Incessant Atrio‐Ventricular Node Reentrant Tachycardia Induced by Unapparent Dual Atrio‐Ventricular Node Conduction

We present the case of a patient with incessant slow‐fast atrio‐ventricular (AV) node reentrant tachycardia induced by dual AV node conduction with aborted conduction to the ventricles. The unapparent conduction over the slow pathway was suspected here because of spontaneous nodal echoes without QRS complexes occurring during sinus rhythm, manifested as isolated premature atrial beats and which repetitively induced the tachycardia.     

Computer Model of the Atrioventricular Node Predicts Reentrant Arrhythmias

Introduction: Following atrial premature beats, the AV node may exhibit sustained reentrant tachyarrhyth-mias, isolated echo beats, or discontinuities in the recovery curve (the plot of conduction time versus atrial cycle length). A computer model was used to examine the hypothesis that spatial variation of AV nodal passive electrical resistance may account for these phenomena. Methods and Results: A computer model of a rectangular lattice of elecirotonically linked elements whose ionic kinetics simulated nodal ionic flux was developed. the model showed that there exists a resistance value that minimizes the effective refractory period, because high resistance prevents depolarization of distal elements, while low resistance allows leakage of depolarizing current by electrotonic transmission, preventing activation of proximal elements. High resistances stabilized reentry by slowing conduction. Simulations incorporating equal resistance values between elements predicted increased AV nodal conduction times with increasing prematurity of atrial impulses. A model with a gradual change in resistance between fibers produced discontinuities and tachycardia, but not both simultaneously. Uniform anisotropy produced preferential transverse block, leading to echo beats and “fast-slow” tachycardia, but not recovery curve discontinuities. Nonuniform anisotropy could produce reentry, but tachycardia often occurred without discontinuities. Dividing the lattice into two electrotonically linked parallel pathways with different resistance values (“dual pathway model”) predicted recovery curve discontinuities, echo beats, and tachycardia. At critical atrial cycle lengths, only the (high resistance) slow pathway conducted antegradely, while the fast pathway conducted retrogradely, to generate the typical “slow-fast” tachycardia. Responses of the dual pathway model to ablation were consistent with clinical data, including the previous observation of a decrease in fast pathway effective refractory period after slow pathway ablation. Conclusion: Differences in passive electrical resistance of electrotonically linked dual pathways within the AV node may account for functional longitudinal dissociation, reentrant arrhythmias, and responses to catheter ablation therapy.     

Double Ventricular Responses to a Single Atrial Depolarization in a Patient with Dual AV Nodal Pathways

Electrophysiological study was performed in a patient with atrioventricular nodal reentrant tachycardia (AVNRT). Double ventricular responses through dual AV nodal pathways were observed by atrial extrastimulus technique followed by initiation of AVNRT. The difference in conduction time between the slow and fast AV nodal pathways was longer than 320 msec. A ventricular extrastimulus delivered during sinus rhythm, which was not followed by ventriculoatrial conduction, also induced AVNRT. These findings indicated the presence of an antegrade critical delay and retrograde block in the slow AV nodal pathway, criteria necessary for the occurrence of a double ventricular response.     

Atrioventricular Node Reentry: Physiology and Radiofrequency Ablation

Atrioventricular (A V) node reentry has heen recognized as a clinical arrhythmia for many years. Earlier basic investigations identified a dual AV conduction system, and atrial echo beats occurred when the refractory period of the slow conduction pathway was shorter than the fast pathway. Subsequent studies in humans confirmed the concept of dual AV node physiology and AV node reentry. Slow-fast AV node reentry (anterograde conduction over the slow pathway and retrograde conduction over the fast pathway) occurs most frequently. The fast-slow and intermediate varieties are much less common. A high (> 95%) cure rate occurs with radiofrequency catheter ablation with experienced electrophysiologists. Most electrophysiologists prefer the posterior approach, which results in absence or very poor conduction over the slow AV node pathway; the PR interval is minimally changed. This approach is highly successful for all three forms of AV node reentry and associated with a 1%–2% incidence of heart block in most experienced laboratories.     

Dual Atrio-ventricular Nodal Pathways and Atrial Fibrillation

The determinants of the ventricular rate during atrial fibrillation were studied in a group of eleven patients demonstrating dual A-V nodal pathways during atrial stimulation. The shortest R-R interval and the mean ventricular cycle length during at least 1 min of pacing-induced atrial fibrillation were compared: a) to the effective and functional refractory period of the fast pathway; b) to the effective refractory period of the slow pathway determined during atrial stimulation, at two or more different basic cycle lengths of pacing; and c) to the shortest cycle length during atrial stimulation followed by 1:1 A-V conduction. A group of 8 patients not demonstrating dual A-V nodal pathway-curves during atrial stimulation was used as a control. In both groups the shortest R-R interval during atrial fibrillation was best predicted by the shortest cycle length followed by 1:1 A-V conduction during atrial stimulation. The mean ventricular cycle length during atrial fibrillation was not accurately predicted by any of the variables studied. The similar results in patients with and without dual A-V nodal pathways suggest that concealed conduction from one to another A-V nodal pathway does not play a role in determining the ventricular response during atrial fibrillation in patients with dual A-V nodal pathways.     

The Effect of Variable Retrograde Penetration on Dual AV Nodal Pathways: Observations Before and After Slow Pathway Ablation LDD

Retrograde VA conduction is usually over the fast pathway and rarely over the slow pathway in patients with dual AV nodal pathways. It is unknown whether this apparent unidirectional conduction of the slow pathway is due to the lack of its retrograde conducting ability or the result of concealment. The effect of variable retrograde AV nodal penetration on antegrade AV nodal conduction was determined in patients with typical AV nodal reentrant tachycardia before and after the slow pathway ablation. Variable retrograde penetration was produced by delivering a ventricular extrastimulus simultaneously with (VE-0), 50 ms after (VE-50), or 100 ms after (VE-100) the last basic atrial stimulus, while atrial extrastimuli were used to determine changes of anterograde AV nodal effective refractory period (ERP) and A-H interval. The AV nodal functions measured without the ventricular extrastimuli served as the baseline. Although the mean slow pathway ERP was not significantly different among the different stimulation protocols, a significant shortening of the slow pathway conduction time (A-H from 348 ± 60 to 324 ±119 ms, P < 0.05) was observed with upper level retrograde penetration of the AV node (VE-0). This facilitating effect became a prolonging effect when the retrograde penetration level moved to the lower level (VE-100, A-H from 324 ± 119 to 366 ± 122 ms, P < 0.05). The fast pathway ERP shortened with an upper level penetration (VE–0) but tended to prolong with a lower level retrograde penetration (VE-100) both before and after the slow pathway ablation (preablation, from 348 ± 143 of the baseline to 302 ± 114 to 360 ± 143 ms, P < 0.05; postablation, from 314 ± 101 of the baseline to 274 ± 118 to 361 ± 143 ms, P < 0.05). The mean A₂?H₂ interval of the slow pathway was significantly shorter than the baseline (350 ± 44 ms) with VE-0 (249 ± 48 ms, P < 0.05) and VE-5O stimulation (285 ± 82 ms, P < 0.05) but not with VE-100 stimulation (330 ± 83 ms, P = NS). Refore slow pathway ablation, the A₂?H₂ interval of the fast pathway at equal coupling intervals was shorter than the baseline (165 ± 53 ms) with VE-0 (144 ± 47 ms, P < 0.01) and VE-50 stimulation (152 ± 43 ms, P < 0.05) but tended to be longer with VE-l00 stimulation (175 ± 47 ms, P = NS). After slow pathway ablation, the mean A₂?H₂ interval at the same coupling interval was shorter than the baseline (173 ± 39 ms) with VE-0 (139 ± 35 ms, P < 0.05), VE-50 (153 ± 32 ms, P = 0.05) but tended to be longer with VE-100 stimulation (178 ± 49 ms, P = NS). We conclude that: (1) concealed retrograde conduction can be demonstrated in both the slow and the fast A V nodal pathways; and (2) concealed retrograde conduction may either shorten or prolong anterograde refractoriness and conduction time, depending on the level of retrograde penetration.     

Randomized study of propofol effect on electrophysiological properties of the atrioventricular node in patients with nodal reentrant tachycardia

BACKGROUND: Atrioventricular nodal reentrant tachycardia (AVNRT) is probably the most common form of paroxysmal supraventricular tachycardia. Percutaneous catheter ablation is a technique to interrupt cardiac conduction pathways selectively. The anesthetist is challenged to provide a safe anesthetic which takes into account the electrophysiologist's requirements for minimal cardiac conduction interference. Propofol is an ideal drug. However, previous studies have shown that the infusion of propofol has sometimes been associated with bradyarrhythmias or conversion of arrhythmias to sinusal rhythm. The purpose of this report is to verify the interferences of propofol in the electrophysiological properties of the atrioventricular (AV) node conduction system in patients with AVNRT. METHODS: Patients were randomly assigned to receive either a placebo or propofol at sedative doses. An electrophysiological study was performed consisting of measuring the anterograde (AERPFP) and retrograde effective refractory period of the fast (RERPFP) and the anterograde effective refractory period of the slow (AERPSP) AV nodal pathway. Reciprocating tachycardia was induced and the cycle length (CL) and atrial-His (AH), His-ventricular (HV), and ventriculoatrial (VA) intervals were measured. RESULTS: Propofol did not cause alteration (P > 0.05) in the AERPFP or RERPFP and the AERPSP AV nodal pathway. The AH, HV, and VA intervals were not affected. Sustained reciprocating tachycardia could be induced in the all patients. All slow pathways were successfully identified and ablated. CONCLUSION: Propofol has no effect on the electrophysiological properties of the AV node conduction system. It is thus a suitable anesthetic agent for use in patients undergoing ablative procedures.     

Dual antegrade response tachycardia induced cardiomyopathy

We report a rare case of tachycardia induced cardiomyopathy resulting from nearly incessant dual antegrade response tachycardia. Criteria necessary for sustaining dual antegrade responses are discussed, including: (1) sufficient antegrade dissociation of the AV node; (2) absence of retrograde conduction over each AV nodal pathway following antegrade conduction over its counterpart; (3) difference between fast and slow pathway conduction times exceeding His-Purkinje refractoriness; and (4) critical timing of sinus impulses relative to preceding AV nodal conduction. Both the arrhythmia and cardiomyopathy were successfully treated by slow pathway ablation.     

Histopathological Study Following Catheter Guided Radiofrequency Current Ablation of the Slow Pathway in a Patient with Atrioventricular Nodal Reentrant Tachycardia

The present study examined histological changes induced by catheter guided radiofrequency current in a patient with AV nodal reentrant tachycardia who underwent cardiac transplantation 1 week after ablation of the slow pathway. During the electrophysiology study AV nodal conduction curves were discontinuous and AV nodal reentry was induced. At the conclusion of the procedure there was no evidence of slow pathway function. Histological sections from the explanted heart demonstrated a sharply demarcated atrial lesion (5 × 5 × 4 mm) extending from the septal portion of the tricuspid annulus to the posterior border of the AV node. The lesion did not encompass the compact AV node. These observations support the hypothesis that the slow pathway is comprised of atrial approaches to the AV node and is distinct from the compact AV node.     

Tachycardiomyopathy secondary to nonreentrant atrioventricular nodal tachycardia: recovery after slow pathway ablation

Nonreentrant atrioventricular (AV) nodal tachycardia is a rare form of arrhythmia due to simultaneous anterograde conduction in dual AV pathways, one atrial impulse triggering two ventricular complexes. We report the case of a 74-year-old man referred for incessant palpitations resistant to antiarrhythmic medication, and effort dyspnea. A nonreentrant AV nodal tachycardia is diagnosed with electrophysiological study. A dilated cardiomyopathy with left ventricular dysfunction is found with gated blood pool single-photon emission computed tomography. A radiofrequency catheter ablation of the slow pathway is successfully performed. The patient is reassessed 11 months after ablation. He is asymptomatic and left ventricular function has fully recovered.     

Multiple Anterograde and Retrograde AV Nodal Pathways: Demonstration by Multiple Discontinuities in the AV Nodal Conduction Curves and Echo Time Intervals

Programmed electrical cardiac stimulation was performed in a 40-year-old man with documented recurrent, sustained ventricular tachycardia which was refractory to standard medical therapy. Both the presence of several discontinuities in the AV nodal conduction curves during atrial and ventricular stimulation and the time intervals of the AV nodal echo phenomena suggested the presence of multiple AV nodal pathways. The results of this study are of interest in further increasing our understanding of the electrophysiologic behavior of the human AV node.     

Radiofrequency Catheter Ablation and Modulation of Atrioventricular Conduction in Patients with Atrial Fibrillation

We attempted radiofrequency ablation of the AV junction with a sequential right- and left-sided approach in 78 patients affected by severely symptomatic, drug refractory atrial fibrillation. Stable third-degree A V block was obtained in 99% of cases and, after 3 months, persisted in 92% of cases. Single session, stepwise, radiofrequency modulation of the AV node was attempted in 13 patients with paroxysmal atrial fibrillation. During sinus rhythm, ablation of the slow and fast AV node pathways was performed in order to increase the nodal refractory period or to slow conduction. Clinically successful modulation of AV conduction was achieved in 15% of cases and persisted during a 3-month follow-up. In conclusion. AV junction ablation is a well-established means of treating atrial fibrillation, but implies the implant of a permanent pacemaker. AV node modulation avoids the pacemaker implant, but is efficacious only in a minority of patients. Thus, in patients affected by paroxysmal atrial fibrillation, AV modulation should be attempted first; if this is ineffective. AV ablation can be performed during the same session.     

Acute effects of simvastatin to terminate fast reentrant tachycardia through increasing wavelength of atrioventricular nodal reentrant tachycardia circuit

Simvastatin (SV) leads to reduction of ventricular rhythm during atrial fibrillation on rabbit atrioventricular (AV) nodes. The aim of our study was (i) to determine the frequency‐dependent effects of SV in a functional model, and (ii) to assess the effects of SV to suppress experimental AV nodal reentrant tachycardia (AVNRT). Selective stimulation protocols were used with two different pacing protocols, His to atrial, and atrial to atrial (AA). An experimental AVNRT model with various cycle lengths was created in three groups of perfused rabbit AV nodal preparations (n = 24) including: SV 3 μm , SV 7 μm , and verapamil 0.1 μm . SV increased nodal conduction time and refractoriness by AA pacing. Different simulated models of slow/fast and fast/slow reentry were induced. SV caused inhibitory effects on the slow anterograde conduction (origin of refractoriness) more than on the fast anterograde conduction time, leading to an increase of tachycardia cycle length, tachycardia wavelength and termination of slow/fast reentrant tachyarrhythmia. Verapamil significantly suppressed the basic and frequency‐dependent intrinsic nodal properties. In addition, SV decreased the incidence of gap and echo beats. The present study showed that SV in a concentration and rate‐dependent manner increased the AV effective refractory period and reentrant tachycardia wavelength that lead to slowing or termination of experimental fast AVNRT. The direction‐dependent inhibitory effect of SV on the anterograde and retrograde dual pathways explains its specific antireentrant actions.     

Automatic Tachycardia Recognition

A microcomputer algorithm for tachycardia identification, suitable for use in un implanted antitachycardia pacemaker, is described. The system employs an atrial and ventricular electrogram, detects a sustained fast rate in either chamber, and awakens the main program to perform detailed analysis of the tachycardia and its immediately preceding beats. The algorithm distinguishes atrial, ventricular, and AV nodal and re-entrant tachycardia from high rates due to sinus tachycardia. For testing of the program, we used a data base of twenty-two tape-recorded and documented arrhythmias provoked during electrophysiologic studies in which atrial and ventricular bipolar electrodes were in place; twenty-one of twenty-two wave successfully detected. These included atrial fibrillation, atrial flutter, atrial tachycardia, AV nodal re-entrant tachycardia, AV re-entrant tachycardia using an accessory pathway, and ventricular tachycardia with and without ventriculo-atrial conduction.     

Extended Protocol for Demonstration of Dual AV Nodal Physiology

The incidence of dual atrioventricular (AV) nodal physiology was evaluated in 22 patients (14 males, 8 females, age 52 ± 18 years) undergoing electrophysiology studies for evaluation of ventricular tachycardia/honsustained ventricular tachycardia (n = 11), supraventricular tachycardia (n = 5), and syncope (n = 6). Patients with AV node reentrant tachycardia were excluded. Thirteen patients had riormal left ventricular function and nine patients (seven with coronary artery disease, two with dilated cardiomyopathy) had depressed left ventricular function. Single atrial extrastimuli (A2) were introduced after eight-beat drives at paced cycle lengths of 550 msec and 400 or 450 msec beginning at coupling intervals of 650 and 500 or 550 msec, respectively. The coupling interval was decreased at 10-msec intervals until AV node or atrial refractoriness. A second atrial extrastimulus (A3) was then added. A2 was fixed at 50 msec greater than the atrial or AV nodal refractory period. A3 was coupled to A2 at 650 and 500 or 550 msec and decremented as with single extrastimulation. Dual AV nodal physiology was defined by a 50-msec increase in A2H2 or A3H3 with a 10-msec decrement in the coupling interval or a discontinuous H1H2 versus A1A2 or H2H3 versus A2A3 curve. Using a single extrastimulus, 1 of 22 patients demonstrated dual AV nodal physiology. Using double extrastimuli, an additional four patients with dual AV nodal physiology were identified. The occurrence of dual AV nodal physiology determined using double extrastimuli is increased compared to using only a single extrastimulus (P = 0.03). In conclusion, dual AV nodal physiology can be demonstrated with greater frequency using an extended rather than a standard protocol.     

Pacemaker Syndrome with AAI Rate Variable Pacing: Importance of Atrioventricular Conduction Properties, Medication, and Pacemaker Programmability

A patient who received an AAI Activitrax rate variable pacemaker for treatment of symptomatic sinus bradycardia is described. disopyramide prolonged the anterograde effective refractory period of the fast conducting atrioventricular (AV) nodal pathway to such an extent, that conduction switched to the slow AV nodal pathway at low atrial pacing rates. This gave rise to symptoms of the pacemaker syndrome during moderate exercise because the paced atrial event was conducted with a long, spike to Q interval with occurrence of the paced atrial event just after the preceding QRS complex. A change of medication solved this problem. Programming a bipolar electrode configuration avoided sensing of far-field QRS signals with the associated problems of resetting the basic pacing interval as well as the upper rate interval. AAI rate variable pacing requires careful evaluation of AV conduction properties, AV conduction intervals as well as the influence of medication to be given. The use of multiprogrammable pacemakers with marker channel capability will significantly facilitate the understanding and resolution of anomalous behavior.     

Radiofrequency Modification of Atrioventricular Conduction by Selective Ablation of the Low Posterior Septal Right Atrium in a Patient with Atrial Fibrillation and a Rapid Ventricular Response

A case is presented of a 58-year-old woman with atrial fibrillation and uncontrolled ventricular responses up to 180 beats/min despite therapy with digoxin. Radiofrequency energy was applied to the low posteroseptai right atrium in an attempt to modify "slow fiber" conduction. This resulted in a decrease in ventricular rate from 125 to 50 beats/min. Follow-up Holter monitor demonstrated an average heart rate of 64 beats/min (range 43–112). On exercise tolerance test, the maximum heart rate was 126. Modification of the low posterosepta right atrium may prove to be an alternative to AV node or His bundle ablation and pacemaker implantation in patients with poorly controlled atrial fibrillation and rapid ventricular response. The mechanism by which this approach was effective may be ablation of slow conducting AV nodal fibers with a short refractory period.     

The annular fat stripe as a fluoroscopic guide to anatomic sites during diagnostic and interventional electrophysiology studies

Few radiographic landmarks are visible during electrophysiology procedures to aid in catheter positioning other than the catheters themselves. In the 35 degrees -45 degrees RAO projection, a linear radio-opacity corresponding to the rings of fat surrounding both annuli can be easily identified. This "fat stripe" can serve as a useful landmark for several important anatomic sites. Intracardiac catheters positioned left of (posterior) the fat stripe lie within an atrial cavity while those positioned to the right (anterior) lie within a ventricular cavity. The superior third of the stripe corresponds to the region of the right and left atrial appendages while the inferior end identifies the site of the coronary sinus os. The middle third serves as a reference for the fast AV nodal pathway and compact AV node. The region corresponding to the slow AV nodal pathway superimposes on the lower third of the fat stripe. Electrophysiological recordings from catheters positioned along the fat stripe always exhibit both an atrial and ventricular component consistent with an annular recording, whether the catheter is septal or free wall in its location. Coronary sinus os engagement and catheterization can be simplified by using the fat stripe as an anatomic guide. In addition to facilitating catheter positioning for evaluating normal AV conduction, the fat stripe can serve as an excellent guide for targeting the majority of structures intended for ablation because of their annular location. These include the compact AV node, the slow AV nodal pathway, the subeustachian isthmus and any accessory pathway. Good ablation catheter tip contact with annular structures is confirmed by observing its movement in unison with the fat stripe.     

Dissociation of Atrioventricular Conduction and Refractoriness Following Application of Radiofrequency Energy to the Canine Atrioventricular Node: Acute and Chronic Observations

The electrophysiology of AV nodal modification induced by radiofrequency energy (n = 5) or a sham procedure (n = 5) was studied in ten dogs. The five dogs that received radiofrequency energy had an AH prolongation > 100% from baseline values and this prolongation persisted throughout the 2-month study. The AV nodal functional refractory period was prolonged only acutely. These data indicate a dissociation between the effects on AV nodal conduction and refractoriness that was induced by this procedure. The five sham treated controls showed no acute or chronic electrophysiological changes. In the dogs that received radiofrequency energy, there was fibrosis of the approaches to the AV node and the region of the A V node itself. It is concluded that chronic modification of AV nodal conduction without concomitant changes in refractoriness can be induced by radiofrequency energy delivered in the proximal portion of the AV node. It would be anticipated that this procedure would not decrease the ventricular response to atrial fibrillation or flutter, but may be effective in preventing AV nodal reentrant tachycardia by interfering with conduction either in the AV node or perinodal region. Since the AV node itself suffers at least moderate pathological damage, there may be an appreciable incidence of the late development of complete heart block after this procedure.     

Electrophysiological characteristics of junctional rhythm during ablation of the slow pathway in different types of atrioventricular nodal reentrant tachycardia

BACKGROUND: Junctional rhythm (JR) is commonly observed during radiofrequency (RF) ablation of the slow pathway for atrioventricular (AV) nodal reentrant tachycardia. However, the atrial activation pattern and conduction time from the His-bundle region to the atria recorded during JR in different types of AV nodal reentrant tachycardia have not been fully defined. METHODS: Forty-five patients who underwent RF ablation of the slow pathway for AV nodal reentrant tachycardia were included; 27 patients with slow-fast, 11 patients with slow-intermediate, and 7 patients with fast-slow AV nodal reentrant tachycardia. The atrial activation pattern and HA interval (from the His-bundle potential to the atrial recording of the high right atrial catheter) during AV nodal reentrant tachycardia (HA(SVT)) and JR (HA(JR)) were analyzed. RESULTS: In all patients with slow-fast AV nodal reentrant tachycardia, the atrial activation sequence recorded during JR was similar to that of the retrograde fast pathway, and transient retrograde conduction block during JR was found in 1 (4%) patient. The HA(JR) was significantly shorter than the HA(SVT) (57 +/- 24 vs 68 +/- 21 ms, P < 0.01). In patients with slow-intermediate AV nodal reentrant tachycardia, the atrial activation sequence of the JR was similar to that of the retrograde fast pathway in 5 (45%), and to that of the retrograde intermediate pathway in 6 (55%) patients. Transient retrograde conduction block during JR was noted in 1 (9%) patient. The HA(JR) was also significantly shorter than the HA(SVT) (145 +/- 27 vs 168 +/- 29 ms, P = 0.014). In patients with fast-slow AV nodal reentrant tachycardia, retrograde conduction with block during JR was noted in 7 (100%) patients. The incidence of retrograde conduction block during JR was higher in fast-slow AV nodal reentrant tachycardia than slow-fast (7/7 vs 1/11, P < 0.01) and slow-intermediate AV nodal reentrant tachycardia (7/7 vs 1/27, P < 0.01). CONCLUSIONS: In patients with slow-fast and slow-intermediate AV nodal reentrant tachycardia, the JR during ablation of the slow pathway conducted to the atria through the fast or intermediate pathway. In patients with fast-slow AV nodal reentrant tachycardia, there was no retrograde conduction during JR. These findings suggested there were different characteristics of the JR during slow-pathway ablation of different types of AV nodal reentrant tachycardia.