Atrioventricular Node Modification Research Articles

Modification of atrioventricular node in a special condition treating paroxysmal supraventricular tachycardia

Modification of atrioventricular node is a usual and necessary operation to cure atrioventricular nodal reentrant tachycardia (AVNRT). In this operation, atrioventricular block is the most severe complication and its prevention is of our great concern. This complication always occurs under some special circumstances with potential risk. So, it is very important to realize such conditions, as in this paper. A patient with paroxysmal palpitation for 10 years, aggravating to shortness of breath with chest distress for 1 year; cardiac electrophysiological examination found slow conduction in both antegrade and retrograde paths of reentrant loop, and typical AVNRT could be induced. During effective ablation there was no junctional rhythm. In some special cases, modification of atrioventricular node should not only rely on the junctional rhythm to determine the ablation effect, but also on the time of cardiac electrophysiological examination, as such to avoid the severe complication of atrioventricular block caused by excessive ablation.

Modification of cardiovascular ion channels by gene therapy

Delivery of genes to the heart and vasculature for therapeutic purposes is an exciting strategy that is approaching clinical reality. Abnormalities of expression or function of ion channels is central to many cardiovascular diseases and gene delivery to modify ion channels is an appealing alternative to traditional therapy with small-molecule drugs. Potential therapeutic targets include hypertrophy and heart failure, atrioventricular node modification in atrial fibrillation, ventricular tachycardia and hypertension. Numerous approaches for gene delivery are under development, including use of tissue-specific promoters in viral vectors. For other applications, such as development of biological pacemakers, cells can be transduced with pacemaker genes in vitro, and then the cells implanted within the heart. There are short-term hurdles to therapeutic gene delivery to modify cardiovascular ion channels, but in the intermediate and longer term, the outlook is promising.

Atrioventricular node modification and ablation for ventricular rate control in atrial fibrillation

M A c a i a p H t s e R q e v p f s 6 p a p a n o ntroduction trial fibrillation (AF) may cause embolic stroke and conestive heart failure (CHF) and increases mortality in paients with CHF. AF causes symptoms in some patients but ay be asymptomatic in others. One of the principal causes f symptoms and ventricular dysfunction is the rapid venricular response (RVR) often associated with AF. In some atients, a high vagal tone, or atrioventricular (AV) nodal isease, limits the ventricular response to AF to nearly ormal heart rates at rest and during exercise. These patients re often asymptomatic and do not develop tachycardiaediated ventricular dysfunction. In other patients, howver, AV nodal conduction is rapid, resulting in excessively igh ventricular rates at rest and during exercise. These atients are often highly symptomatic and may have tachyardia-mediated ventricular dysfunction, requiring AV odal blocking drugs such as beta receptor blockers, calium channel blockers, and digitalis, alone or in combinaion, to control ventricular rate. However, pharmacological rate control is often difficult, nd AV node–blocking drugs may cause side effects, inluding hypotension, CHF, and marked bradycardia or auses. Consequently, the nonpharmacological approaches f AV node modification or AV node ablation and paceaker implantation were developed and widely impleented in patients with AF and pharmacologically refracory RVR. This paper will review the role of AV node odification and AV node ablation with pacemaker implanation as methods for ventricular rate control in patients ith AF.

Analysis of surface electrocardiograms in atrial fibrillation: techniques, research, and clinical applications

Atrial fibrillation (AF) is the most common arrhythmia encountered in clinical practice. Neither the natural history of AF nor its response to therapy is sufficiently predictable by clinical and echocardiographic parameters. The purpose of this article is to describe technical aspects of novel electrocardiogram (ECG) analysis techniques and to present research and clinical applications of these methods for characterization of both the fibrillatory process and the ventricular response during AF. Atrial fibrillatory frequency (or rate) can reliably be assessed from the surface ECG using digital signal processing (extraction of atrial signals and spectral analysis). This measurement shows large inter-individual variability and correlates well with intra-atrial cycle length, a parameter which appears to have primary importance in AF maintenance and response to therapy. AF with a low fibrillatory rate is more likely to terminate spontaneously and responds better to antiarrhythmic drugs or cardioversion, whereas high-rate AF is more often persistent and refractory to therapy. Ventricular responses during AF can be characterized by a variety of methods, which include analysis of heart rate variability, RR-interval histograms, Lorenz plots, and non-linear dynamics. These methods have all shown a certain degree of usefulness, either in scientific explorations of atrioventricular (AV) nodal function or in selected clinical questions such as predicting response to drugs, cardioversion, or AV nodal modification. The role of the autonomic nervous system for AF sustenance and termination, as well as for ventricular rate responses, can be explored by different ECG analysis methods. In conclusion, non-invasive characterization of atrial fibrillatory activity and ventricular response can be performed from the surface ECG in AF patients. Different signal processing techniques have been suggested for identification of underlying AF pathomechanisms and prediction of therapy efficacy.

Impact of Transforming Growth Factor-β1 on Atrioventricular Node Conduction Modification by Injected Autologous Fibroblasts in the Canine Heart

Atrioventricular (AV) nodal ablation for management of atrial fibrillation (AF) is irreversible and requires permanent pacemaker implantation. We hypothesized that as an alternative, implantation of autologous fibroblasts in the perinodal region would focally modify AV nodal conduction and that this modulation would be enhanced by pretreatment with transforming growth factor-beta1 (TGF-beta1), a stimulant of fibroblasts. Skin biopsies were taken from 12 mongrel dogs, and derived fibroblasts were dissociated and grown in culture for 2 weeks. Multiple injections (0.25 mL) were made through an 8F NOGA catheter along the fast/slow AV nodal pathways as guided by an electroanatomic mapping system. Seven dogs received fibroblasts alone (1x10(6) cells/mL), 7 dogs received TGF-beta1 (5 microg), 4 dogs received fibroblasts and TGF-beta1 (1x10(6) cells/mL+5 microg), and 4 dogs received saline only. AV node function was assessed at baseline and after 4 weeks. Saline (80 mL) with assigned therapy (0.25 mL per injection) was injected into the peri-AV nodal region in each dog. At baseline, the AH interval (66+/-3 ms) and the average RR interval (331+/-17 ms) in pacing-induced AF were similar in each cohort. The increase in AH interval in normal sinus rhythm was longer after fibroblast (23+/-4 versus 5+/-5 ms; P=0.05) and fibroblast plus TGF-beta1 (50+/-5 versus 5+/-5 ms; P<0.001) injections than with saline alone, with similar findings during high right atrium and distal coronary sinus pacing. The AH interval was not significantly increased after TGF-beta1 injections. The AH interval was significantly longer after fibroblast plus TGF-beta1 injections than with either therapy (TGF-beta1 or fibroblasts) alone. The RR interval during AF was increased in dogs that received fibroblasts alone (110+/-36 versus -41+/-34 ms) and to a greater extent with the addition of TGF-beta1 (294+/-108 versus -41+/-34 ms). No AV block was seen in any cohort at 4 weeks. Labeled fibroblasts that expressed vimentin were identified in all dogs that received cell injections at 4 weeks. AV nodal modification can be achieved with injected fibroblasts without the creation of AV block. The effect on AV node conduction is substantially enhanced by pretreatment of fibroblasts with TGF-beta1. These data have therapeutic potential for the management of rapid ventricular rate during AF without pacemaker implantation.

Radiofrequency Modification for Inducible and Suspected Pediatric Atrioventricular Nodal Reentry Tachycardia

AV Node Reentry Tachycardia (AVNRT) is the second most common supraventricular tachycardia (SVT) undergoing pediatric radiofrequency ablation behind accessory pathway reentry tachycardias. AVNRT can be difficult to induce during electrophysiology study (EPS) and dual atrioventricular nodal (AVN) pathways physiology may not be demonstrated in young patients. This report is the largest single center long term pediatric experience of radiofrequency modification of slow AVN input fibers for inducible or suspected (non-inducible) AVNRT. One hundred thirty-two patients underwent slow input AVN modification from 1993 to 2002. The mean patient age was 13.7 years (4-20 yrs) with 62M/70F. Outpatient tachycardia was documented by ambulatory monitoring in all patients. AVNRT was induced in 98/132 patients during EPS (group A) with mean SVT cycle length of 324 msec (230-570 msec). Initial AVN modification (group A) was successful in 97/98 patients (99%). During 34/132 EPS, AVNRT was non-inducible; dual AVN physiology was present in 19/34 (group B), and 15/34 did not show evidence for dual AVN physiology (group C). These 34 patients underwent empiric AVN modification following discussion with patients' families. Freedom of recurrence from SVT at 1 year was 96% for group A (94/98), 89% (17/19) for group B and 93% (14/15) for group C. 1 major and 6 minor complications occurred. AVN modification for AVNRT can be performed safely and effectively in pediatric patients with good long-term results. Empiric slow pathway AVN modification for non-inducible SVT results in a high rate of freedom from recurrence of tachycardia.

Chronic favorable modification of AV nodal conduction with an injected autologous fibroblast cell line in a canine model

Background: Radiofrequency ablation of the atrioventricular node (AVN) is a recognized treatment for atrial fibrillation (AF), but results in permanent ventricular pacing and possible unfavorable long-term ventricular function. Modification of AVN conduction using other approaches has been difficult. This study was undertaken to assess the feasibility of AVN modification with strategically injected fibroblasts to modulate conduction.

1034-207 Mechanism for rate slowing by anterior atrioventricular node modification during atrial fibrillation: Partial damage of the compact node rather than past pathway ablation

1034-207 Mechanism for rate slowing by anterior atrioventricular node modification during atrial fibrillation: Partial damage of the compact node rather than past pathway ablation

Atrioventricular nodal fast pathway modification: mechanism for lack of ventricular rate slowing in atrial fibrillation.

Atrioventricular node (AVN) modification is one of the alternatives for ventricular rate control in patients with drug refractory atrial fibrillation (AF). However, the underlying mechanisms, and in particular the role of the dual pathway electrophysiology is not clear. By using a novel index, His electrogram (HE) alternans, we have previously demonstrated in rabbits that both the slow (SP) and the fast pathways (FP) are involved in AVN conduction during AF. This electrophysiological-morphological study was designed to address the role of selective FP ablation on AVN conduction during AF. In 12 rabbit AVN preparations dual pathway conduction was confirmed by HE alternans during A1A2 pacing protocol, as well as during AF. On average 48% of the conducted beats during AF utilized the FP. Selective FP ablation (n=12) guided by HE alternans resulted in only-SP conduction, with longer AVN conduction time at basic beats, but without change of AVN effective refractory period (ERP). Interestingly, despite elimination of all FP-conducted beats during AF, the selective FP ablation allowed previously concealed SP beats to be conducted, resulting in little net effect on the ventricular rate (average His-His interval 199+/-10 ms before versus 201+/-13 ms after FP ablation, p>0.05). Morphological evidence indicated that FP ablation created lesions within the transitional cells of the superior approaches at the junction between the central fibrous body and the AVN. However, extension of FP ablation lesion into the compact AVN domain resulted in non-selective AVN modification and slowing of ventricular rate during AF. Despite its longer ERP, FP is responsible for a substantial number of ventricular beats during AF. However, selective FP ablation has a minor effect on ventricular rate. The most likely mechanism for this phenomenon is that FP ablation allows previously concealed SP beats to be conducted. On the other hand, ventricular rate slowdown could be achieved if FP ablations caused collateral damage in the compact node. This study highlights the usefulness of HE alternans as a novel tool to monitor dual pathway conduction during AF and to guide AVN modification.

His electrogram alternans reveal dual atrioventricular nodal pathway conduction during atrial fibrillation: the role of slow-pathway modification.

Traditional tools to study dual-pathway atrioventricular nodal (AVN) electrophysiology are not applicable in subjects with permanent atrial fibrillation (AF). The presence of fast-pathway (FP) and slow-pathway (SP) wavefronts and their possible modification remain uncertain in this condition. We demonstrated previously that His electrogram (HE) alternans can determine whether the FP or the SP reaches the His bundle on a beat-by-beat basis. We have now applied this novel index to monitor dual-pathway conduction and the effects of SP modification during AF. In 12 rabbit AVN preparations, HE alternans were confirmed during a standard A(1)A(2) pacing protocol. During AF, in 9 of the 12 hearts, HE alternans indicated the presence of dual pathways. Successful SP modification guided by the HE alternans eliminated the SP, resulting in a predominantly FP conduction during AF in all hearts. This increased the average His-His interval (204+/-14 versus 276+/-51 ms, P<0.001). Morphological studies revealed that SP modification damaged only the posterior extension of the AVN. We have demonstrated for the first time in rabbits that HE alternans permit "visualization" of dual-pathway electrophysiology and confirmed the presence of both FP and SP wavefronts during AF. This novel index has been used in a selective SP ablation that resulted in a significant slowing of the ventricular rate. HE alternans provide a new insight into the mechanisms of AVN conduction and could guide AVN modification for ventricular rate control in AF clinically.

Atrioventricular node modification in patients with chronic atrial fibrillation. Role of morphology of RR interval variation

Atrioventricular node modification in patients with chronic atrial fibrillation. Role of morphology of RR interval variation

The 1998 NASPE prospective catheter ablation registry.

The results of the NASPE Prospective Voluntary Registry are reported. A total of 3,357 patients were entered. For those undergoing atrioventricular (AV) junctional ablation (646 patients), the success rate was 97.4% and significant complications occurred in 5 patients. A total of 1,197 patients underwent AV nodal modification for AV nodal reentrant tachycardia, which was successful in 96.1% and the only significant complication was development of AV block (1%). Accessory pathway ablation was performed in 654 patients and was successful in 94%. Major complications included cardiac tamponade (7 patients), acute myocardial infarction (1 patient), femoral artery pseudoaneurysm (1 patient), AV block (1 patient), pneumothorax (1 patient), and pericarditis (2 patients). A total of 447 patients underwent atrial flutter ablation and acute success was achieved in 86% of patients. Significant complications included inadvertent AV block (3 patients), significant tricuspid regurgitation (1 patient), cardiac tamponade (1 patient), and pneumothorax (1 patient). Atrial tachycardia was attempted for 216 patients and the success rate was higher for those with right atrial (80%) or left atrial (72%) compared to those with septal foci (52%). A total of 201 patients underwent ablation for ventricular tachycardia. The success rate was higher for those with idiopathic ventricular tachycardia compared to those with ventricular tachycardia due to ischemic heart disease or cardiomyopathy. While the number of AV junction ablation were higher for those > 60 years of age, there was no significant difference in the success rate or incidence of complication comparing patients > or = 60 to those < 60 years of age. In addition, we found no differences in incidence of success or complications comparing large volume centers (> 100 ablation/year) with lower volume centers or between teaching and non-teaching hospitals.

Prevalence of coronary artery disease in a general population without suspicion of coronary artery disease: angiographic analysis of subjects aged 40 to 70 years referred for catheter ablation therapy.

The prevalence of coronary vessel wall alterations in the general population is not known. Therefore, the aim of our study was to determine the prevalence of coronary artery disease in persons in whom the underlying disease was not related to coronary artery disease and could therefore be regarded as a near normal population. We included 331 consecutive patients (173 men, 158 women, aged between 40 and 70 years) who were referred for catheter ablation of an accessory pathway (67.4% ) or atrioventricular-node modification (32.6%) and who underwent coronary angiography as part of their routine baseline evaluation before radiofrequency current application. Most of the patients (79%) of this cohort were free of symptoms of coronary artery disease. Based on visual inspection of coronary angiograms in multiple projections, patients were classified to have one-, two- or three-vessel disease if stenoses greater than 50% of lumen diameter were present. In addition, diffuse vessel wall alterations were assessed using two different score systems. The prevalence of coronary artery disease in this near normal population was 7.3%, with a significant difference in coronary asymptomatic (3.8%) vs symptomatic patients (17.1%). Mean levels of total cholesterol and other risk factors were not significantly different in patients with coronary artery disease compared to those without. But levels of low-density lipoprotein (LDL) cholesterol and lipoprotein(a) were significantly higher and high-density (HDL) cholesterol lower in patients with a stenosis or extent score higher than zero compared to a score of zero. The values of all vessel scores evaluating the extent of critical and diffuse coronary vessel alterations were very low in patients affected with coronary artery disease, indicating a low degree of diffuse alteration of the vessel wall. The prevalence of coronary artery disease with at least one critical stenosis in subjects aged 40-70 years with an average cholesterol level of 238+/-42 mg. dl(-1)is 7.3%.

Catheter-ablative techniques for the treatment of atrial fibrillation.

Atrial fibrillation is the most commonly encountered arrhythmia in clinical practice and is associated with significant morbidity and mortality. Pharmacologic therapy, although useful for rate control, has proven much less effective in the long term maintenance of sinus rhythm. The utility of implantable atrial defibrillators or pacing to prevent atrial fibrillation remains largely untested. This article describes four catheter-based therapies for atrial fibrillation: His ablation, atrioventricular nodal modification, the Maze procedure, and the ablation of pulmonary vein foci which initiate the arrhythmia. Whereas the first two procedures are largely palliative and recommended for patients with symptomatic, drug-refractory atrial fibrillation, the latter two offer the potential for a curative intervention.

Variable effects of adenosine on retrograde conduction in patients with atrioventricular nodal reentry tachycardia.

Adenosine has been demonstrated to reliably produce transient block of atrioventricular nodal (AVN) conduction, and has been advocated as a method of differentiating retrograde conduction via the atrioventricular node from accessory pathway conduction. However, the response of retrograde AVN to adenosine in patients with typical atrioventricular nodal reentry tachycardia (AVNRT) remains unclear. We evaluated 13 patients (mean age 45 +/- 20 years) with typical AVNRT prior to AVN modification. During right ventricular pacing, a rapid bolus of adenosine (0.2 mg/kg; maximum 18 mg) was administered. Adenosine sensitivity, defined by transient ventriculoatrial block, was observed in six patients, while in seven patients ventriculoatrial conduction was unaffected. An adenosine bolus administered during sinus rhythm or atrial pacing resulted in antegrade atrioventricular block in all the adenosine resistant patients in whom this was performed (n = 6). Comparisons of AVN electrophysiological characteristics between the adenosine sensitive and adenosine resistant patients were performed. There was no difference with respect to ventriculoatrial effective refractory period, ventriculoatrial Wenckebach, AVNRT cycle length, and His to atrial echo interval in AVNRT. However, there was a trend toward a longer antegrade fast pathway ERP in the adenosine sensitive group (P = 0.07). Electrophysiological properties do not predict retrograde AVN adenosine sensitivity. Adenosine does not cause retrograde AVN block in all patients with AVNRT, and therefore cannot reliably distinguish between retrograde conduction via the AVN or an accessory pathway.

Comparison of Power- and Temperature-Guided Radiofrequency Modification of the Atrioventricular Node

The purpose of this study was to compare the performance and clinical outcome of radiofrequency ablation of the substrate of atrioventricular (AV) nodal reentrant tachycardia (AVNRT) when guided by power output or temperature monitoring. Two sequential multicenter studies of power-controlled and open-loop, temperature-controlled radiofrequency ablation were analyzed in 171 patients undergoing AV node modification for the treatment of AVNRT. After successful ablation of AVNRT, complete elimination of slow AV node pathway function was accomplished more often with than without temperature monitoring (92% vs 69%, p = 0.005). Greater power was delivered to each patient with than without temperature monitoring (median 47 W, range 10 to 57, vs median 35 W, range 5 to 68, p = 0.001). Acute elimination of tachycardia (100% vs 96%), 3-month recurrence (6% vs 8%), procedural times (162 vs 170 minutes), fluoroscopy times (24.6 vs 29.5 minutes), complications (6% vs 3%), and catheter removals to check for coagulum (8% vs 6%) did not differ between patients treated with and without temperature monitoring, respectively. Power- and temperature-controlled radiofrequency techniques are highly successful with low complication rates for slow pathway ablation. Temperature monitoring may allow the safe delivery of more power, and the more complete elimination of slow AV node pathway function.

Using the right drug. A treatment algorithm for atrial fibrillation.

Atrial fibrillation is the commonest sustained cardiac arrhythmia. Its incidence increases with age and in association with organic heart disease, in particular valvular heart disease, left ventricular dysfunction and in association with thyrotoxicosis and alcohol excess. Atrial fibrillation may present as paroxysms of self-terminating arrhythmia or as a sustained arrhythmia. In the former instance, management is directed towards suppression of paroxysms and will commonly involve class 1C, class 2 or class 3 agents. If atrial fibrillation is sustained, a decision as to the desirability of cardioversion must be made. If this can be achieved successfully, particularly if the episode was of brief duration and associated with a reversible cause, sinus rhythm may be preserved without further antiarrhythmic therapy. Otherwise prophylactic therapy as used for paroxysmal atrial fibrillation is appropriate. In patients who fail to respond to cardioversion, or in those with advanced organic heart disease, long-standing atrial fibrillation or marked dilatation of the left atrium in which case cardioversion is unlikely to be successful, the principal therapeutic strategy is to control ventricular rate. Classically, digoxin is used for this purpose. Additional agents which will slow the ventricular rates, such as beta-blockers, amiodarone or calcium channel antagonists (verapamil or diltiazem), may be necessary if the ventricular rate remains uncontrolled and continues to produce severe symptoms. In the event of failure of medical therapy to control ventricular rate, atrioventricular nodal modification or ablation may be appropriate.

Cardiac arrest following holiday heart syndrome

We describe the case of a patient who, after a binge, had an episode of ventricular fibrillation (holiday heart syndrome) and was successfully resuscitated. In the electrophysiological study, we found dual atrioventricular nodal pathways, an atrioventricular effective refractory period of 210 ms, and an inducible atrial fibrillation with a ventricular response of 210 bpm that produced hemodynamic collapse. Atrioventricular nodal modification by radiofrequency ablation was successfully performed. The patient stopped drinking alcohol and has remained completely asymptomatic. In this case, ventricular fibrillation was probably caused by the fibrillating atria combined with a fast AV node.

Mechanism of ventricular rate control after radiofrequency modification of atrioventricular conduction in patients with atrial fibrillation.

Modification of atrioventricular (AV) conduction during atrial fibrillation (AF) may be achieved by radiofrequency ablation in the posteroseptal region of the tricuspid annulus. We tested the hypothesis that elimination of the posterior atrionodal input rather than direct damage to the compact AV node accounts for the decrease in ventricular rate after AV nodal modification. Twenty-four patients with the typical form of AV nodal reentrant tachycardia (AVNRT) underwent selective radiofrequency ablation of the slow AV nodal pathway in the posteroseptal tricuspid annulus. AF was induced before ablation (phase 1), 30 minutes after ablation (phase 2), and during follow-up 24 hours after ablation (phase 3), both with and without concurrent infusion of isoproterenol (4 micrograms/min). Successful elimination of AVNRT was achieved in all patients. During phase 3, 11 patients (46%) had residual dual pathway physiology. AV nodal Wenckebach cycle length (AVNW-CL) increased progressively during each phase of the protocol (356 +/- 72 versus 371 +/- 78 ms versus 432 +/- 104 ms, P < .0001), as did the effective refractory period of the AV node (279 +/- 60 versus 304 +/- 67 ms versus 372 +/- 56 ms, P < .0001). Minimal, mean, and maximal RR intervals during AF progressively increased immediately after ablation and 24 hours later (485 +/- 88 versus 533 +/- 116 ms versus 637 +/- 142 ms for mean RR, P < .0001). The changes in AVNW-CL, AV nodal effective refractory period, and ventricular response during AF were independent of residual dual pathway physiology after ablation. Similar observations were observed during isoproterenol infusion. Modification of AV nodal conduction during AF by radiofrequency ablation in the posteroseptal tricuspid annulus is independent of the presence or absence of a residual slow AV nodal pathway. On the basis of these observations, the mechanism of AV nodal modification is consistent with elimination of the posterior atrionodal input.

Catheter-induced atrioventricular nodal block during radiofrequency ablation

This study examined the incidence and significance of catheter-induced atrioventricular nodal block (AVNB) during a radiofrequency ablation procedure that uses stiff large-tip steerable ablation catheters. AVNB was noted in 10 (1.6%) of 613 consecutive patients undergoing radiofrequency ablation therapy for atrioventricular nodal (AVN) reentrant tachycardia (592 patients) or atrioventricular reentry tachycardia incorporating a midseptal accessory pathway (21 patients). Of these 10 patients, 9 underwent AVN modification for AVN reentrant tachycardia and 1 for ablation of a midseptal accessory pathway. One patient had two episodes of AVNB during two sessions undertaken because of recurrence of tachycardia. No patient had a preexisting conduction defect before the study. In all 10 patients, AVNB was transient, and it lasted for a mean of 9.1 ± 19 minutes. It occurred during positioning of the ablation catheter in the junctional area before (8 patients) or after (2 patients) the start of radiofrequency current applications. Complete AVNB was noted on six occasions, second-degree AVNB on four occasions, and first-degree AVNB on one occasion. All blocks were associated with narrow QRS ventricular beats and with a site of block proximal to the His bundle. The mean ventricular heart rate during AVNB was 60 ± 23 beats/min. Two patients had transient asystole, with one having loss of consciousness. No patient required special treatment for heart block. One-to-one conduction resumed after repositioning of the catheters, and the subsequent ablation procedure was successfully completed in 8 of the 10 patients. During a follow-up of 20 ± 12 months, none of the patients had severe dizziness or syncope, and none required implantation of a permanent pacemaker. In conclusion, transient AVNB due to mechanical injury occurs during positioning of a stiff large-tip steerable ablation catheter in the junctional area. Delivery of radiofrequency current to the site that provokes catheter-induced AVNB should be avoided.