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PubMed2001

Ablation of atrial tachycardia originating from the vicinity of the atrioventricular node: significance of mapping both sides of the interatrial septum.

OBJECTIVES: The purpose of the study was to examine the value of right- and left-sided mapping to identify the site of tachycardia origin. BACKGROUND: Focal atrial tachycardia may originate from the vicinity of the atrioventricular node from either side of the interatrial septum. METHODS: In 16 patients undergoing radiofrequency catheter ablation of perinodal atrial tachycardia, activation mapping of the right and left side of the interatrial septum was performed. RESULTS: Atrial tachycardia originated from the right side of the interatrial septum in 10 patients (group A) and from the left side in 6 patients (group B). On the right side, earliest atrial activity preceded the onset of the P-wave by 49 +/- 15 ms in group A and by 38 +/- 8 ms in group B (NS), and it preceded the signal recorded from the right atrial appendage by 59 +/- 19 ms in group A and by 60 +/- 13 ms in group B (NS). On the left side, earliest activity preceded the onset of the P-wave by 27 +/- 16 ms in group A and by 51 +/- 6 ms in group B (<0.01), and it preceded the signal obtained from the right atrial appendage by 38 +/- 19 ms in group A and by 73 +/- 9 ms in group B (<0.01). Atrial tachycardias were successfully eliminated in all patients without impairment of atrioventricular conduction. During follow-up, two patients had a recurrence of tachycardia. CONCLUSIONS: Mapping of only the right side cannot exclude a left-sided origin. Therefore, mapping of both sides of the interatrial septum is required prior to ablation of focal atrial tachycardia originating from the vicinity of the atrioventricular node.

Adult↗
PubMed2006

Localization of Na+ channel isoforms at the atrioventricular junction and atrioventricular node in the rat.

BACKGROUND: The electrical activity of the atrioventricular node (AVN) is functionally heterogeneous, but how this relates to distinct cell types and the 3-dimensional structure of the AVN is unknown. To address this, we have studied the expression of Na(V)1.5 and other Na+ channel isoforms in the AVN. METHODS AND RESULTS: The rat AVN was identified by Masson's trichrome staining together with immunolabeling of marker proteins: connexin40, connexin43, desmoplakin, atrial natriuretic peptide, and hyperpolarization-activated and cyclic nucleotide-gated channel 4. Na+ channel expression was investigated with immunohistochemistry with isoform-specific Na+ channel antibodies. Na(V)1.1 was distributed in a similar manner to Na(V)1.5. Na(V)1.2 was not detected. Na(V)1.3 labeling was present in nerve fibers and cell bodies (but not myocytes) and was abundant in the penetrating atrioventricular (AV) bundle and the common bundle but was much less abundant in other regions. Na(V)1.5 labeling was abundant in the atrial and ventricular myocardium and the left bundle branch. Na(V)1.5 labeling was absent in the open node, penetrating AV bundle, AV ring bundle, and common bundle but present at a reduced level in the inferior nodal extension and transitional zone. Na(V)1.6 was not detected. CONCLUSIONS: Our findings provide molecular evidence of multiple electrophysiological cell types at the AV junction. Impaired AV conduction as a result of mutations in or loss of Na(V)1.5 must be the result of impaired conduction in the AVN inputs (inferior nodal extension and transitional zone) or output (bundle branches) rather than the AVN itself (open node and penetrating AV bundle).

Animals↗
PubMed1990

Autonomic modulation of the frequency-dependent actions of diltiazem on the atrioventricular node in anesthetized dogs.

Calcium antagonists have rate-dependent effects on atrioventricular node refractoriness in autonomically blocked dogs. Autonomic reflexes can attenuate diltiazem's actions and could alter their frequency-dependence. We evaluated the effects of four steady-state drug concentrations in each of seven dogs with intact autonomic tone, six with muscarinic blockade (atropine) and eight with combined muscarinic and beta adrenergic blockade. Diltiazem depressed atrioventricular nodal function less in autonomically intact dogs than in the other two groups. The concentration-response relationship for increases in Wenckebach cycle length (compared to intact dogs) was twice as steep among dogs with muscarinic blockade (P less than .001) and three times as steep with combined blockade (P less than .001). For an equal dose of diltiazem, the slope of drug-induced refractory period prolongation vs. pacing cycle length was similar (-0.20 +/- 0.11%/msec, mean +/- S.D.) in intact dogs compared to atropinized dogs (-0.21 +/- 0.10%/msec) and dogs with combined blockade (-0.24 +/- 0.14%/msec). Amplification of diltiazem's actions by the rapid atrial rate during atrial fibrillation was associated with increases in mean RR interval which were 8.3 times as large as changes in refractory period produced by the drug at slow heart rates. We conclude: 1) autonomic reflexes reduce diltiazem's effect for any given plasma concentration; 2) changes in vagal tone can play an important role in the autonomic response to diltiazem; and 3) despite altering the magnitude of diltiazem's effects, autonomic mechanisms do not prevent frequency-dependent drug action.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1989

Ionic mechanisms of the depression of automaticity and conduction in the rabbit atrioventricular node caused by hypoxia or metabolic inhibition and protective action of glucose and valine.

The effects of hypoxia and a metabolic inhibitor, sodium cyanide (NaCN), on the spontaneous action potential and membrane current systems were studied in small preparations (0.2 x 0.2 x 0.1 mm) of rabbit atrioventricular node. When the PO2 of the superfusate was lowered from 500 to less than 20 mm Hg, all the preparations initially showed reductions in the spontaneous firing frequency (due to the decreased rate of diastolic depolarization) and maximal rate of depolarization, which were followed by a cessation of automatic activity with subsequent membrane hyperpolarization to -57 +/- 3 mV (n = 4). Voltage clamp experiments using double microelectrode techniques revealed that hypoxia reduced the slow inward current by 20 to 80% without affecting its inactivation kinetics. The delayed rectifying potassium current tail was also reduced or abolished by severe hypoxia, whereas the background outward current was greatly increased. The hyperpolarization-activated inward current was decreased by hypoxia. Similar changes in the spontaneous action potential and membrane currents were obtained on adding 0.1 to 0.5 mM NaCN to the superfusate under conditions of normal PO2. Hypoxia-induced suppression of automaticity was reversed completely by 5 mM glucose, and partially by 40 mM valine. These results suggest that (1) hypoxia impairs atrioventricular nodal conduction by reducing the slow inward current and the delayed rectifying potassium current; (2) hypoxia depresses automaticity by increasing the background outward current and, to some extent, by reducing the slow inward current; and (3) glucose and valine contribute to the generation of high-energy phosphates in cytoplasm and mitochondria, respectively, and protect the atrioventricular node from hypoxia.

Action Potentials↗
PubMed1988

Cryosurgical modification of atrioventricular conduction for treatment of atrioventricular node reentrant tachycardia.

Cryosurgical modification of atrioventricular (AV) node conduction was performed in five patients with AV node reentrant tachycardia that used dual AV nodal pathways and was refractory to drug therapy. The procedure alleviated the tachycardia in all patients without the development of complete heart block and without any associated surgical morbidity or mortality. These results suggest that cryosurgical modification of AV node conduction is a promising and potentially curative method of treating AV node reentrant tachycardia.

Adolescent↗
PubMed1990

[Effects of 2-[p-(dimethylamino)styryl] pyridine methiodide on conduction and refractory period of atrioventricular node in rat].

The effects of 2-[p-(dimethylamino)styryl] pyridine methiodide (DSPM) on rat ECG and HBE were studied. The P-R and R-R intervals of ECG were lengthened 40.3% and 115.4% respectively, after iv injection of DSPM 2 mg/kg. DSPM (1.5 and 2 mg/kg) affected the A-H interval in a dose-dependent manner with no change in the H-V interval of HBE. DSPM 0.5 mumol/L lengthened the A-H interval of isolated perfused hearts in frequency-dependent manner, with greater prolongation at higher frequency. The effect of verapamil on the A-H interval was less than that of DSPM. Propranolol had no effect on the frequency-dependent delay of atrioventricular node. DSPM 0.5 mumol/L lengthened the functional and effective refractory periods of atrioventricular node by 26.8% and 31% respectively. These phenomena support that DSPM may be a calcium antagonist.

Animals↗
PubMed1995

[Refractory periods of cardiac tissues and the filtering properties of the atrioventricular node in the isolated rabbit heart].

It is generally believed that the atrioventricular node (AVN) possesses filtering properties (FP) capable of preventing excess atrial impulses or earlier atrial premature beat from reaching the ventricle. In the present study, the refractory periods (RP) of cardiac tissues and the FP of the AVN were investigated in isolated rabbit hearts (n = 18). It was found that: (1) The relative RP of AVN was the longest at shorter basic cycle lengths (BCL) (200-300 ms) while the relative RP of His-Purkinje system (HPS) was the longest at longer BCL (600, 700 ms). (2) The effective RP of AVN was shorter than the functional RP of the atrium in most cases (16/18) at any BCL. (3) During rapid atrial pacing at cycle length of 140 ms in 7 cases, AVN maintained 1:1 conduction. (4) The atrioventricular nodal conduction curve was smooth at BCL from 200 to 700 ms. The present results suggest that AVN in the isolated perfused rabbit heart do not have the FP and any dual atrioventricular pathways in a physiological sense.

Animals↗
PubMed2002

Pharmacological and electrophysiological characterization of junctional rhythm during radiofrequency catheter ablation of the atrioventricular node: possible involvement of neurotransmitters from autonomic nervous system.

Catheter ablation of the atrioventricular node (AVN) with radiofrequency current is closely associated with the short-term onset of a junctional rhythm. The origin of this rhythm was analyzed in Beagle dogs which were anesthetized with pentobarbital sodium. Atrioventricular (AV) conduction block was induced first using a standard catheter ablation technique for the AVN, so that the sinus automaticity could not override the junctional ectopy during the following energy delivery. The ablation catheter was kept in the initial position and the delivery of radiofrequency energy was repeated. The pattern of ECG changes suggests that the dominant pacemaker may shift from the distal portion of the AV junctional area to the proximal portion during the energy delivery. This enhanced junctional automaticity was suppressed by the beta-blocker esmolol, but was not affected by M-antagonist atropine. Moreover, the beta-agonist isoproterenol did not induce the same type of junctional tachycardia, but the pacemaker shift was induced by the increased sympathetic tone after transient asystole by ventricular overdrive pacing or acetylcholine administration. These results suggest that proximal portion of the AV junctional area has extremely slow pacemaker activity, but responds to locally released norepinephrine with an abrupt rise and fall in rate, resulting in a typical pattern of junctional tachycardia during the ablation of the AVN.

Acetylcholine↗
PubMed1998

Predictors of atrial rhythm after atrioventricular node ablation for the treatment of paroxysmal atrial arrhythmias.

OBJECTIVE: To assess the natural history of the atrial rhythm of patients with paroxysmal atrial arrhythmias undergoing atrioventricular node ablation and permanent pacemaker implantation. DESIGN AND SETTING: A retrospective cohort study of consecutive patients identified from the pacemaker database and electrophysiology records of a tertiary referral hospital. PATIENTS: 62 consecutive patients with paroxysmal atrial arrhythmias undergoing atrioventricular node ablation and permanent pacemaker implantation between 1988 and July 1996. MAIN OUTCOME MEASURES: (1) Atrial rhythm on final follow up ECG, classified as either ordered (sinus rhythm or atrial pacing) or disordered (atrial fibrillation, atrial flutter or atrial tachycardia). (2) Chronic atrial fibrillation, defined as a disordered rhythm on two consecutive ECGs (or throughout a 24 hour Holter recording) with no ordered rhythm subsequently documented. RESULTS: Survival analysis showed that 75% of patients progressed to chronic atrial fibrillation by 2584 days (86 months). On multiple logistic regression analysis a history of electrical cardioversion, increasing patient age, and VVI pacing were associated with the development of chronic atrial fibrillation. A history of electrical cardioversion and increasing patient age were associated with a disordered atrial rhythm on the final follow up ECG. CONCLUSIONS: Patients with paroxysmal atrial arrhythmias are at high risk of developing chronic atrial fibrillation. A history of direct current cardioversion.

Age Factors↗
PubMed1997

Subthreshold stimulation in the region of the slow pathway during atrioventricular node reentrant tachycardia: correlation with effect of radiofrequency catheter ablation.

OBJECTIVES: The present study sought to investigate the role of subthreshold stimulation in patients with atrioventricular node reentrant tachycardia (AVNRT) undergoing catheter ablation of the slow pathway. BACKGROUND: Subthreshold stimulation applied to right atrial sites has been demonstrated to terminate AVNRT but has not been correlated with the effects of radiofrequency current delivery to the area of the slow pathway. METHODS: Eighteen patients with common AVNRT were prospectively included in the study. Sustained AVNRT was reproducibly inducible in all patients (cycle length 334 +/- 58 ms). Anatomic and electrogram guided mapping of the slow pathway was started posteroseptally and continued to more midseptal sites if required. Subthreshold stimulation (3 s, up to 5 mA) during induced AVNRT was performed at each site eligible for slow pathway ablation until termination of AVNRT or capture was observed. Irrespective of the effect of subthreshold stimulation, radiofrequency current was delivered at each site after exclusion of catheter dislocation. RESULTS: Termination of AVNRT due to block of the anterograde slow pathway induced by subthreshold stimulation occurred without apparent capture in 15 of 18 patients. This phenomenon was exclusively observed at successful posteroseptal to midseptal ablation sites. Subthreshold stimulation was not successful at any of 30 target sites with ineffective radiofrequency current delivery. Thus, subthreshold stimulation identified successful target sites with 83% sensitivity and 100% specificity. Atrioventricular node reentrant tachycardia was abolished in all patients after a median of two (range one to nine) radiofrequency current applications. CONCLUSIONS: Subthreshold stimulation delivered to the region of the slow pathway terminates AVNRT with high safety and efficacy. High sensitivity and specificity for prediction of the effect of radiofrequency current application suggest that subthreshold stimulation may become a new tool for identifying target sites for slow pathway ablation.

Adult↗
PubMed1995

[Junctional arrhythmias in radiofrequency modification of the atrioventricular node].

UNLABELLED: Accelerated junctional rhythm (JR) is known as a response of the atrioventricular node to thermal injury and a common finding in radiofrequency ablation for AV node reentrant tachycardia. We studied JR during 1314 radiofrequency current deliveries in 172 patients with AV node reentrant tachycardia or paroxysmal atrial fibrillation in relation to the ablation result. JR in a successful RF delivery were characterized by cycle length and conduction. RESULTS: Selective slow pathway ablation was performed in 100 patients (Group A), selective fast pathway ablation in 41 patients (Group B), and total AV junction ablation in 31 patients (Group C). A successful radio-frequency ablation without JR was rare (sensitivity: 98.8%; specificity: 51.2%). JR during slow pathway ablation had a longer cycle length (X +/- SD; CL: 494 +/- 138 ms) and a lower cycle length dispersion (delta CL: 178 +/- 199 ms) than JR during fast pathway ablation (CL: 399 +/- 108 ms; delta CL: 345 +/- 145 ms) or before total AV block (CL: 439 +/- 163 ms; delta CL: 338 +/- 195 ms). JR with bundle branch block aberration or ventriculoatrial block were more often found in group B and group C than in group A (BBB: 29% vs. 23% vs. 12%; VA-Block: 80% vs. 82% vs. 33%). Group B and group C did not differ significantly. CONCLUSION: JR leading to fast pathway ablation or heralding total AV block are characterized by a short cycle length, wide cycle length dispersion, and predominantly present ventriculoatrial block. Thus, JR is a useful marker to prevent inadvertent AV block in slow pathway ablation.

Adult↗
PubMed1977

Positive dromotropic effect of dibutyryl cyclic adenosine 3',5'-monophosphate on the atrioventricular node.

The effect of atrioventricular (A-V) conduction of N6-2'-0-dibutyryl cyclic 3',5'-adenosine monophosphate (dibutyryl cyclic AMP) was investigated in comparison with those of norepinephrine, cyclic 3',5'-adenosine monophosphate (cyclic AMP), adenosine-5'-monophosphate (5'-AMP), and adenosine by the use of the isolated, blood-perfused A-V node preparation of the dog. Single injections of dibutyryl cyclic AMP (3-300 micronmol) and norepinephrine (0.1-1 nmol) into the posterior septal artery of the preparation (the upper part of the A-V node is mainly perfused through this artery) produced a dose-dependent decrease in the A-V conduction time. The time to the peak effect and the duration of the effect of dibutyryl cyclic AMP were much longer than with norepinephrine. The positive dromotropic effect of dibutyryl cyclic AMP was resistant to the beta-adrenoceptor blocking action of propranolol. Unlike dibutyryl cyclic AMP, cyclic AMP (above 30 nmol), 5'-AMP and adenosine (above 1 nmol) injected into the posterior septal artery prolonged the A-V conduction time in a dose-dependent manner. The results indicate that dibutyryl cyclic AMP has a mode of action on A-V nodal cells which differs distinctly from that of either norepinephrine or cyclic AMP, 5'-AMP, and adenosine.

Adenosine↗
PubMed1989

[Topographical anatomy of the atrioventricular node of Tawara--findings by macro-microscopic dissection under dissecting microscope].

The atrioventricular node of Tawara was dissected macroscopically under dissecting microscope with scalpel and microforceps. The node is a flat and fan-shape mass of the specialized cardiac muscular tissue, which is sandwiched between the floor of the right atrium and the right fibrous trigone as an epi- or extra-myocardial structure, in the center of the heart as a whole. The node is situated in the apical (anterior) angle of the triangle of Koch, and does not show any individual variation in its location, occupying the same site topographically. Orifice of the coronary sinus is not proper to indicate the location of the node, because orifice of the coronary sinus changes its position individually. Clinically, the location of the node can be presumed correctly by identifying the important anatomical landmarks; postero-inferior angle of the membranous portion of the interventricular septum, commissure between the septal and the accessory (or anterior) cusps of the tricuspid valve, attachment line of the septal cusp, and the tendon of Todaro.

Adult↗
PubMed1990

Vagal modulation of the rate-dependent properties of the atrioventricular node.

Vagal effects on atrioventricular (AV) nodal conduction are accentuated by increases in heart rate. To establish the mechanism of these rate-dependent negative dromotropic actions, we studied the properties governing AV nodal adaptation to changes in heart rate in chloralose-anesthetized dogs in the absence and presence of bilateral cervical vagal nerve stimulation (20 Hz, 0.2 msec). Stimulation protocols were applied to evaluate the contributions of changes in AV nodal recovery, facilitation, and fatigue independently of each other. Vagal stimulation slowed AV nodal recovery in a voltage-dependent way, increasing the time constant of recovery (tau r) from 80 +/- 7 to 194 +/- 16 msec (mean +/- SEM, p less than 0.01) at the highest voltage studied. The facilitating effect of a premature (A2) beat was manifested by a leftward shift of the recovery curve (A3H3 versus H2A3) of a subsequent A3 beat. The magnitude of shift depended on the A1A2 coupling interval and was reduced by vagal stimulation at all A1A2 intervals (maximum shift: control, 63 +/- 12 msec; vagus, 24 +/- 11 msec; p less than 0.01). When recovery and facilitation were kept constant, abrupt increases in AV nodal activation rate caused a slow (tau = 75 beats) increase in AH interval (fatigue). Vagal stimulation increased the magnitude of this process (maximum: control, 11 +/- 2 msec; vagus, 27 +/- 3 msec; p less than 0.001), without altering its time course. At activation rates comparable to sinus rhythm in humans, vagal stimulation at an intermediate voltage increased the AH interval by 25 msec. As heart rate increased, vagally induced changes in dynamic processes amplified AH prolongation up to fivefold at maximum rate. The role of vagal changes in individual functional properties depended on heart rate, but slowing of recovery was the single most important factor, constituting over 50% of overall vagal action at rapid rates. We conclude that vagal stimulation alters the ways in which the AV node responds to changes in activation rate and that at rapid rates most of the negative dromotropic action of the vagus is due to changes in the AV nodal response to tachycardia. Alterations in rate-dependent AV nodal properties are a novel and potentially important mechanism through which interventions may affect AV nodal conduction.

Animals↗
PubMed1986

Effects of sympathetic tone on vagally induced phasic changes in heart rate and atrioventricular node conduction in the anesthetized dog.

We examined the effects of stellate ganglia stimulation on the phase-dependent chronotropic and dromotropic responses to brief vagal bursts in open-chest anesthetized dogs. Stellate stimulation affected the phasic vagal effects on heart rate by shortening the latent period, shifting the phase at which maximum decrease in heart rate occurred to earlier phases, and reducing the maximum decrease in heart rate. These effects were due primarily to an increase in the basic heart rate. No significant sympathetic-parasympathetic interaction occurred for heart rate, indicating that accentuated antagonism did not occur with brief vagal bursts. Stellate stimulation primarily decreased the amplitude of the phasic vagal effects on atrioventricular nodal conduction, regardless of the underlying heart rate, and a significant sympathetic-parasympathetic interaction was associated with this effect. The peak of the phase-dependent vagal effects on heart rate and atrioventricular nodal conduction were phase-shifted with one another. From these findings, we postulate the small changes in sympathetic tone might shift the predominant phase-dependent vagal effect from one on heart rate to one on atrioventricular nodal conduction. Furthermore, our results suggest that dynamic vagal control of heart rate and atrioventricular node conduction involves both phase-dependent and phase-independent factors. Sympathetic activity appears to affect only the phase-independent factor(s) in the control of heart rate, whereas it affects both phase-dependent and phase-independent factors in the control of atrioventricular node conduction.

Animals↗
PubMed1984

Retrograde concealed conduction in the atrioventricular node: differential manifestations related to level of intranodal penetration.

Although concealed conduction in the atrioventricular node (AVN) has been the focus of numerous experimental and clinical studies, little is known about the differential effects on AVN functional behavior of prior concealed retrograde impulse penetration alone vs prior anterograde or dual AVN activation. This study was undertaken specifically to investigate this aspect of human AVN physiology in patients without intact ventriculoatrial conduction to provide a model with which to analyze concealed retrograde AVN conduction. In 13 such patients AVN behavior during a subsequent anterograde input was characterized for each of three different manners of prior AVN activation: anterograde alone (method I), simultaneous anterograde and retrograde excitation (method II), or equivalently timed retrograde concealed AVN penetration alone (method III). In all patients evidence for retrograde AVN concealment was documented by longer anterograde conduction in the AVN during method III than that observed when the retrograde impulse was omitted (method IV). Furthermore, in these patients lacking intact ventriculoatrial conduction, anterograde conduction in the AVN was facilitated and refractoriness was decreased during dual excitation vs anterograde activation alone (method II vs method I). However, when each of methods I and II were compared with concealed retrograde AVN penetration alone (method III), two patterns of AVN responses were observed: In 11 of 13 patients (group A) conduction in the AVN was "worse" and refractoriness was greater both in methods I and II compared with method III; in the remaining two patients (group B) the opposite relationships were observed. The results suggest that among patients with no ventriculoatrial AVN conduction there exist at least two subpopulations whose AVN functional characteristics differ markedly when the effects of anterograde and dual excitation are compared with equivalently timed concealed retrograde activation alone. These findings may be related to differences in level of retrograde AVN concealment in groups A and B, which can be unmasked by the outlined pacing techniques.

Adult↗
PubMed1998

Structural characteristics of Koch's triangle in patients with atrioventricular node reentrant tachycardia.

The aim of this study is to investigate whether patients with atrioventricular node reentrant tachycardia (AVNRT) present different structural characteristics of Koch's triangle from patients with atrioventricular (AV) reentrant tachycardia and other control patients. Fifty-eight patients with arrhythmia or chest pain underwent selective coronary sinus angiography so that the diameter of the coronary sinus could be measured. The patients with arrhythmia also underwent electrophysiological study and measurement of the height of Koch's triangle. Patients with AVNRT had large coronary sinus ostial diameters compared with patients with AV reentrant tachycardia and those with chest pain (13.6 +/- 2.2 mm vs. 10.6 +/- 2.7 mm [p < 0.005] and 10.0 +/- 2.1 mm [p < 0.002], respectively), while there were no differences in distal diameter. The ostial diameter in patients with dual AV node pathways but noninducible AVNRT (11.8 +/- 1.5 mm) tended to be smaller than that in patients with AVNRT. No differences in the height of Koch's triangle and electrophysiological characteristics, including AV node properties, were found among the study groups. In conclusion, an increased size of the coronary sinus ostium (the base of Koch's triangle) is a structural characteristic in patients with AVNRT and may be the substrate needed for the appearance of AVNRT.

Adolescent↗