the tachycardia and earliest retrograde atrial activation at the right superoseptum (n=2) or midseptum (n=4). The tachycardias were entrained from the RV and resumed with V-A-V sequence after cessation of entrainment pacing. SP ablation at right inferoseptum was unsuccessful in all F/F forms. Successful ablation was achieved at right superoseptum (n=2) or midseptum (n=4) without creating AV block. Conclusions: F/F forms of AVNRT not involving SP in TC were observed in 0.5% of all AVNRT. It was suggested the TC was smaller and confined to the superior part of AV nodal area in this extremely rare form of AVNRT.

FIX-R338L (FIX Padua) as a Successful Alternative for the Treatment of Canine Severe Hemophilia B.

Abstract 694Hemophilia B (HB) is a severe bleeding disorder affecting 1 in 30,0000 men and results from the deficiency of FIX clotting activity. The current treatment involves infusion of either plasma derived or recombinant FIX. We have recently described a novel naturally occurring gain-of-function mutation in the FIX gene found associated with hyperfunctional activity of the protein (N Engl J Med, 2009). The proband presented with 776% FIX clotting activity (FIX:C), but normal FIX antigen levels (FIX:Ag of 92% of normal), and after detailed analysis the causative mutation was found to be a transversion of R338L in FIX (FIX-Padua) that segregates in a classical X-linked fashion. Furthermore, in vitro expression of FIX-Padua confirmed that the protein had a specific activity that was 8 fold higher than FIX-wild type. Arginine at 338 is highly conserved in FIX from mammals but is unique among other human vitamin K-dependent proteins. We sought to determine whether FIX-Padua would be an attractive strategy for novel therapy of hemophilia B by introducing this mutation in the canine FIX gene (cFIX) and testing in HB dog models. The HB colony at Chapel Hill is an outbred, immunocompetent large animal model that have a missense mutation in the cFIX gene and have no detectable circulating levels of cFIX antigen or activity, and its disease phenotype closely correlates with that seen in humans.Adeno-associated viral (AAV) vector encoding the cFIX-Padua and cFIX-wt under control of the CMV promoter was generated and administered to HB dogs. AAV6 was chosen as the serotype to overcome the high prevalence of neutralizing antibodies to AAV2 in the general population. Delivery of AAV6-cFIX wild type by intravascular delivery to the skeletal muscle via anterograde limb perfusion (ALP) coupled with transient immunosuppression (duration of 5 weeks) resulted in FIX:Ag and FIX:C of 2-5% of normal with partial shortening the whole blood clotting time. Post AAV6-cFIX Padua injection we observed a remarkable correction of the WBCT to the normal range (8-10 min) within the first 7 days that has continued for the duration of the study. One dog's (M55) FIX:Ag levels were ∼250 ng/mL (5% of normal) at the peak and 180 ng/mL (3.6%) at the plateau. Notably, his FIX:C levels were 49% at peak and 35% at plateau, indicating a specific activity ∼10 fold higher than wild type cFIX. Treatment of a second dog (M59) resulted in FIX:Ag levels of 175 ng/mL (3.5%) at the peak and 60 ng/mL (1.2%) at plateau. This is in contrast with his FIX:C levels that were 35% at peak and 12% at plateau levels, respectively. Like M55, the specific activity was 10 fold higher than wild type cFIX. An important consideration is the potential for an immune response against the cFIX-Padua neo-antigen. Notably, there is no evidence of formation of inhibitor to cFIX in these dogs for a cumulative observation period of 6 months post-immunosuppression.We have demonstrated that the cFIX-Padua mutant protein has 10-fold higher specific activity in a canine model of HB. This is significant as it allows for lower doses of AAV vectors to be used for the treatment of HB without compromising efficacy, thereby increasing the safety profile of clinical gene therapy for HB. In addition, FIX Padua provides an excellent alternative to overcome the limited ability of skeletal muscle to synthesize fully posttranslational modified functional FIX (Blood, 2001). Thus, FIX-Padua improves both the efficacy and safety of skeletal muscle-mediated FIX resulting in FIX:C levels sufficient to convert the severe HB phenotype to mild hemophilia (10-35% of normal) at vector doses already tested clinical trials. This strategy has the potential of improving other gene and/or cell therapy for HB targeting ectopic targets as well as the liver. Disclosures:High:Genzyme: Patent licensed to Genzyme, but Dr. High has waived all financial interest, Patents & Royalties.

Abstract 5678: Fast-Fast Form of Atypical AV Nodal Reentrant Tachycardia: Incidence, Electrophysiological Characteristics and Results of Catheter Ablation

Both the typical (slow-fast (S/F)) and atypical (slow-slow (S/S) and fast-slow (F/S)) forms of the AV nodal reentrant tachycardias (AVNRT) are usually amenable to the classical slow pathway (SP) ablation at the inferoseptal atrial region. However, rare cases of unusual forms AVNRT do not involve an SP in the tachycardia circuits (TC), and they are resistant to the classical SP ablation. The characteristics of the atypical AVNRTs not involving an SP in the TCs remain to be elucidated. A total of 1252 AVNRTs induced during the electrophysiological study in 950 cases were analyzed. Both the anterograde and retrograde limbs of the TC were classified into the fast pathway (FP) or SP according to the A-H (AHI) and H-A intervals (HAI) during the tachycardia; the anterograde FP: AHI of <220 ms, anterograde SP: AHI of ≥220 ms, retrograde FP: HAI of <120 ms, and retrograde SP: HAI of ≥120 ms. Accordingly, each tachycardia was classified into one of the S/F, S/S, F/S and fast-fast (F / F) forms . There were 998 S/F forms (79.7%), 119 S/S forms (9.5%), 129 F/S forms (10.3%) and 6 F / F forms (0.5%). The F / F forms were induced by atrial or ventricular extrastimulation without an associated jump-up in the AHI and HAI, and they were characterized by a shorter tachycardia cycle length (260±55 ms), short AHI (153±39 ms) and HAI (107±19 ms) during the tachycardia, earliest retrograde atrial activation (ERAA) at the right superoseptum (n=2) or midseptum (n=4), and 2nd degree AV block without a tachycardia interruption. The retrograde atrial activation sequence during the F / F forms was identical to that during ventricular pacing. The tachycardias could be entrained from the RV, and they resumed with a V-A-V sequence after the cessation of the entrainment pacing. The classical SP ablation at the right inferoseptal region was unsuccessful in all 6 cases with the F / F forms . The successful ablation was achieved at the right superoseptum (n=2) or midseptum (n=4) without creating AV block in all 6 cases. The F / F forms of atypical AVNRT not involving a classical SP in the TC were observed in 0.5% of all AVNRT cases. The results of this study suggested that the TC was smaller and confined to the superior part of the AV nodal area in this extremely rare form of AVNRT.

A Novel Method of Regional Intravenous Delivery of AAV Vector to Skeletal Muscle Results in Correction of Canine Hemophilia B Phenotype.

Previously we demonstrated that intramuscular (IM) injection of AAV-F.IX in humans was safe and resulted in long-term >gene transfer and expression of injected muscle biopsied at time points up to 10 months post injection. However, at the doses administered, it did not result in sustained circulating levels >1%. Although access to the skeletal muscle can be easily obtained by direct IM injection, achievement of target doses in humans has proved impractical because of hundreds of injections required. We sought to exploit techniques that allowed transduction of large numbers of muscle fibers by injecting AAV vectors via intravascular. The major obstacle to vector distribution to large areas of skeletal muscle is the vascular endothelial barrier. However, the network of capillaries can be chemically and/or mechanically modified to ensure vascular leakage of fluid containing vectors. Earlier we showed that intravascular delivery of AAV2-CMV-canine F.IX, at doses in the range of 2–4 x 1012 vg/kg, by infusion vector through isolated femoral artery in the presence of histamine to increase capillary permeability (isolated limb perfusion), results in long-term expression (> 3 years) of therapeutic levels (4–14% normal) of F.IX, and phenotypic correction of severe canine hemophilia B. Here we report a novel approach, anterograde limb perfusion (ALP), in which the vector is injected through a superficial saphenous vein in the distal part of the limb under elevated hydrostatic pressure without vasoactive drug. Briefly, a tourniquet was placed at the level of the proximal thigh. Access to the target vessel was achieved by a small incision of the skin overlying the saphenous vein and an intravascular catheter was placed. The vector was diluted in 20 ml of PBS/kg and infused rapidly using a pressure of 300 mmHg. The vector-containing solution dwells for 15 minutes before tourniquet release. The procedure was well tolerated and muscle enzyme levels increased transiently (up to day 2 post-infusion) in 1 of 3 dogs. We treated two dogs (15 and 16 kg) with AAV2-CMV-cF.IXvector at dose of 3 x1012 vg/kg. Circulating F.IX antigen levels slowly increased to 292 and 299 ng/ml at day 14, reaching levels of 674 and 876 ng/ml day 21 (13 and 17 % of normal, ongoing observation). The shortening of the aPTT and the whole blood clotting time to nearly normal values confirmed that F.IX is biologically active. A third ALP-treated dog received 8 x1012 vg/kg of the AAV vector; F.IX levels rose to 577 ng/ml (>10% of normal), at days 13. This dose seems to be excessive since we documented the development of low-level of a non-neutralizing antibody to F.IX that likely increased the clearance of the transgene product. Thus, ALP provides an efficient, non-invasive strategy for widespread delivery of vector to skeletal muscle in the absence of vasoactive drugs. The doses required to achieve therapeutic F.IX levels are similar to those proved to be safe in earlier clinical trials. Furthermore, ALP abolishes the dose advantage in gene transfer of liver-directed over muscle-directed gene transfer for hemophilia B. These results establish an experimental basis for clinical studies of this delivery method in humans with hemophilia B.

Electrophysiologic characteristics of diverse accessory pathway locations of antidromic reciprocating tachycardia

This study assessed antidromic reciprocating tachycardia (ART) in patients with paraseptal accessory pathways (APs). Previous clinical experience suggests that paraseptal APs are unable to serve as the anterograde limb during ART. Based on the reentry wavelength concept, we hypothesized that anatomic location of a paraseptal AP may not preclude occurrence of ART. If wavelength criteria were met due to prolonged conduction time retrogradely in the atrioventricular node or anterogradely in the AP, ART may be sustained. All patients who had ART in the electrophysiologic laboratory at our institution (1991 to 1998) were studied. Based on fluoroscopically guided electrophysiologic mapping and radiofrequency ablation, AP location was classified as paraseptal, posterior, or lateral. Conduction time and refractoriness measurements were made for all components of the ART circuit. Of 24 patients with ART, 5 (21%) had ART utilizing a paraseptal AP. Anterograde conduction time through the AP and retrograde atrioventricular nodal conduction time were significantly longer in patients with paraseptal versus lateral pathways. Isoproterenol was required for ART induction in 38% of patients with a posterior AP, 36% with lateral AP location, but not in patients with a paraseptal AP. There were no significant differences in tachycardia cycle length or refractoriness of anterograde and/or retrograde components of the macroreentry circuit between the 3 pathway locations. Thus, ART can occur in patients with a paraseptal AP. Slower anterograde pathway conduction, or retrograde atrioventricular nodal conduction renders the wavelength critical for completion of the antidromic reentrant circuit.

Coexistent Atrioventricular and Nodoventricular Pathways in a Patient with Hypertrophic Cardiomyopathy

A 17-year-old girl with concentric hypertrophic cardiomyopathy presented with a wide complex tachycardia and underwent electrophysiological study. She was found to have an antidromic tachycardia utilizing a decremental atrioventricular fiber as the anterograde limb with retrograde conduction occurring through the septum. Ablation of a right free-wall pathway rendered tachycardia noninducible, yet ventricular preexcitation remained. After ablation there was evidence of a second nodoventricular connection. We believe this to be the first report of coexistent "Mahaim" fibers; one a decremental atrioventricular connection and the second nodoventricular.

Intermittent bundle branch blocks in a patient with uncommon-type atrioventricular nodal reentrant tachycardia and enhanced atrioventricular nodal conduction

We report on a patient with uncommon-type atrioventricular (AV) nodal reentrant tachycardia with a short tachycardia cycle length (235–270 ms), in whom transient wide QRS tachycardia with both left bundle branch block and right bundle branch block aberrancy were followed by narrow QRS complexes. In addition, His-ventricular (H-V) block and a sudden prolongation of the H-V interval occurred during the tachycardia. As the determinant of these unusual findings, the possibility that the anterograde limb of the reentry circuit has an enhanced AV nodal conduction property is discussed, as is the clinical significance of this type of tachycardia.

Slow-fast Form of Atrioventricular Nodal Reentrant Tachycardia with Eccentric Retrograde Left-sided Activation.

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

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.

Double loop figure-of-8 reentry as the mechanism of multiple atrioventricular node reentry tachycardias

Seven patients with multiple atrioventricular node reentry tachycardia were analyzed to unravel the mechanism of these tachycardias. Six of the seven patients showed anterograde dual atrioventricular node pathways and one showed anterograde conduction through the fast pathway. Three types of retrograde pathways were noted among these seven patients: (1) the fast pathway with the earliest atrial activation at the His bundle area; (2) the intermediate pathway with the earliest atrial activation at the ostium of the coronary sinus; and (3) the slow pathway with the earliest atrial activation at the ostium of the coronary sinus. All seven patients used the intermediate pathway for retrograde conduction. However, one patient showed evidence of retrograde slow pathway conduction with demonstrable retrograde dual pathways, and another showed evidence of retrograde fast pathway conduction with a shift of atrial activation sequence when conduction switched to the intermediate pathway. Four different types of reetry circuits using either the fast or the slow pathway as the anterograde limb and one of the three retrograde pathways as the retrograde limb were demonstrated in these seven patients, resulting in two types of tachycardias in four patients and three types of tachycardias in three patients. A change in tachycardia type could be induced with atrial or ventricular stimulation. A radiofrequency current delivered to the inferior aspect of Koch's triangle along the tricuspid anulus in five patients resulted in selective ablation or modification of the intermediate pathway or the slow pathway, with preservation of anterograde atrioventricular conduction and abolition of tachycardias. The findings suggest that a double loop figure-of-8 reentry circuit including a fast pathway, a slow pathway, and an intermediate pathway is responsible for multiple atrioventricular node reentry tachycardias.

Atrioventricular nodal reentrant tachycardia with retrograde block induced by aprindine

Two patients are described who had atrioventricular nodal reentrant tachycardia (AVNRT) with 1:1 relationship in the control state, but in whom a varying degree of VA block during AVNRT was observed during therapy with aprindine. Aprindine, however, did not cause anterograde blockade of conduction over the slow AV nodal pathway during tachycardia. These observations support the conclusion that the bulk of atrial muscle is not a requisite part of the tachycardia circuit in AVNRT and that antiarrhythmic drugs may have disparate effects on conduction in the retrograde and anterograde limbs of the circuit.

Catheter Ablation of the Atrial Origin of a Decrementally Conducting Atriofascicular Accessory Pathway by Radiofrequency Current

Radiofrequency Ablation of Pseudo‐Mahaim Fibers. Introduction: A young woman with refractory recurrent supraventricular tachycardia was referred for catheter ablation. Methods and Results: Electrophysiologic studies revealed the mechanism of tachycardia to be atrioventricular (AV) reentry, utilizing a decrementally conducting atriofascicular accessory pathway as the anterograde limb of the circuit and the normal intraventricular conducting system as the retrograde limb. Pace mapping in the right atrium during sinus rhythm suggested an atrial origin of the accessory pathway several centimeters distant from the AV node. Multiple radiofrequency lesions at the distal insertion of the accessory pathway in or near the right bundle branch failed to abolish preexcitation. In contrast, radiofrequency current applied to the ventricular side of the anterolateral tricuspid ring, adjacent to the atrial origin of the accessory pathway, was successful in abolishing preexcitation and inducible supraventricular tachycardia without affecting AV nodal conduction. Conclusion: Radiofrequency ablation can provide curative therapy for intractable supraventricular tachycardia due to decrementally‐conducting atriofascicular accessory pathways. The risk of AV block in such patients as a consequence of the procedure should be quite low.

Use of intracardiac recordings to determine the site of drug action in paroxysmal supraventricular tachycardia

Paroxysmal supraventricular tachycardia most often results from atrioventricular (AV) reentry using an accessory AV pathway (Wolff-Parkinson-White syndrome) or reentry within the region of the AV node. In AV reentry, using an accessory pathway, suppression of the tachycardia may be achieved by depressing either anterograde AV nodal conduction or retrograde accessory pathway conduction. Intracardiac recordings and programmed electrical stimulation have established that β-adrenergic antagonists and calcium channel blockers principally affect AV nodal conduction (anterograde limb of the reentrant circuit), whereas class IA and IC agents principally affect the accessory AV pathway (retrograde limb). Pharmacologic therapy has been more effective when directed at the limb in which conduction is most marginal at the tachycardia rate (weak limb). In individual patients, intracardiac recordings and programmed electrical stimulation can be used to identify the weak limb, indicating the class of agents most likely to be effective. Specialized techniques allowing direct recording of accessory pathway activation suggest that limitations in accessory pathway conduction may be explained by anatomic impediments. Conduction is most limited at the atrial interface of the accessory pathway in some patients, whereas in others the ventricular interface may be the limiting factor. Class IA and IC agents appear to have the greatest effect at sites where conduction is most tenuous, i.e., at the anatomic impediments. Similar considerations apply to AV nodal reentry. Anterograde slow AV nodal pathway conduction is most often depressed by digitalis preparations, β-adrenergic antagonists, and calcium channel blockers, whereas retrograde fast AV nodal pathway conduction is more often depressed by class IA and IC agents. Intracardiac recordings and programmed electrical stimulation can also be used in these patients to identify the weak limb and direct pharmacologic therapy. Direct catheter recordings of AV nodal conduction remain elusive, limiting knowledge of the different conduction properties of the anterograde and retrograde limbs and the site(s) of drug action. Studies in progress, comparing the retrograde AV nodal conduction time during tachycardia with that during ventricular pacing at the same rate, suggest that the His bundle may be incorporated in the reentrant circuit in some patients. It appears that verapamil more readily depresses retrograde fast pathway conduction in these patients than in those in whom the His bundle does not form part of the reentrant circuit, but the reasons for this are unknown.

Linking by collision initiated in the absence of preexisting reentrant tachycardia

Dynamic functional block in 1 limb of a reentrant circuit (“linking”) can be maintained by either repetitive interference or collision of successive impulses entering the circuit. Occurrence of linking by collision during attempted overdrive pacing of reentrant tachycardias accounts for the entrainment phenomenon. To investigate whether linking by collision can be initiated in the absence of preexisting tachycardia, a human reentrant circuit model was studied. The model consisted of the atrioventricular node and His-Purkinje system as anterograde limb and an electronic stimulator that served as “retrograde limb” by initiating a paced atrial impulse at a predetermined ventriculoatrial interval following each sensed ventricular depolarization. In 3 patients with intact ventriculoatrial conduction, “reentrant tachycardia” was initiated by a ventricular extrastimulus (V 2), which retrogradely blocked bilaterally below the His bundle. When this same V 2 was followed, instead, by a paced V 2V 2 train at a cycle length equal to the programmed ventriculoatrial interval of the “tachycardia,” it could be shown that each beat of the train not only “traversed” the simulated “retrograde limb” but also retrogradely collided with a prior circulating impulse in the anterograde limb of the circuit, thereby constituting linking by collision at a supra-Hisian level with inability of even a single “reentrant cycle” to be completed; “tachycardia” became manifest only after termination of the V 2V 2 train. The findings suggest the existence of a unique mechanism for initiation of certain clinical reentrant tachycardias during incremental pacing.

Transcatheter ablative techniques for treatment of the permanent form of junctional reciprocating tachycardia in young patients

Five patients with medically refractory incessant supraventricular tachycardia due to a posterior septal, slowly conducting accessory connection underwent transcatheter closed chest ablative treatment. The tachycardia characteristics were consistent with the permanent form of junctional reciprocating tachycardia. In each patient the ablative attempts resulted in independent interruption of either the anterograde limb (atrioventricular node-His bundle conduction) or the retrograde limb (accessory connection) of the tachycardia circuit. Permanent retrograde pathway ablation was achieved in only one patient and followed separate permanent transcatheter His bundle ablation. In three of the other four patients the ablation attempt caused temporary interruption of retrograde conduction. Each patient had improved control of tachycardia related to the ablation attempt. Of the five patients, four required pacemaker implantation. With further refinements, selective ablation of the retrograde limb of the tachycardia circuit may be possible. This experience confirms the anatomic independence of the anterograde and retrograde limbs of the tachycardia circuit.

Intracardiac electrode catheter recordings of atrioventricular bypass tracts in Wolff-Parkinson-White syndrome: Techniques, electrophysiologic characteristics and demonstration of concealed and decremental propagation

Atrioventricular bypass tract deflections were recorded in five patients with the Wolff-Parkinson-White syndrome using standard, closely spaced (5 mm) electrode catheters. Three right paraseptal and two left-sided Kent bundles were recorded at the level of the tricuspid valve on the His bundle catheter and in the coronary sinus, respectively. Characteristics of the bypass tracts were studied during atrial pacing, programmed premature atrial stimulation, induction of supraventricular tachycardias and programmed ventricular stimulation. During atrial pacing, as pre-excitation increased, the stimulus to bypass tract deflection time remained unchanged. In five patients normalization of the QRS complex coincided with loss of the bypass tract deflection during incremental atrial pacing. Two patients demonstrated fragmentation of the bypass tract deflection before block. In one patient fragmentation of the bypass deflection coincided with normalization of the QRS complex. The effective refractory periods of the bypass tracts coincided with loss of bypass tract deflections in three of the five patients. In one patient, the effective refractory period of the bypass tract at its ventricular insertion preceded that at its atrial insertion, whereas in the remaining patient, the effective refractory period of the bypass tract was not attained because of atrial refractoriness. During orthodromic supraventricular tachycardia, the bypass tract deflections disappeared in the anterograde limb in all patients. In one patient, the bypass tract deflection was recorded during atrial fibrillation with pre-excitation. Bypass tract deflections can be recorded with a closely spaced electrode catheter. Right paraseptal bypass tracts are located close to the His bundle. The anterograde effective refractory period of the bypass tract usually reflects its atrial insertion, but concealment through the bypass tract can occur with block at the ventricular insertion. Decremental conduction within the bypass tract can occur before block, suggesting concealed and overt Wenckebach block within the bypass tract. Recordings of bypass tract deflections increase the potential of closed chest ablation of right paraseptal and left-sided bypass tracts.