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PubMed2004

Electrophysiological effects of nitric oxide on spontaneous activity of rabbit atrioventricular node cells.

The electrophysiological effects of nitric oxide (NO) on spontaneous activity of rabbit atrioventricular (AV) node cells were examined using intracellular microelectrode technique. The results obtained are as follows. (1) NO donors sodium nitroprusside (SNP, 1~1000 micromol/L) and 3-morpholinosydnonimine (SIN-1, 100, 1000 micromol/L) decreased the amplitude of action potential (APA), rate of spontaneous firing (RSF), velocity of diastolic (phase 4) depolarization (VDD), and maximal rate of depolarization (V(max)) in a concentration-dependent manner. (2) Pretreatment with L-type calcium channel agonist Bay K8644 (0.25 micromol/L) completely reversed the effects of SNP (100 micromol/L) on AV node cells. (3) Elevation of Ca(2+) concentration (5 mmol/L) in superfusate antagonized the effects of SNP on AV node cells. (4) Perfusion with Ca(2+)-free K-H solution, completely abolished the effects of SNP on AV node cells. (5) Application of methylene blue (50 micromol/L), a guanylyl cyclase inhibitor, failed to abolish the inhibitory effects of SNP (100 micromol/L). All these results suggest that NO exerts a negative effect on spontaneous activity of AV node cells in rabbits. These effects are likely due to reduction in calcium influx via a cGMP-independent mechanism.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1989

An interindividual variability in the sensitivity of atrioventricular node to diltiazem in patients with paroxysmal supraventricular tachycardia.

To study the sensitivity of atrioventricular (AV) node to diltiazem in seven patients with paroxysmal supraventricular tachycardia (PSVT), we analyzed the plasma concentration-response relationship of this Ca-antagonist using AH interval as an index for assessing its Ca channel blocking effect on the AV node after an IV infusion (0.4 mg/kg). The postdose AH intervals were prolonged compared with the baseline, and their percentage changes correlated significantly (P less than 0.01) with log-diltiazem concentrations in all patients. However, drug concentrations associated with a 20% prolongation of AH interval differed considerably among the patients (range; 65 to 260 ng/ml), indicating a large interindividual variability in the sensitivity of AV node to diltiazem. These results suggest that the interindividual difference in the responsiveness of AV node to diltiazem-induced Ca channel blocking effect may be one of the possible explanations for the therapeutic failure of this Ca-antagonist for terminating PSVT or preventing its recurrences in certain patients.

Adult↗
PubMed2006

First postpacing interval after tachycardia entrainment with correction for atrioventricular node delay: a simple maneuver for differential diagnosis of atrioventricular nodal reentrant tachycardias versus orthodromic reciprocating tachycardias.

BACKGROUND: The difference between the first postpacing interval (PPI) after tachycardia entrainment from the right ventricular apex and the tachycardia cycle length (TCL) can be used as an index of proximity to the circuit. OBJECTIVES: The purpose of this study was to determine whether the response to entrainment of tachycardia during ventricular stimulation with correction for AV node delay is a useful, simple maneuver for differentiating AV nodal reentrant tachycardia (AVNRT) from orthodromic reciprocating tachycardia (ORT) using a concealed accessory pathway. METHODS: The study consisted of 193 consecutive patients who underwent electrophysiologic study and ablation of regular paroxysmal supraventricular tachycardia without preexcitation during sinus rhythm. Tachycardia entrainment was attempted through trains of 5 to 15 right ventricular apex pacing pulses. The increment in AV nodal conduction time in the first PPI was subtracted from the PPI-TCL difference (corrected PPI-TCL). RESULTS: Electrophysiologic study demonstrated ORT in 84 patients and AVNRT in 109 patients. Transient entrainment was achieved in all but 12 patients. The mean corrected PPI-TCL difference was significantly shorter in 77 patients with ORT (66 +/- 27 ms) than in 104 AVNRT patients (151 +/- 28 ms; P <.0001). Patients with septal accessory pathways had shorter corrected PPI-TCL differences than patients with free-wall accessory pathways. The presence of a corrected PPI-TCL difference <110 ms identified all but one patient with ORT, and no patients with AVNRT had such a difference. CONCLUSION: The return cycle after tachycardia entrainment by right ventricular apex stimulation with correction for AV node delay is a rapid, useful maneuver for differential diagnosis of AVNRT vs ORT in patients without preexcitation. The presence of a corrected PPI-TCL <110 ms accurately identified with high reliability those patients with ORT.

Adult↗
PubMed2001

Differentiation of atypical atrioventricular node re-entrant tachycardia from orthodromic reciprocating tachycardia using a septal accessory pathway by the response to ventricular pacing.

OBJECTIVES: The purpose of this study was to determine whether the response to ventricular pacing during tachycardia is useful for differentiating atypical atrioventricular node re-entrant tachycardia (AVNRT) from orthodromic reciprocating tachycardia (ORT) using a septal accessory pathway. BACKGROUND: Although it is usually possible to differentiate atypical AVNRT from ORT using a septal accessory pathway, a definitive diagnosis is occasionally elusive. METHODS: In 30 patients with atypical AVNRT and 44 patients with ORT using a septal accessory pathway, the right ventricle was paced at a cycle length 10 to 40 ms shorter than the tachycardia cycle length (TCL). The ventriculo-atrial (VA) interval and TCL were measured just before pacing. The interval between the last pacing stimulus and the last entrained atrial depolarization (stimulus-atrial [S-A] interval) and the post-pacing interval (PPI) at the right ventricular apex were measured on cessation of ventricular pacing. RESULTS: All 30 patients with atypical AVNRT and none of the 44 patients with ORT using a septal accessory pathway had an S-A-VA interval >85 ms and PPI-TCL >115 ms. CONCLUSIONS: The S-A-VA interval and PPI-TCL are useful in distinguishing atypical AVNRT from ORT using a septal accessory pathway.

Adult↗
PubMed1994

Catheter ablation of the atrioventricular node using radiofrequency energy.

BACKGROUND: Catheter ablation of the atrioventricular (AV) junction using stored direct current (DC) energy from a standard DC Cardioverter defibrillator was first reported in 1982. Since then many patients have been treated using this procedure for refractory supraventricular arrhythmias, usually atrial fibrillation and flutter. Undesirable thermal effects such as barotrauma and arcing are largely responsible for complications associated with the use of DC energy. This report details our experience of catheter ablation of the AV junction using radiofrequency (RF) energy in a series of 30 consecutive patients. METHODS: RF ablations were performed using steerable Mansfield (Webster Laboratories) 4 mm tipped electrodes and locally assembled RF energy delivery system. RESULTS: The procedure was successful in 27/30 (90%) patients using RF energy, while three patients required DC energy to achieve successful AV junction ablation. General anaesthesia was required in nine patients, six of whom required this for cardioversion to sinus rhythm so that an adequate His Bundle spike could be recorded and three for DC ablation. Dual chamber permanent pacemakers with automatic mode switching were implanted in four patients who had paroxysmal atrial fibrillation or flutter and the remainder had ventricular rate responsive pacemakers. CONCLUSIONS: In patients with drug refractory paroxysmal atrial fibrillation and flutter and in patients with established atrial fibrillation where control of the ventricular rate is difficult, catheter ablation of the AV junction using RF energy is a safe and effective procedure with a high success rate.

Atrial Fibrillation↗
PubMed1988

Selective functional characteristics of rate-induced fatigue in rabbit atrioventricular node.

The slowly developing rate-induced prolongation in atrioventricular nodal conduction time, termed "fatigue," was selectively studied using specifically designed stimulation protocols in isolated rabbit heart preparations. A nodal recovery curve (A2H2 versus H1A2 intervals; nodal conduction time of each premature beat plotted against corresponding recovery time) was obtained before and after a stable and nearly maximum fatigue had been reached by driving the atrium for 5 minutes at a fast rate close to the upper limit of 1:1 nodal conduction. The fatigue uniformly prolonged all A2H2 intervals (12.3 +/- 1.3 msec) and systematically increased the minimum H1A2 interval at which complete nodal block occurred (24.8 +/- 4.0 msec) (p less than 0.01, n = 6). To study the rate and time dependence of fatigue, nodal conduction times were obtained during three rapid 5-minute pacings corresponding to 50%, 75%, and 100% shortening of the pacing interval in the 1:1 nodal conduction range. The respective maximum fatigue-induced increases in conduction time were 5.4 +/- 1.8, 9.0 +/- 2.7, and 12.5 +/- 2.1 msec (p less than 0.01, n = 6). However, the pacing interval had no significant effect on the time required to reach either 50% (17.1 +/- 3.5 seconds) or 90% (92.6 +/- 15.4 seconds) of the fatigue observed after 5 minutes of fast rate. At the termination of any rapid stimulation, the fatigue effect dissipated with a time course that was inverse but symmetrical to that of its induction. These findings support the existence of an independent, slow, nodal memory process by which the conduction time changes according to past events with a long time constant.

Animals↗
PubMedDate not supplied

Reentrant tachycardia using two discrete atrioventricular nodes and a concealed atriofascicular pathway.

We describe a case of reentrant supraventricular tachycardia using two discrete atrioventricular (AV) nodes in the antegrade direction and a concealed atriofascicular pathway in the retrograde direction in a 21-year-old woman with superior-inferior ventricles and ventricular inversion. Using the Carto endocardial mapping system, two discrete AV nodes were identified as well as a separate decremental AV pathway located midway between the two nodes. Ablation of the separate pathway resulted in elimination of inducible tachycardia without loss of either AV node.

Adult↗
PubMed2002

Intrinsic sinus and atrioventricular node electrophysiologic adaptations in endurance athletes.

OBJECTIVES: In the present study, we evaluated sinus and atrioventricular (AV) node electrophysiology of endurance athletes and untrained individuals before and after autonomic pharmacologic blockade. BACKGROUND: Endurance athletes present a higher prevalence of sinus bradycardia and AV conduction abnormalities, as compared with untrained individuals. Previous data from our laboratory suggest that nonautonomic factors may be responsible for the longer AV node refractory period found in well-trained athletes. METHODS: Six aerobically trained male athletes and six healthy male individuals with similar ages and normal rest electrocardiograms were studied. Maximal oxygen uptake (O(2)max) was measured by cardiopulmonary testing. The sinus cycle length (SCL), AV conduction intervals, sinus node recovery time (SNRT), Wenckebach cycle (WC) and anterograde effective refractory period (ERP) of the AV node were evaluated by invasive electrophysiologic studies at baseline, after intravenous atropine (0.04 mg/kg) and after addition of intravenous propranolol (0.2 mg/kg). RESULTS: Athletes had a significantly higher O(2)max as compared with untrained individuals. The SCL was longer in athletes at baseline, after atropine and after the addition of propranolol for double-autonomic blockade. The mean maximal SNRT/SCL was longer in athletes after atropine and after propranolol. The WC and anterograde ERP of the AV node were longer in athletes at baseline, after atropine and after propranolol. CONCLUSIONS: Under double-pharmacologic blockade, we demonstrated that sinus automaticity and AV node conduction changes of endurance athletes are related to intrinsic physiology and not to autonomic influences.

Adaptation, Physiological↗
PubMed1998

Predictors of outcome after radiofrequency catheter ablation of the atrioventricular node for atrial fibrillation and congestive heart failure.

BACKGROUND: Although radiofrequency catheter ablation of the atrioventricular (AV) node is an established treatment for atrial fibrillation (AF) with uncontrolled ventricular response, factors that predict clinical outcome in patients with associated congestive heart failure (CHF) are unknown. METHODS AND RESULTS: AV node ablation and permanent pacemaker implantation was performed in 44 consecutive patients (mean age 71+/-10 years) with CHF and AF associated with uncontrolled ventricular response. Immediately before ablation, mean left ventricular ejection fraction (EF) measured by 2-dimensional echocardiogram was 34.6%+/-9.8%, mean exercise tolerance time was 2.6+/-1.8 minutes, and mean quality of life score was 62.3+/-19.7. Complete AV block was achieved in all 44 patients but was complicated by death in 1 patient from cardiogenic shock soon after ablation. By 1 month after ablation, EF increased to 43.8%+/-13.7% (P < .01), exercise tolerance time was 4.0+/-2.5 minutes (P < .01), and mean quality of life score decreased to 35.6+/-18.1 (P < .01). Improved cardiac performance (increase in EF > or = 9% over baseline EF) was detected in 20 (45%) of the patients. During a mean follow-up of 17+/-9 months, 5 patients died suddenly of presumed ventricular tachyarrhythmia and 4 others died of progressive CHF. Multivariate Cox survival analysis identified baseline EF < or = 30%, presence of significant mitral regurgitation (>2+) before ablation, and failure to exhibit improved cardiac performance by 1 month after ablation as the only independent predictors of death. CONCLUSIONS: Baseline variables and failure of EF to improve soon after AV node ablation identifies patients with CHF and AF who have a high mortality rate. Adjunctive therapy to reduce sudden death and progressive heart failure should be evaluated in this subgroup.

Aged↗
PubMed1992

Effects of flecainide on the rate dependence of atrial refractoriness, atrial repolarization and atrioventricular node conduction in anesthetized dogs.

UNLABELLED: Flecainide is effective against certain supraventricular arrhythmias (atrial fibrillation and atrioventricular [AV] node reentrant tachycardia), but its mechanisms of action are unknown. Previous in vitro work suggests that flecainide attenuates rate-dependent action potential duration shortening, producing tachycardia-dependent prolongation of the refractory period. This study was designed to assess whether similar changes occur in vivo and whether the effects of flecainide on AV node conduction depend on heart rate and on direction of propagation (anterograde vs. retrograde). The effects of flecainide at three clinically relevant concentrations were assessed in open chest, morphine-chloralose-anesthetized dogs. Flecainide increased atrial refractory period in a concentration- and rate-related fashion (e.g., dose 3 increased the atrial effective refractory period by 9 +/- 4% at a cycle length of 1,000 ms but by 36 +/- 5% and 55 +/- 10% at a basic cycle length of 400 and 300 ms, respectively; p less than 0.001 for each). Flecainide attenuated the action potential duration accommodation (measured by monophasic action potentials) to heart rate, causing tachycardia-dependent action potential duration prolongation and accounting for most of the rate-dependent atrial effective refractory period changes. Flecainide increased Wenckebach cycle length, but the concentration-response curve was much steeper in the retrograde (slope 41 +/- 7 ms/mumol.liter-1) than in the anterograde direction (17 +/- 4 ms/mumol.liter-1; p less than 0.01), indicating more potent effects on retrograde conduction. The depressant action of the drug on the AV node was also rate dependent, with an effect on the AH interval at a basic cycle length of 400 ms that averaged 1.8, 1.5 and 2 times that at a basic cycle length of 1,000 ms for doses 1 (p less than 0.05), 2 (p less than 0.01) and 3 (p less than 0.001), respectively. CONCLUSIONS: 1) Flecainide suppresses atrial action potential duration accommodation to heart rate changes in vivo, leading to rate-dependent atrial effective refractory period prolongation, which may be important in suppressing atrial fibrillation. 2) The drug has frequency- and direction-dependent effects on AV node conduction, which may lead to selective antiarrhythmic actions during AV node reentry.

Action Potentials↗
PubMed1984

Adenosine-5'-triphosphate-sensitive single potassium channel in the atrioventricular node cell of the rabbit heart.

The patch-clamp method was applied to single atrioventricular (a.v.) node cells of the rabbit heart to study the characteristics of the K+ channel. When the electrode contained 5.4 mM-K+, depolarizations of the cell-attached patch membrane induced outward single channel currents characterized by burst-like openings; the open-state probability increased from 0.005-0.01 at -40 mV to 0.07-0.1 at +20 mV of membrane potential. The reversal potentials of the current at K+ concentrations of 5.4, 20 and 130 mM in the electrode agreed with those given by the Nernst equation, indicating that this channel is selective for K+ ions. The slope conductance of the channel decreased beyond 60-90 mV positive to the reversal potential (inward-going rectification). The conductance near the reversal potential increased with increasing K+ concentrations on either side of the membrane: from 31-32 pS at 5.4 mM-K+ to 41-42 pS at 20 mM-K+ on the outside, and from 19 pS at 90 mM-K+ to 29.3 pS at 130 mM-K+ on the inside. Superfusion of the cell with 5.4 mM-CN-, glucose-free Tyrode markedly increased the number of channel openings in the cell-attached patch. In the inside-out patch, application of 1 mM-adenosine-5'-triphosphate (ATP) at the inner surface of the patch membrane blocked reversibly the channel activity, while 1 mM-adenosine-5'-diphosphate (ADP) failed to block it. The conductance and kinetics of the channel were not modified by increasing the Ca2+ concentration from 10(-8) M to 5 X 10(-6) M on the inner side of the membrane, while a further increase in Ca2+ to 10(-4) M decreased the open-state probability. The probability density for the open time fitted well with an exponential distribution (time constant of 5.4 ms at 60 mV positive to the resting potential), while that for the closed time was separated into a fast and a slow component (time constants of 4.0 and 132.0 ms, respectively). The time constant of the slow component decreased significantly with depolarization in some preparations. However, neither the time constant of the fast component of the closed-time histogram nor that of the open-time histogram was voltage-dependent.

Action Potentials↗
PubMed1990

Modification of the atrioventricular node. A new approach to the treatment of supraventricular tachycardias.

Atrioventricular nodal modification appears to be a relatively safe and effective treatment option for patients with refractory AV nodal reentrant tachycardia. Hopefully, the long-term results will be as encouraging as the initial experience. Newer surgical and catheter techniques, together with a better understanding of the mechanisms underlying AV nodal reentrant tachycardia, may lead to improved efficacy and safety. In the future, AV nodal modification may obviate the need for drug therapy in patients with symptomatic AV nodal reentrant tachycardia and be applied to the treatment of other supraventricular tachycardias.

Anti-Arrhythmia Agents↗
PubMed1986

Angiomatous variant of so-called mesothelioma of the atrioventricular node.

A case is presented of an elderly woman found to have an angiomatous tumor involving the atrioventricular (AV) node. The entire AV node was not involved, which explains her lack of symptomatology during her life. The divergent histologic patterns observed in these tumors suggest that the term AV node tumor is preferable to the term mesothelioma.

Aged↗
PubMed1993

Nonatherosclerotic narrowing of the atrioventricular node artery and sudden death.

OBJECTIVES: This study was undertaken to determine whether thickening of the atrioventricular (AV) node artery is a cause of sudden cardiac death. BACKGROUND: Thickening of the AV node artery has been implicated as a cause of sudden death primarily on the basis of case reports. Few pathologic studies have compared subjects who died of sudden cardiac death with normal control subjects who died traumatically. METHODS: The AV node artery in 27 patients with unexplained sudden cardiac death (mean age 24.8 +/- 7.4 years) was compared with that in 17 control subjects who died traumatically (mean age 25.6 +/- 7.0 years). No anatomic cause of death was found at autopsy in the subjects with sudden death, all of whom died of presumed cardiac arrhythmias. The conduction system of all hearts was studied by semiserial sections and Movat pentachrome stains. At the point of greatest narrowing of the AV node artery, the outer circumference and lumen outline were traced by computerized morphometry, the ratio of outer vessel area to lumen area was calculated and the histopathologic changes were noted. RESULTS: The rank-sum of ratios was significantly greater in the sudden death group than in the control group (p = 0.031, Wilcoxon rank-sum/Mann-Whitney statistic). A dysplastic AV node artery with significant acid mucopolysaccharide deposition was seen almost exclusively in the sudden death group (12 of 27 vs. 1 of 17, p = 0.006). In 10 subjects with sudden death a dysplastic AV node artery was narrowed > 2 SD over the control value; half of this subgroup died during exercise and one third had a family history of sudden unexplained cardiac death. CONCLUSIONS: Dysplasia of the AV node artery may contribute to death in a substantial portion of patients with unexplained sudden death, and such death is often associated with exercise and a family history of unexplained sudden death.

Adult↗
PubMed1988

The atrioventricular node of the golden hamster (Mesocricetus auratus): a light and electron microscopic study including immunocytochemistry.

The atrioventricular (AV) node of the golden hamster is situated unusually high in the interatrial septum when compared to other species such as the rat. 2 main cell types, characterized by electron-lucent or electron-dense cytoplasm respectively, are found in the node; although both types contain numerous myofilaments these are irregularly arranged and sarcomeric banding is poor. A third variety comparising transitional cells, with features intermediate between the main nodal cells and general atrial myocardial cells, are found at the periphery of the node. Similar electron-lucent and electron-dense cells are also found in the bundle and the mean diameter of bundle cells increases as one passes from the node to the bundle bifurcation. In the node, specific heart granules (SHG) identified by ANP-28 immunoreactivity are found only in transitional cells and even here they are very sparse, unlike general atrial myocytes in which they are plentiful. Numerous nerve varicosities are present throughout the node and bundle and 5-hydroxydopamine (5-OHDA) labelling demonstrates that most of them have features of either noradrenergic or cholinergic terminals; a few non-cholinergic, non-adrenergic varicosities are also present.

Animals↗
PubMed2002

Demonstration of a left atrial input to the atrioventricular node in humans.

BACKGROUND: During right atrial stimulation, the anterior and posterior approaches provide inputs to the atrioventricular (AV) node. The purpose of the present study was to determine how activation proceeding from the left atrium reaches the AV node. METHODS AND RESULTS: We studied AV nodal conduction during right and left atrial (coronary sinus) stimulation in 46 patients (27 women and 19 men; mean age, 46+/-4 years) who had structurally normal hearts. At an identical cycle length (600 ms), left atrial stimulation resulted in shorter A-H intervals than right atrial stimulation (73+/-3 ms versus 99+/-3 ms; P<0.05). In addition, atrial electrograms recorded close to the His bundle changed from near to far field potentials when stimulation was shifted to the left atrium. The A-H interval prolonged as the site of pacing was progressively moved from the distal to the proximal coronary sinus. During constant pacing from the distal coronary sinus, atrial activation close to the His bundle could be advanced by late extrastimuli delivered at the anterior and posterior approaches (up to 11+/-2 ms and 9+/-1 ms, respectively), without altering His bundle activation time. In contrast, late extrastimuli delivered at the inferoparaseptal mitral annulus advanced both the A and H electrograms in 19 of 20 patients, which is consistent with a left-sided input to the AV node. Right and left atrial stimulation resulted in similar AV nodal function. CONCLUSION: The mitral annulus provides a left atrial input to the human AV node.

Atrial Flutter↗
PubMed1978

[Electrophysiological demonstration of more structures in the atrioventricular node (author's transl)].

Three types of atrioventricular nodal conduction curves, relating A1A2 to H1H2, generated with atrial extrastimulus technique, are known. The first type is smooth, suggesting the homogeneous structure of A-V node. The second type, with abrupt increase in H1H2 response over a critical range of A1A2 coupling intervals, suggests the presence of fast and slow A-V nodal pathways. We have found in five patients the third tipe of A-V conduction curve, giving evidence of an intranodal final common pathway, distal to the fast and slow A-V nodal pathways. The thyrd type of curve enables us to know also some alectrophysiological properties of final common pathway. Indeed we have defined effective and functional refractory periods of fast, slow and final common pathways as far as we can in this type of curve. Paced heart rate variations and atropine medications have led the third type of A-V conduction curve to change into the second type in three cases, into first type in one case. These changes of A-V nodal conduction curves are related to different influence of cardiac cycle lenghts and autonomic nervous system on refractory periods and conduction velocity of the outlined intranodal structures.

Adolescent↗