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PubMed1986

A comprehensive model describing conduction through the atrioventricular node.

An algorithm which models conduction over two conduction pathways through the atrioventricular (AV) node has been derived and tested. Output from the node has been previously related to input, the coupling intervals of extrastimuli introduced during programmed atrial stimulation. An exponential model of conduction in a single pathway was used with the general form: A2 H2 = K1 + K2 exp (-A1 A2/K3) with K1, K2, K3 parameters The algorithm for identification of dual pathways minimised residual sums of squares from two such functions. Potential 'bifurcation' points were selected by significant deviation of the computed single curve of best fit. The algorithm was tested using data obtained during electrophysiology study. Three trials of programmed stimulation were performed in 15 patients after pacing at 100 bpm. Computations using the model suggested single and dual functions (and therefore pathways) respectively in 19 and 25 of 44 trials. An electrophysiologist independently examining the data usually agreed (83% of trials). As the reasons for discordance were minor the model was reasonably verified.

Adolescent↗
PubMedDate not supplied

Long-term follow-up of patients with P-R prolongation after catheter ablation of slow pathway for atrioventricular node re-entrant tachycardia.

BACKGROUND: Long-term impact of interval between P wave and R wave (P-R) prolongation on prognosis of patients with successful catheter ablation of slow atrioventricular nodal pathway was investigated. METHODS: Among 436 patients undergoing slow-pathway ablation for atrioventricular node re-entrant tachycardia (AVNRT), 17 (3.9%) experienced permanent P-R prolongation. Ablation target sites where conduction block was induced were located in mid- or anteroseptum. Fast junctional rhythm with ventriculoatrial conduction block was observed in eight patients immediately before atrioventricular block. RESULTS: Antegrade slow-pathway conduction was eliminated in 16 patients, and retrograde fast- and slow-pathway conduction was abolished in all patients. There was no recurrence of AVNRT after an average of 38 +/- 12 month follow-up. There was no deterioration of atrioventricular block in these patients. Average PR interval prior to hospital discharge and at the end of follow-up was 0.24 +/- 0.02 sec and 0.23 +/- 0.02 sec, respectively (p >0.05). Left ventricular ejection fraction remained unchanged in these patients (p >0.05). CONCLUSIONS: Radiofrequency catheter ablation of slow pathway for AVNRT is associated with a small risk of atrioventricular block. PR prolongation after successful slow-pathway ablation is associated with benign prognosis.

Adult↗
PubMed1987

Electrophysiologic effects of nicorandil, a new antianginal agent, on action potentials and membrane currents of rabbit atrioventricular node.

Electrophysiologic effects of nicorandil, a newly developed coronary vasodilator, on the atrioventricular (AV) node were studied using space-clamped small preparations of the rabbit AV node. At the concentrations of 10(-6), 10(-5) and 10(-4) mol/l, this drug did not cause significant changes in the action potential characteristics including the spontaneous firing frequency, overshoot, maximum diastolic potential, maximum rate of depolarization and action potential duration. When the resting membrane potential of the AV node was obtained by a superfusion with verapamil and then nicorandil was added to the perfusate, no hyperpolarization was observed. This was in sharp contrast to the reported hyperpolarizing action of this drug on the atrial muscle, Purkinje fibres and vascular smooth muscle where the resting potential is much more negative. On the other hand, voltage clamp experiments using double microelectrode techniques revealed that 10(-5) to 10(-4) mol/l nicorandil increased the steady-state outward current at potentials positive to -40 mV and the steady-state inward current at potentials negative to -40 mV. Such a nicorandil-sensitive component of the steady-state current had an average reversal potential of -41.8 mV (n = 5). This component was considered to reflect changes in the time-independent background current, although, at more negative potential levels, it may partially reflect an increase in the hyperpolarization activated inward current (ih). Nicorandil, at the concentrations of 10(-5) and 10(-4) mol/l, increased the slow inward current (isi) by 10.8% (n = 5, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed2001

Clinical study on the treatment of 325 cases of atrioventricular node reentrant tachycardia by radiofrequency catheter ablation.

In order to improve the efficacy of modified inferior method or middle method of radiofrequency catheter ablation (RFCA) in the treatment of atrioventricular node reentrant tachycardia (AVNRT), the clinical data of 325 cases of AVNRT from March 1992 to Feb. 2000 being subjected to the treatment of RFCA were retrospectively analyzed. The results showed that the successful rate was increased and recurrence was decreased year by year. In the recent 4 years the effective rate was up to 100%. The complication of three grade of AVB occurred in 3% and recurrent rate in 9.1% before March 1996, but both of them were zero in the last 3 years. The time of RFCA procedure and X-ray exposure was significantly reduced. It was concluded that ablating more than 3 targets by modified inferior method or middle method with energy titrating and strict endpoint was the crux of obtaining satisfactory therapeutic effects and preventing recurrence.

Adolescent↗
PubMed1992

Evidence of spare A1-adenosine receptors in guinea pig atrioventricular node.

In normoxic, isolated perfused guinea pig hearts instrumented for measurement of atrioventricular nodal conduction time (AVCT), an analysis utilizing the irreversible A1-adenosine (Ado) antagonist, meta-1,3-phenylene diisothiocyanate xanthine amine cogener (m-DITC-XAC), a novel isothiocyanate derivative of 1,3-dialkylxanthine, was used to investigate whether spare A1-Ado receptors exist in the guinea pig atrioventricular (AV) node and the degree of amplification (reserve) between A1-Ado receptor occupancy and dromotropic response (e.g., AVCT slowing). The potency, dose dependency, and kinetic profile (time dependence of washout and washin) of m-DITC-XAC was determined and compared with those of known competitive (reversible) A1-Ado receptor antagonists. In the presence of m-DITC-XAC, Ado and N6-cyclopentyladenosine (CPA) produced submaximal dromotropic responses. In a series of 19 hearts, m-DITC-XAC caused 100% apparent antagonism of the effect of Ado on AVCT even after 60 min of washout. In contrast, greater than 90% of 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) and XAC-induced antagonism of the effect of Ado on AVCT dissipated within 35 min. Unlike XAC, which caused maximal attenuation of Ado's AVCT effect within 5 min and remained constant thereafter, m-DITC-XAC showed marked time- and concentration-dependent behavior. It was found that 5 min of 0.5 microM m-DITC-XAC pretreatment irreversibly inactivated 72% of the A1-Ado receptors mediating the dromotropic effect, and the estimated agonist equilibrium dissociation constant for CPA was 84 +/- 4 nM. The percent of spare A1-Ado receptors at the EC50 and extrapolated maximal S-H interval prolongation levels was 20 and 54%, respectively, and the reserve (coupling amplification) varied from 1 to 2.3 within the 0-50% maximal response range. In summary, m-DITC-XAC appears to specifically and irreversibly antagonize the negative dromotropic effect of Ado and CPA, and guinea pig AV nodal tissue possesses spare A1-Ado receptors.

Adenosine↗
PubMed2006

Long-term outcome of patients with atrioventricular node reentrant tachycardia.

BACKGROUND: Little information is available on the natural history of patients with AVNRT. The purpose of this study was to compare the outcome of patients with Atrioventricular node reentrant tachycardia (AVNRT) who underwent ablation with those on antiarrhythmic therapy and those not receiving drugs. METHODS: 93 consecutive patients (mean age=33.5+/-18.1 years) with AVNRT referred to our institution from 1988 to 1993 were prospectively followed-up for a mean of 13.2+/-2.0 years (range=11.4-16.1 years). RESULTS: 18 patients underwent ablation (group 1), 24 received antiarrhythmic therapy (group 2), 38 received no drugs or remained on drug therapy for only few months (group 3), 3 died and 10 were lost to follow-up. The frequency of symptoms at the baseline was higher in group 1 than in groups 2 and 3 (7.8+/-3.7, 3.5+/-2.3, 2.3+/-1.9 episodes/month, respectively; p<0.02 in group 1 vs. group 3). At the end of the follow-up 18/18 (100%) of group 1, 14/23 (61%) of group 2 and 17/38 of group 3 (44.7%) reported being asymptomatic for the previous 3 years. Group 3 patients who became asymptomatic had a shorter duration of symptoms before enrolment (3.7+/-1.5 vs. 7.1+/-3.6 years, p<0.05) and a shorter mean length of the tachycardia episodes (3.8+/-2.4 vs. 42.6+/-17.8 min, p<0.02) than patients from the same group who remained symptomatic. CONCLUSIONS: The main result of this study is that during a long-term follow-up a considerable number of untreated patients with AVNRT become asymptomatic. This finding should be considered for choosing treatment modality and for calculating healthcare costs of ablation vs. medical therapy.

Adolescent↗
PubMed2002

Is electrical stimulation during administration of catecholamines required for the evaluation of success after ablation of atrioventricular node re-entrant tachycardias?

OBJECTIVES: The purpose of this study was to answer the question of whether stimulation after administration of catecholamines is mandatory for identifying unsuccessful ablations of atrioventricular node re-entrant tachycardia (AVNRT). BACKGROUND: The success of radiofrequency (RF) catheter ablation in AVNRT is confirmed in many centers by noninducibility of tachycardias during stimulation after the administration of catecholamines. METHODS: A total of 131 patients (81 women and 50 men; mean age 53.6 +/- 13.7 years [range 20 to 77]) were studied. Electrical stimulation was performed without and with the beta-adrenergic amine Orciprenaline (metaproterenol) before and after RF catheter ablation. RESULTS: In 100 patients (76.3%; confidence interval [CI] 68.1% to 83.3%) an AVNRT was inducible without administration of Orciprenaline. Thirty minutes after the initially successful ablation in 95 patients, tachycardia was inducible in none of these patients, not even after Orciprenaline administration. In the 31 patients (23.7%; CI 16.7% to 31.9%) in whom there was no tachycardia inducible before ablation, Orciprenaline was given, and the stimulation protocol was repeated. In only five patients (3.8%; CI 1.3% to 8.7%) was there still no tachycardia inducible. After an initially successful ablation in the 26 patients who had inducible tachycardias with Orciprenaline before ablation, no tachycardia could be re-induced. After Orciprenaline, the tachycardia was inducible again in only one patient. CONCLUSIONS: Only patients who require catecholamines for tachycardia induction before ablation need catecholamines for control of the success of the ablation of AVNRT.

Adrenergic beta-Agonists↗
PubMed1987

Transient entrainment and interruption of atrioventricular node tachycardia.

The possibility of transiently entraining and interrupting the common type of atrioventricular (AV) node tachycardia (anterograde slow, retrograde fast AV node pathway) was studied using atrial and ventricular pacing in 18 patients with paroxysmal AV node tachycardia. Transient entrainment occurred in all patients. During atrial pacing, localized block in the AV node for one beat followed by anterograde conduction over the fast pathway was observed in three patients. During ventricular pacing, localized block for one beat followed by retrograde conduction over the slow pathway was not observed in any patient. Neither atrial nor ventricular fusion beats were observed during entrainment. These observations indicate in a way not previously shown that reentry involving two functionally dissociated pathways in the AV node is the underlying mechanism of paroxysmal AV node tachycardia. The inability to demonstrate atrial or ventricular fusion beats during entrainment suggests a true intranodal location of the reentrant circuit. Finally, the ability to transiently entrain intranodal tachycardia demonstrates that this electrophysiologic phenomenon is not exclusively limited to macroreentrant circuits.

Adult↗
PubMed1993

Experimentally created atrioventricular node reentrant tachycardia in the dog: evidence of a brake system for nodal reentry in the anterior interatrial septum.

OBJECTIVES: The purpose of the study was to investigate the hypothesis that nodal approaches of both anterior and posterior atrial input sites of the atrioventricular (AV) node contribute to part of the circuit of AV node reentrant tachycardia. Thus, tachycardia might be elicited by a premature atrial impulse that arrived at the AV node through one input site while blocked at another. BACKGROUND: Atrioventricular node reentrant tachycardia is the most common supraventricular tachycardia in humans, yet the exact pathway of the reentrant circuit is unknown. METHODS: In eight dogs, an operation that blocked atrial impulses from the anterior input site to the AV node was performed through a right thoracotomy with the inflow occlusion method. The right atrial free wall and the anterior atrial septum between the sinoatrial node and the AV node were completely divided, whereas the tissues within the triangle of Koch remained intact. Thus, atrial impulses were blocked from the anterior input site in the right atrium and the atrial septum and were conducted only through the left atrial free wall to the posterior atrial septum into the AV node. RESULTS: In a baseline electrophysiologic study before operation, dual AV conduction pathways were demonstrated in seven of eight dogs, but none of the seven had inducible AV node reentrant tachycardia. A repeat study 1 week postoperatively revealed that 1) both PR and AH intervals were prolonged during sinus rhythm (p < 0.01); 2) anterograde and retrograde conduction of the AV node showed no significant changes; and 3) AV node reentrant tachycardia was induced in four dogs (50%), of which three had sustained tachycardia. CONCLUSIONS: These results are compatible with the hypothesis that both nodal approaches of atrial input sites of the AV node contribute to part of the circuit of AV node reentrant tachycardia. They also confirm Moe's hypothesis of the existence of a brake system that prevents sustained AV node reentry. Our data suggest that the brake system is located in the anterior atrial septum.

Animals↗
PubMed2002

Atrial activation sequence during junctional tachycardia induced by thermal stimulation of Koch's triangle in canine blood-perfused atrioventricular node preparation.

Junctional tachycardia is observed during radiofrequency ablation of the slow pathway. The authors investigated the atrial activation sequence during junctional tachycardia induced with thermal stimulation in canine blood-perfused atrioventricular node (AVN) preparation. The canine heart was isolated (n = 7) and cross-circulated with heparinized arterial blood of the support dog. The activation sequence in the region of Koch's triangle (15 x 21 mm) was determined byrecording 48 unipolar electrograms. Atrial sites anterior to the coronary sinus ostium (site AN), close to the His-potential recording site (site N) and superior to site N (site F), were subjected to a continuous temperature rise from 38 degrees C to 50 degrees C with a heating probe. The temperature of the tissue adjacent to the heating site was monitored simultaneously. Junctional tachycardia at a rate of 92+/-12 beats/min with the His potential preceding the atrial one in the His-bundle electrogram was induced during thermal stimulation at site AN (temperature 42.1 degrees C+/-0.9 degrees C) in all seven preparations, whereas junctional tachycardia was induced during stimulation at site N in one and at site F in none. In each case, the temperature rose only at the site of stimulation. The earliest activation site during junctional tachycardia induced by site AN stimulation was at the His-potential recording site in five preparations and the middle of Koch's triangle in the other two. After creating an obstacle between sites AN and N, atrial tachycardia at a rate of 85+/-11 beats/min was induced during site AN stimulation. The earliest activation site during this tachycardia was site AN. Thus, junctional tachycardia induced by thermal stimulation was suggested to originate from the AN thermal stimulation site. The impulse from the stimulation site appeared to conduct via the posterior input to the compact AVN and junctional tachycardia was generated. When the posterior input was interrupted, atrial tachycardia was generated.

Animals↗
PubMed2000

Inhibition by agmatine on spontaneous activity of rabbit atrioventricular node cells.

AIM: To study the effects of agmatine on spontaneous activity of atrioventricular (AV) node and its action mechanisms. METHODS: Action potentials in AV node cells were recorded using intracellular microelectrode technique. RESULTS: Agmatine not only reduced the amplitude of action potential (APA), maximal rate of depolarization (Vmax), velocity of diastolic (phase 4) depolarization (VDD), and rate of spontaneous firing (RSF), but also prolonged 90% duration of action potential (APD90) in a concentration-dependent manner. The effects of agmatine (10 mmol/L) could be blocked completely by pretreatment with idazoxan (0.1 mmol/L), an imidazoline receptor (IR) and alpha 2-adrenergic receptor (alpha 2-AR) antagonist. Pretreatment with NG-nitro-L-arginine methyl ester (L-NAME, 0.5 mmol/L), a nitric oxide (NO) synthase inhibitor, did not affect the effects of agmatine on AV node cells. Elevation of Ca2+ concentration (5 mmol/L) in perfusate antagonized the effects of agmatine (10 mmol/L). Lemakalim (30 mumol/L), an ATP-sensitive potassium channel opener, inhibited the prolonging effects of agmatine on repolarization. CONCLUSION: The inhibitory effects of agmatine on spontaneous activity of AV node cells in rabbits were likely mediated by IR and/or alpha 2-AR, and were related to the reduction in calcium influx and potassium efflux.

Action Potentials↗
PubMed1992

Transcatheter modification of the atrioventricular node using radiofrequency energy.

120 consecutive patients with symptomatic atrioventricular nodal reentrant tachycardia (AVNRT) underwent catheter ablation using radiofrequency energy. Fast pathway ablation was attempted in the first 16 consecutive patients by application of radiofrequency current in the anterior and superior aspect of the tricuspid annulus. Successful results were accomplished in 13 patients, complete AV block occurred in three. The other 104 patients initially underwent ablation of the slow pathway in the posterior and inferior aspects of the tricuspid annulus which was successful in 98 patients. The remaining six patients subsequently underwent a fast pathway ablation with successful results in four and AV block in two. Therefore, 102 (98%) of the last 104 patients became free of AVNRT while maintaining intact AV conduction. This study demonstrates that both AV nodal conduction pathways can be selectively ablated. However, slow pathway ablation seems safer and should be considered as the first approach.

Atrioventricular Node↗
PubMed1993

A simple technique for selective radiofrequency ablation of the slow pathway in atrioventricular node reentrant tachycardia.

OBJECTIVES: A simple technique was designed for radiofrequency ablation therapy of atrioventricular (AV) node reentrant tachycardia. BACKGROUND: This technique was based on the hypothesis that slow pathway conduction reflects conduction through the compact node and its posterior atrial input. METHODS: A total of 100 consecutive patients were studied; there were 37 men and 63 women, with a mean age of 48 +/- 15 years. All 100 patients had induction of sustained tachycardia with (51 patients) or without (49 patients) administration of isoproterenol or atropine, or both. The ablation catheter was initially manipulated to record the largest His bundle deflection from the apex of Koch's triangle. It was then curved downward and clockwise to the area of the compact node when His deflection was no longer visible and the ratio of atrial to ventricular electrogram was < 1. The radiofrequency current was delivered from the 4-mm tip electrode a mean of 5 +/- 7 times at a power of 25 +/- 4 W for a duration of 21 +/- 4 s. The total fluoroscopic time was 19 +/- 11 min. RESULTS: Selective ablation (56 patients) or modification (26 patients) of the slow pathway without affecting anterograde and retrograde fast pathway conduction was achieved in 82 patients. Ablation or modification of both the retrograde fast pathway and the slow pathway but with preservation of anterograde fast pathway conduction was noted in 12 patients. Ablation or modification of the retrograde fast pathway alone or both anterograde and retrograde fast pathway conduction was noted in three patients. Complete AV node block occurred in three patients. Seventy-three patients had no induction of echo beats or tachycardia and 24 patients had induction of a single echo beat after ablation. Follow-up study was performed in 62 patients 76 +/- 18 days after ablation. Thirty-nine patients had no induction of echo beats or tachycardia, 22 had induction of echo beats alone and 1 patient had induction of sustained tachycardia. CONCLUSION: Selective ablation of the slow AV node pathway can be achieved by a simple procedure with a high success rate and few complications.

Adolescent↗
PubMed1995

Anatomic substrate of the experimentally-created atrioventricular node re-entrant tachycardia in the dog.

Despite major success in the treatment of atrioventricular (AV) node reentrant tachycardia using either catheter ablation or surgery, the morphologic basis underlying AV node reentry is not yet clear. A canine model of AV node reentrant tachycardia was used to examine the histologic features of the reentry circuit. AV node reentrant tachycardia was created in 4 of 8 dogs by a right atrial division which divided the right atrial free wall and the atrial septum into upper and lower portions on a plane between the mid-right atrial free wall and the fossa ovalis. The AV junctional area of all dogs were serially sectioned on a plane that was perpendicular to the AV annulus and the septum. The slices were stained with Masson's trichrome technique. The connections between atrial fibers and the compact AV node and the common AV bundle were examined, and comparison of the histologic features between dogs with and without AV nodal re-entry was made. The histologic examinations showed that, in all dogs, the operation scar was remote from the AV junctional area leaving the Koch's triangle intact. The compact node received its atrial inputs mainly from the anterosuperior and posterior aspects of the Koch's triangle. However, both atrial inputs gave off superficial (subendocardial) fibers that by-passed the compact node to terminate at the base of tricuspid valve. These superficial fibers might function as the proximal link between the dual AV nodal inputs by means of lateral connections. There was no bypass connection between atrial fibers and the common AV bundle. The histologic features of the AV junctional area was not different between dogs with and without AV nodal reentry. In conclusion, AV nodal reentry involves the anterior and posterior atrio-nodal inputs which function as dual AV nodal pathways, and the superficial bypass fibers form the proximal linkage between the two inputs. These structures, together with the compact node, complete the reentry circuit.

Animals↗
PubMed2004

Electrophysiological effects of capsaicin on spontaneous activity of rabbit atrioventricular node cells.

To study the electrophysiological effects of capsaicin on spontaneous activity of rabbit atrioventricular (AV) node cells, parameters of action potential in AV node were recorded using intracellular microelectrode technique. Capsaicin (1-30 micromol/L) not only decreased the amplitude of action potential, maximal rate of depolarization (V(max)), velocity of diastolic (phase 4) depolarization, and rate of pacemaker firing, but also prolonged the duration of 90% repolarization of action potential (APD(90)) in a concentration-dependent manner. Both application of L-type Ca(2+) channel agonist Bay K8644 (0.5 micromol/L) and elevation of calcium concentration (5 mmol/L) in superfusate antagonized the effects of capsaicin on pacemaker cells. Pretreatment with ruthenium red (10 micromol/L), a capsaicin receptor blocker, did not affect the effects of capsaicin on AV node cells. Capsaicin exerted an inhibitory action on spontaneous activity of AV node cells in rabbits. These effects were likely due to reduction in calcium influx, but were not mediated by VR1.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗