[1:2 atrioventricular conduction of dual pathway in atrioventricular node].
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Atrioventricular Node↗
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Congenital polycystic tumor of the atrioventricular node.
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Atrioventricular Node↗
Ultrastructure of the atrioventricular node of the big brown bat, Eptesicus fucus.
This investigation describes the ultrastructure of the atrioventricular node of Eptesicus fuscus. Two conducting cells types (nodal and transitional) are indentified which differ in location, myofibrillar content, and types of intercellular junctions. Centrally located nodal cells display variable staining intensity and contain disorganized myofibrils which rarely form sarcomeres. Desmosomes and nexus-like junctions connect the nodal cells. Transitional cells, situated peripherally, exhibit distinct sarcomeres and are attached to the adjacent cells through desmosomes and underdeveloped intercalated discs. Longitudinal arrangement of the mitochondrial cristae is frequently seen in both cells types. In the connective tissue stroma, numerous capillaries (with micropinocytotic vesicles), axons, and possibly axonal terminals, some filled with vesicles, are observed. A large ganglionated nerve trunk is present on the nodal periphery. True nexuses and neuromuscular junctions are not observed. It is suggested that nodal cell types previously reported in different vertebrates under various names are merely simple variations of the two basic types of conducting cell--nodal and transitional. No interspecific differences are observed between these cells of the big brown bat compared with those in other vertebrates.
Animals↗
Radiofrequency catheter atrioventricular node ablation in patients with permanent cardiac pacing systems.
Following successful RF ablation of the atrioventricular node (AVN), temporary pacing is necessary prior to insertion of a permanent pacemaker. The risks and inconvenience of temporary pacing could be avoided if a permanent pacemaker is already in place. This study reports the feasibility of RF ablation of the AVN in 27 patients (age 55 +/- 17 years, 15 males) with hypertrophic cardiomyopathy and pacemakers. Indications for AVN ablation were drug refractory atrial fibrillation in 24 patients, and rapid AVN conduction preventing septal pre-excitation by DDD pacemaker, inserted for relief of left ventricular outflow obstruction, in three cases. Sixteen patients had DDD devices and 11 patients had VVI devices. During RF ablation, each pacemaker was programmed to VVI at 50 beats/min. The ablation catheter was manipulated with fluoroscopic control to avoid close contact with or disturbance of the pacing leads. In 16 patients, RF ablation was performed immediately following pacemaker implantation but in the remaining patients, the AVN was ablated 6-32 months after pacemaker implantation. The power applied was 25-50 watts for a duration of 15-60 seconds. AV block was achieved in all cases but required 34 +/- 36 applications for 16.5 +/- 17.8 min/case. RF ablation consistently caused reversion to magnet rate in one patient and temporarily inhibited appropriate pacemaker discharge in another. However, no other pacemaker or lead malfunction was detected so that temporary pacing was not required in any case. At 6 +/- 3 months follow-up, all pacemakers were functioning normally without alteration in pacing parameters from baseline.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Muscarinic inhibition of basal L-type calcium current in pacemaker cells from the rabbit atrioventricular node.
Effects of acetylcholine (ACh) on the L-type calcium current were examined in isolated atrioventricular nodal cells that exhibited spontaneous contractions. ACh (0.1 to 10 microM) inhibited basal calcium current dose-dependently. This inhibition was eliminated by dialysis with 8Br cAMP or cAMP-dependent kinase inhibitory peptide. Both extracellular N-ethylmaleimide 50 microM and intracellular GDPssS 0.2 mM abolished the ACh effect. Dialysis with cGMP or NG-monomethyl-L-arginine did not significantly affect ACh inhibition of basal calcium current. Similarly, cGMP-dependent protein kinase inhibitor KT5823 (1 microM) and the type II phosphodiesterase inhibitor erythro-9-(2-hydroxy-3-nonyl) adenine (30 microM) did not attenuate the ACh effect. Therefore, ACh inhibits the basal calcium current in the atrioventricular node mainly by suppressing cAMP synthesis through the inhibitory GTP-binding protein.
Acetylcholine↗
Comparison of the direct effects of nifedipine and verapamil on the electrical activity of the sinoatrial and atrioventricular nodes of the rabbit heart.
We compared the effects of nifedipine and verapamil on the rabbit sinus and atrioventricular nodes. Both drugs slowed the rate of impulse initiation by sinus node cells. Verapamil exerted a greater negative chronotropic effect at low concentrations, but at higher concentrations verapamil and nifedipine were equipotent. Nifedipine also reduced the amplitude of sinus node action potentials and the Vmax of phase O, effects which are identical to those previously described for verapamil. Both drugs slowed AV nodal conduction and prolonged refractory periods, but verapamil was more potent than nifedipine. Nifedipine reduced the amplitude of AV nodal action potentials and Vmax of phase O the same as verapamil. Nifedipine and verapamil, therefore, have nearly identical direct effects on the nodes. The failure of nifedipine to depress AV nodal conduction in situ and abolish reentrant AV nodal tachycardia is probably a result of the decreased sensitivity of the AV node to nifedipine compared to verapamil.
Animals↗
[Arterial vascularization of the sinoatrial and atrioventricular node (preliminary study apropos of 15 anatomic parts].
Arterial supply to the sino-atrial and atrioventricular node is studied after coronary RHODOPAS injection on 15 adult hearts taken off during autopsy. Both coronaries were injected in 7 cases, left ostium in 2 cases and the right on in 6 cases. The sino-atrial node is supplied by the right sino atrionodal artery (S.A.N.A) in 6 cases upon 7 and in 3 cases by the left S.A.N.A. Anastomoses exist in 2 cases between the right S.A.N.A. and the left S.A.N.A. The atrio-ventricular nodal artery arises from the retro-ventricular trunk branching from the right coronary artery mainly. The authors emphasize that care must be taken to protect the vascular supply to the conduction tissue during cardiac surgery.
Adult↗
Time- and voltage-dependent block of the delayed K+ current by quinidine in rabbit sinoatrial and atrioventricular nodes.
The modes in which quinidine blocks the delayed K+ current (IK) of rabbit sinoatrial and atrioventricular nodes were investigated by voltage clamp experiments using small preparations. Depolarizing pulses were applied from a holding potential of -50 mV and resultant IK current was evaluated. At a concentration of 2 x 10(-6) M, quinidine blocked 52 +/- 5% of IK with a 1000-msec test pulse of 0 mV, whereas it inhibited the slow inward current by only 5 to 10%. IK inhibition was enhanced with increasingly larger depolarizations. The activation curve obtained with the use of 1000-msec test pulses shifted toward hyperpolarization by 3.0 mV and its slope factor increased from 7.3 to 8.8, suggesting a voltage-dependent mechanism for IK blockage. Short and small depolarizing pulses from the holding potential of -50 mV hardly affected II. The activation of IK in the presence of quinidine did not show any delay. These results indicated a low affinity of quinidine to the closed (deactivated) channels. The deactivation time constant of IK was significantly prolonged from 120 to 145 msec at -50 mV. By applying the modulated receptor model to the K+ current, the tail current in the presence of quinidine was well reconstructed when the time constant of drug-channel interactions was 300 msec at -50 mV and 2000 msec at -30 mV. It is suggested that the unblocking of quinidine slows the decay of the IK tail current.
Animals↗
Evidence of quadruple anterograde atrioventricular nodal pathways in a patient with atrioventricular node reentry.
Functional longitudinal dissociation of the atrioventricular (AV) node exhibiting two discrete discontinuities in AV nodal conduction curves suggestive of triple AV nodal pathways has been described. The authors report here unusual electrophysiologic properties of the AV node in a patient with documented episodes of paroxysmal supraventricular tachycardia. Programmed atrial extrastimuli introduced at A1-A2 coupling intervals of 390 ms with a driven cycle length of 500 ms produced a sudden marked increase of 75 ms at the A2-H2 intervals suggesting failure of the fast pathway with conduction proceeding through a slower pathway with a shorter refractory period. With further decreasing coupling intervals, a second sudden jump of 70 ms and a third one of 150 ms occurred at A1-A2 coupling intervals of 330 and 290 ms, respectively. Beyond the first sudden jump, atrial echoes occurred when sufficiently slow pathway delay permitted recovery of the fast pathway for retrograde conduction. The atrial echo zone was 170 ms. These electrophysiologic demonstrations of reentry within the AV node in a patient with clinically documented supraventricular tachycardia and the existence of four ranges of AH conduction times and refractory periods strongly suggest the presence of quadruple anterograde AV nodal pathways and a variety of potential loops available for the development of sustained AV nodal reentrant tachycardia.
Adult↗
Is vagal innervation to the atrioventricular node impaired after radiofrequency ablation of the slow atrioventricular nodal pathway?
To assess the potentially adverse effects of RF catheter ablation (RFCA) of the slow AV nodal pathway on the parasympathetic innervation to the AV node in patients with AV nodal reentrant tachycardia (AVNRT), AV nodal conduction was evaluated following vagal stimulation by means of a phenylephrine bolus injection (200 micrograms) before and after RFCA in ten patients (mean age, 37 +/- 14 years). Nine patients with AV reentrant tachycardia (AVRT) due to a left free wall accessory pathway served as a control group (mean age of 37 +/- 12 years). Whereas no prolongation of the AH interval was observed in the AVNRT group following the phenylephrine bolus during sinus rhythm, despite a significant slowing in sinus rate, phenylephrine administration in AVRT patients was associated with both slowing of the sinus rate and prolongation of the AH interval. Following successful RFCA, the same responses were observed. To delineate the indirect effect of heart rate on AV conduction in response to the phenylephrine bolus, the AH interval was also measured during fixed atrial pacing. A marked prolongation of the AH interval occurred in both groups following phenylephrine administration. This prolongation was biphasic in 50% of AVNRT patients before ablation, suggesting a predominant effect of vagal stimulation on the fast AV nodal pathway. RFCA was associated with disappearance of discontinuous AV conduction in all but one patient with AVNRT. Vagal stimulation caused the same amount of AH interval prolongation as before RFCA in both study groups. In conclusion, patients with AVNRT have a preserved modulation of AV nodal conduction in response to vagal stimulation during sinus rhythm. In addition, vagal stimulation seems to exert a predominant effect on the fast AV nodal pathway. RFCA of the slow AV nodal pathway in patients with AVNRT does not cause detectable damage to the vagal innervation to the AV node.
Adult↗
Skeletonization of the atrioventricular node for AV node reentrant tachycardia: experience with 32 patients.
We describe our experience with operative therapy for atrioventricular (AV) node tachycardia using an anatomically guided procedure. The operative rationale was to dissect the AV node from most of its atrial inputs (AV node "skeletonization") with the intent of altering the perinodal substrate and preventing reentry. The anteroseptal and posteroseptal regions were initially approached epicardially to facilitate identification of anatomical structures. Under normothermic cardiopulmonary bypass, the right atrial septum was mobilized and the intermediate AV node was exposed anterior to the tendon of Todaro. Atrioventricular node conduction was monitored electrocardiographically throughout the procedure. Ablation of concomitant accessory pathways was done prior to AV node skeletonization. Thirty-two patients aged 9 to 67 years (mean age, 30 years) underwent operation. Five patients had concomitant accessory pathways in addition to AV node reentry. At electrophysiological study before discharge, no patient had AV block although anterograde and retrograde Wenckebach cycle lengths were significantly prolonged. Six patients had retrograde AV block. Twenty-nine patients are free from arrhythmia and require no antiarrhythmic medication after a follow-up of 1 month to 45 months (mean follow-up, 17 months). Three patients had recurrence of tachycardia ten days, 2 months, and 7 months postoperatively. All patients subsequently had a successful reoperation.
Adolescent↗
[Enzyme activity in the normal atrioventricular node and in the bundle of His in young children].
The authors examined by histochemical methods the atrioventricular node and the bundle of His in five infants who died from unnatural deaths and in a four-and-half-year-old child who died immediately following haemorrhagic infarction of the gut. Both structures differed, similarly as in adult age, from working muscle by a lower oxidation capacity, higher activity of the pentose-phosphate shunt and a high acetylcholine esterase activity.
Atrioventricular Node↗
Effect of slow pathway ablation in atrioventricular nodal reentrant tachycardia on the electrophysiologic characteristics of the inferior atrial inputs to the human atrioventricular node.
The inferior atrial extensions of the atrioventricular (AV) node have been related to the anatomic substrate of the slow pathway, but their role in AV nodal reentrant tachycardia (AVNRT) is unknown. Ten patients with slow-fast AVNRT were studied before and after successful slow pathway ablation. Simultaneous His bundle recordings from the right and left sides of the septum were made during right and left inferoparaseptal pacing. Longer stimulus to His (St-H) intervals were measured during right inferoparaseptal pacing than during left inferoparaseptal pacing (284 +/- 55 vs 246 +/- 46 ms, p = 0.005 for right His recordings and 283 +/- 56 vs 244 +/- 46 ms, p = 0.005 for left His recordings) at similar coupling intervals during AVNRT induction. After ablation, the St-H intervals at the maximum AV nodal conduction decrement were similar during right inferoparaseptal and left inferoparaseptal pacing (217 +/- 32 vs 207 +/- 21 ms, p = 0.10 for right His and 215 +/- 32 vs 206 +/- 20 ms, p = 0.13 for left His) at similar coupling intervals. The difference (DeltaSt-H) between St-H intervals during AVRNT induction or at the maximum conduction decrement and during constant pacing for right His recordings with right inferoparaseptal pacing were significantly greater than DeltaSt-H measured with left His during left inferoparaseptal pacing (173 +/- 64 vs 137 +/- 55 ms, p = 0.005) before ablation, but not after (117 +/- 39 vs 100 +/- 40 ms, p = 0.44). Resetting of AVNRT with delivery of left inferoparaseptal extrastimuli was achieved in 7 of 10 patients. In conclusion, the electrophysiologic characteristics of the right and left inferior atrial inputs to the human AV node in patients with AVNRT and their response to slow pathway ablation provide further evidence that the inferior nodal extensions represent the anatomic substrate of the slow pathway.
Adult↗
Distinction between atrioventricular reciprocating tachycardia and atrioventricular node re-entrant tachycardia in the adult population based on P wave location; should we reconsider the value of some ECG criteria according to gender and age?
AIMS: Distinction between atrioventricular node re-entrant tachycardia (AVNRT) and atrioventricular reciprocating tachycardia (AVRT) is sometimes difficult using location of retrograde P waves on ECG. METHODS: P wave location was retrospectively determined in 137 anterior slow-fast AVNRT (85%) and 26 orthodromic AVRT (15%) with narrow QRS occurring in 161 successive patients without pre-excitation. Mechanism of arrhythmia was assessed by electrophysiological study and confirmed by the efficacy of radiofrequency ablation. P waves were classified as invisible, visible after the QRS, or as R' in V(1) and/or S in II. Correlations with arrhythmia mechanism were made according to gender and age (>or= or <65 years old). RESULTS: Mechanism was related to gender but not to age, with a higher proportion of AVNRT in women (89/97, 91%) than in men (48/66, 72%) (P=0.001). AVRT presented with visible P waves in 26/26 cases (100%) while AVNRT presented with invisible P waves in 36/137 (27%), R'V(1)/SII in 79/137 (57%) and visible P waves in 22/137 (16%). P wave location during AVNRT was related to age but not to gender, with a higher proportion of AVNRT with visible P waves in elderly than in younger patients: 8/27 (29%) vs 14/110 (12%) (P=0.03). Visible P wave during AVNRT was mainly caused by a delay in nodal retrograde conduction in 17/22 patients (77%). Mechanism of tachycardia with visible P waves was related to gender (AVNRT in 14/22 women (64%), AVRT in 18/26 men (70%), P =0.02) and to age, although non-significantly (AVNRT in 8/13 (62%) old vs 14/35 (40%) young patients, P=0.18). A visible P wave was predictive of AVNRT in 25% and in 60% of the men and women younger than 65 years old, and in 50% and in 71% of older men and women respectively (P=0.08 - borderline significance). CONCLUSIONS: Correct distinction between anterior slow-fast AVNRT and orthodromic AVRT can be reliably made regardless of gender or age in case of R'V(1)/SII or invisible P wave. AVRT as the expected mechanism should be reconsidered in the case of visible P waves in the elderly and in the female gender in the absence of pre-excitation.
Age Factors↗
A microcomputer system for on-line study of atrioventricular node accommodation.
An automated on-line programmable stimulator and interval measurement system was developed to study atrioventricular node (AVN) accommodation. This dedicated microcomputer system measures and stores the stimulus-to-His bundle (S-H) interval from His bundle electrogram (HBE) recordings. Interval measurements for each beat are accurate to within 500 microsecond. This user-controlled system has been used to stimulate at any rate up to 6.5 Hz and to measure intervals up to 125 ms in isolated perfused guinea pig hearts. A built-in timer-reset mechanism prevents failure of the system in the absence of a His potential (i.e., 2:1 AV block). It may be modified for use in clinical studies or other experimental systems and has the ability to measure other physiological intervals. The system provides the precision in pacing and accuracy in the measurement of AVN conduction time that is necessary for meaningful analysis of AVN accommodation and has the simplicity of design and use that is not available in previously described systems. Furthermore, this computer system can be used not only in studies involving AV conduction, but also in any setting where programmed stimulation and interval measurement and recording need to be performed simultaneously.
Animals↗
Structure and function of specific regions in the canine atrioventricular node.
The functional subregions of the rabbit atrioventricular (AV) node have been examined in detail, but it has not been possible to subject the normal canine AV node to such rigorous scrutiny. Arterial perfusion and beveled microelectrodes have now allowed us to explore the anatomic and functional regions of the isolated canine AV node. The atria and AV junctional tissues of 20 young dogs were excised and selectively perfused with physiological solution through the nutrient arteries to the sinus node, AV node, and His bundle. AV node action potentials had shapes similar to those of the rabbit AV node and were conducted slowly (56 +/- 7 mm/s); slowest conduction (16 +/- 14 mm/s) was observed in the distal AV node where diastolic depolarization was always recorded and where maximum upstroke velocity of the action potential was slowest. From subsequent anatomic studies of the same preparations we found that the proximal region of the canine AV node was predominantly composed of interwoven slender transitional cells and that the distal region contained bundles of transitional cells and small but conspicuous aggregations of P-cells. The proximal portion of the canine AV node appeared to be organized for triage of atrial input during sinus rhythm. Electron microscopic examinations revealed numerous relatively long (greater than 1.0 micrometers) gap junctions between proximal AV node cells. The large gap junctions may provide an anatomic basis for electrotonic interaction during summation and conduction of AV node inputs. The distal AV node is the site of slowest AV conduction and also where most forms of AV junctional rhythm originate.
Action Potentials↗
Origin, domain, and dynamics of rate-induced variations of functional refractory period in rabbit atrioventricular node.
Different aspects of the intrinsic regulation of rate-induced variations of functional refractory period of atrioventricular node (FRPN) were studied in isolated rabbit heart preparations. First, the hypothesis that these variations originate from the net interaction between facilitation and fatigue was tested. For a constant fast rate, selective effects of faciliation and of steady-stage fatigue were independently shown to shorten and prolong, respectively, FRPN while their combined effects were shown to result in intermediate changes corresponding to the sum of their individual effects. Second, selective and combined effects on FRPN were shown to start for rates corresponding to the upper half of the 1:1 nodal conduction range and to reach their maximums at the fastest rate tested. Third, the time-courses of fatigue-induced prolongations in nodal conduction time and FRPN were shown to be closely linked. Facilitation effects on conduction time and FRPN were confirmed, as previously shown for in situ dog hearts, to be linked, but time-independent. Fourth, FRPN was shown not to correspond to particular limits in its subintervals, but to be, nevertheless, related to nodal refractoriness. Fifth, it was demonstrated that, in conditions of combined facilitation and transient fatigue such as those prevailing in current endocavitary investigations of nodal function, FRPN could be shortened, left unchanged or prolonged by a constant fast rate depending on its duration. In conclusion, the present study demonstrates the dual origin of rate-induced FRPN variations, their rate and time dependence, their relation to changes in nodal refractoriness, and their involvements in various nodal responses.
Animals↗
Characteristics of single cells isolated from the atrioventricular node of the adult guinea-pig heart.
To date, data regarding the cellular electrophysiology of the atrioventricular node (AVN) have derived from AVN cells isolated from the rabbit heart. The aim of this study was to characterise for the first time the electrophysiological properties of single cells isolated from the AVN of the guinea-pig heart. Cells were isolated from the AVN region by a combination of enzymatic and mechanical dispersion. Mean (+/-SEM) cell dimensions were 110.8+/-2.3 microm in length by 11.4+/-1.3 micro m in width (n=76 cells). Electrophysiological recordings were made using the whole-cell patch-clamp technique at 37 degrees C. Mean cell capacitance was 25.1+/-0.9 pF (n=43) and mean cell input resistance was 1,377+/-178 Muomega (n=21). Spontaneously active cells exhibited action potentials characteristic of cardiac pacemaker tissue. Under whole-cell voltage clamp, the mean 'zero current' potential was -39.7+/-4.1 mV (n=21). Voltage commands of 500 ms duration to a range of test potentials from a holding potential of -40 mV revealed a number of distinct current components. At potentials positive to -40 mV an early inward current was observed that exhibited a bell-shaped current voltage (I-V) relation, typical of L-type calcium current. A delayed outward current that increased progressively with test potential magnitude was also observed. Analysis of the outward current 'tails' on repolarisation to -40 mV showed this to be comprised of two components with half-maximal activation voltages of -17.2+/-1.8 mV, and +27.1+/-3.6 mV (n=13). 'Transient outward' current appeared absent from guinea-pig AVN cells. Hyperpolarising test pulses activated net inward current, for which three components could be observed: a barium-sensitive (100 microM Ba(2+)) inwardly rectifying current evident at the start of the voltage command and prominent at potentials negative to the diastolic potential range; a time-dependent, hyperpolarisation-activated current, and a residual background current. On repolarisation to -40 mV, a large inward current spike typical of cardiac Na current was observed in some cells. Notably, the following electrophysiological characteristics of guinea-pig AVN cells are distinct from those characteristics previously reported for the rabbit AVN: (1) an absence of transient outward current, (2) the presence of two components of delayed outward current, and (3) the presence of a Ba(2+)-sensitive inwardly rectifying current at negative voltages. The guinea-pig AVN isolated cell preparation may be valuable in providing additional insights into the cellular electrophysiology of this important region of the heart.
Action Potentials↗