Effect of verapamil on retrograde conduction in atrioventricular nodal reentrant tachycardia

Using His bundle electrograms, incremental ventricular pacing and the ventricular extrastimulus (V2) technique, the effects of intravenous verapamil, 0.2 mg/kg, on retrograde atrioventricular (AV) nodal conduction during ventricular pacing, premature ventricular stimulation (H2A2 interval) and paroxysmal supraventricular tachycardia (SVT) (H-Ae interval) were evaluated in 11 patients with AV nodal reentrant tachycardia. During the control study, SVT could be induced in all 11 patients. After verapamil administration, SVT or atrial echo beats could be induced in 5 patients. Verapamil produced ventriculoatrial (VA) block at a longer cycle length than that during the control study in 10 of 11 patients (295 +/- 27 vs 352 +/- 40 ms, p less than 0.01), but prolonged H2A2 interval in only 5 of 11 patients (37 +/- 6 vs 60 +/- 31 ms, p less than 0.05). In all 5 patients with persistence of inducible SVT or atrial echo beats after verapamil treatment, the H-Ae interval remained unchanged even though in 4 of these 5 patients VA conduction time or H2A2 interval was prolonged. Correlation between the paced cycle length which induced VA block, the shortest V1H2 interval achieved during premature ventricular stimulation and the cycle length of SVT revealed that in all instances in which verapamil induced VA block at a longer cycle length than in controls but did not prolong H2A2 or H-Ae interval, the shortest V1H2 interval and the cycle length of SVT (H-H interval) were significantly longer than the ventricular paced cycle length which produced VA block.(ABSTRACT TRUNCATED AT 250 WORDS)     

Procainamide and retrograde atrioventricular nodal conduction in man

Recent studies that show a depressant effect of procainamide (PA) on retrograde conduction in patients with atrioventricular (AV) nodal reentrant tachycardia (RT) have suggested possible incorporation of AV nodal bypass tracts. Electrophysiologic effects of i.v. PA, 10 mg/kg, on retrograde AV nodal conduction were examined in 13 patients without RT, demonstrable AV nodal refractory period curves, or accessory pathways. Ventriculoatrial (VA) conduction was recorded before and after PA using intracardiac electrograms, incremental ventricular pacing and extrastimulation. With incremental pacing during the control, VA block occurred at a mean cycle length (CL) of 364.6 +/- 87.9 msec. After PA, VA conduction was abolished in five of 13 patients due to onset of retrograde block in the AV node; in seven of 13, VA block occurred at a longer paced CL after PA (344.2 +/- 51.2 msec vs 477.1 +/- 93.2 msec). In one patient, PA did not affect VA conduction. PA invariably produced prolongation in the VA interval at comparable CL of pacing. With ventricular premature stimulation, the retrograde H2A2 intervals during the control period were short (less than 50 msec) in seven of 13, intermediate (60-100 msec) in three of 13 and long (greater than 100 msec) in three of 13 cases. PA either abolished H2A2 conduction (H2 but no A2) or prolonged the H2A2 intervals by 5-20 msec in most cases in this series. The data suggest that i.v. PA almost uniformly depresses retrograde AV nodal conduction in the intact human heart. This depressant response to PA is not indicative of presence of partial or complete AV nodal bypass tracts.     

Effect of concealed anterograde impulse penetration on retrograde atrioventricular nodal conduction in man

The manner in which concealed anterograde impulse penetration may affect retrograde atrioventricular nodal conduction was studied systematically in 12 patients with intact ventriculoatrial (VA) conduction. After the last beat of a basic atrial drive (A1), an extrastimulus (A2) was introduced 20 msec inside the effective refractory period of the atrioventricular node. A ventricular extrastimulus (Vp) was then introduced at a progressively shorter A1Vp coupling interval both in the presence (method I) and absence (method II) of A2. In two patients, Vp was never conducted retrogradely to the atria with method I despite the presence of VA conduction during method II. In the remaining 10 patients, the VpAp interval was longer with method I vs method II; moreover, retrograde block of Vp ultimately occurred at a mean A2Vp coupling interval of 359 +/- 153 msec (range 190 to 540 msec) during method I despite the persistence of VA conduction during method II at comparable A1Vp coupling intervals. Before onset of retrograde block in method I, the VpAp curve took one of the following three forms: (1) crescendo, a progressively increasing VpAp interval; (2) flat, a constant VpAp interval, (four cases); or (3) discontinuous, a marked jump in the VpAp interval before the onset of retrograde block (two cases). Our findings may serve to elucidate some poorly understood electrophysiologic phenomena.     

Rapid autonomic tone regulation of atrioventricular nodal conduction in man

The changes in P-P intervals and atrioventricular nodal (AVN) conduction during the Valsalva maneuver were studied in 17 patients. In spite of a significant decrease in the sinus P-P interval during phase II of the maneuver (733 +/- 143 to 520 +/- 86 msec, p less than 0.005) and prolongation during phase IV (884 +/- 171 msec, p less than 0.01), there was no change in the AH interval (control: 78 +/- 15: phase II: 76 +/- 15: phase IV: 72 +/- 14 msec, N.S.). In six patients consecutive P-P intervals during phase II were recorded in solid-state memory and were used to trigger pacing of the high right atrium at rest. This showed a significant increase in the AH interval (75 +/- 10 to 123 +/- 45 msec, p less than 0.05). Valsalva maneuver during constant rate atrial pacing resulted in a significant decrease in the AH interval during phase II (115 +/- 36 to 80 +/- 15 msec, p less than 0.001). During phase IV there was prolongation of the AH interval (156 +/- 58 msec) but in 11 patients (61%) a variable degree of Wenckebach periodicity appeared. Thus autonomic tone modulates the changes in AVN conduction induced during physiologic heart rate variation, resulting in maintenance of adequate 1:1 AVN conduction.     

Effects of the autonomic nervous system on the refractory periods of atrioventricular conduction in man

The purpose of the work is to evaluate in clinical setting the effects of autonomic nervous system on the refractory periods of atrio-ventricular (A-V) conduction. Electrophysiological study was carried out, both during basal state and after autonomic blockade induced by i.v. administration of propranolol 0.2 mg/Kg and atropine 0.04 mg/Kg, in 21 subjects with normal atrio-ventricular node conduction (A-H less than or equal to 120 msec) and normal sinus rate (mean age: 54.3 +/- 16.3 years). Following autonomic blockade the sinus cycle length decreased significantly (P less than 0.01), whereas A-H interval, A1-H1 interval at cycle length of 460 msec and the longest atrial pacing cycle length inducing Wenckebach block did not change significantly. Effective and functional refractory periods of the A-V node did not show significant variations after autonomic blockade (342.2 +/- 41 versus 337.2 +/- 54.2 msec and 435.9 +/- 58.9 versus 430 +/- 60.9 msec, respectively); however, these refractory periods changed variably from subject to subject; in some patients they increased and in others there was a marked decrease. There were no significant variations of atrial effective and functional refractory periods after autonomic blockade (249.5 +/- 29.6 versus 256.6 +/- 31.9 msec and 276.4 +/- 27.1 versus 287.7 +/- 33.4 msec, respectively); they too showed a variable response from subject to subject. The relative refractory period of His-Purkinje system, evaluated in 3 patients, increased in all after autonomic blockade (420 +/- 20 versus 463.3 +/- 15.2 msec).(ABSTRACT TRUNCATED AT 250 WORDS)     

A new mechanism for atrioventricular nodal gap-vagal modulation of conduction

The well-known paradoxic behavior of atrioventricular conduction, the so-called gap phenomenon, that occurs when impulses within a certain range of coupling intervals are blocked while impulses with shorter coupling intervals are conducted is attributed to differences in properties of refractoriness in neighboring regions of the conduction system. In contrast, in the present study a model was developed showing a similar phenomenon, dependent on different electrophysiologic mechanisms and localized within the atrioventricular node in an isolated rabbit heart tissue preparation (n = 11). The hearts were paced at cycle length of 400-500 msec, and atrioventricular nodal conduction times (A2H2) were measured versus atrial extrastimulus (A1A2) coupling intervals by standard extrastimulus techniques. Postganglionic vagal stimulation was applied in the atrioventricular node as short bursts of subthreshold (for myocardium) stimuli with duration of 50-150 msec, amplitude of 20-800 microA, and absolute phase (delay after A1) of 0-500 msec. Vagal bursts with appropriate parameters consistently produced bimodal conduction curves. Initially, gradual shortening of the A1A2 coupling interval was associated with an increasing A2H2, with an accentuated increase (or even atrioventricular block) within an intermediate A1A2 range. However, further shortening of the A1A2 coupling interval produced a decrease in A2H2, which subsequently was followed by a block at the effective refractory period. Microelectrode recordings indicated that this characteristic bimodal pattern of conduction curves, demonstrating a gap, reflected transient vagally induced hyperpolarization in the N region of the node. In those instances where conduction block occurred and gap was manifest, the most marked hyperpolarization coincided with the time of arrival of midcycle premature extrastimuli, whereas the conduction of extrastimuli with either more or less prematurity was under less-marked vagal influence. Thus, this study demonstrates a new electrophysiologic mechanism producing anomalous conduction curves and the gap phenomenon within the atrioventricular node based on vagal-induced nonuniform recovery of diastolic excitability.     

Depressant effect on the retrograde atrioventricular nodal conduction of beta-adrenergic blockade by propranolol in humans

Propranolol is known to have a depressant effect on anterograde atrioventricular (AV) nodal conduction in normal subjects and in those with AV nodal reentrant tachycardia. Using His bundle recording and programmed ventricular stimulation, the effect of propranolol-induced beta-adrenergic blockade (1 mg/kg intravenously) on retrograde AV nodal conduction was studied in 17 patients without (group I) and nine with (group II) AV nodal reentrant tachycardia. During baseline studies the ventricular pacing cycle length that induced ventriculoatrial block was 338 +/- 60 ms (range 260 to 450 ms) in group I and 305 +/- 39 ms (range 260 to 375 ms) in group II patients (not significant). After injection of propranolol, the ventricular pacing cycle length that induced ventriculoatrial block in group I patients was 416 +/- 97 ms (range 300 to 550 ms) (P less than 0.001, compared to baseline state) in 15 patients, and complete block occurred in two patients. In group II patients ventriculoatrial block occurred at a ventricular pacing cycle length of 375 +/- 97 ms (range 260 to 510 ms) (P less than 0.02 compared to baseline value) in eight patients, and complete block occurred in one patient. Retrograde AV nodal conduction expressed as the H2A2 interval was 75 +/- 33 ms (range 35 to 150 ms) in group I and 49 +/- 16 ms (range 20 to 80 ms) in group II patients (P less than 0.05). Following the administration of propranolol, the H2A2 interval was prolonged in group I patients by 10 to 45 ms in 11 patients, no retrograde AV nodal conduction was observed in three patients, and there was no effect in two patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

离子通道及自主神经系统与房室结折返性心动过速关系的研究进展

房室结折返性心动过速(atrioventricular nodal reentrant tachycardia,AVNRT)是临床上最常见的阵发性室上性心动过速.目前认为房室结双径路或多径路是AVNRT发生的机制,但确切的病理生理机制以及解剖定位至今尚未阐明.近年来,射频消融术治疗AVNRT的成功率可高达95％.分子蛋...     

Cryoablation in pediatric atrioventricular nodal reentry: Electrophysiologic effects on atrioventricular nodal conduction

BACKGROUND: Cryoablation for treatment of atrioventricular nodal reentrant tachycardia (AVNRT) is safe and efficacious. Information on the effects of cryoablation on atrioventricular (AV) nodal conduction is limited. OBJECTIVES: The purpose of this study was to evaluate the effects of cryoablation on AV nodal conduction in pediatric patients with AVNRT. METHODS: We retrospectively analyzed electrophysiologic studies before and after successful cryoablation. Patients were divided into two groups: group 1 (n = 22, age 14 +/- 3 years) had baseline discontinuous atrial-to-His interval (AH) conduction curves; and group 2 (n = 13, age 12 +/- 4 years, P = .054) had continuous curves. RESULTS: At baseline, group 1 had longer measurements of maximal AH with A1A2, AV nodal effective refractory period, and AV block cycle length. Postcryoablation, both group 1 and group 2 showed decreases in maximal AH with A1A2 pacing or atrial overdrive pacing and in the finding of PR > or = RR with atrial overdrive pacing (group 1: 55% vs 5%, P < .001; group 2: 69% vs 0%, P < .001). A significant increase in overall AV effective refractory period and a decrease in AV block cycle length were found in group 1 but not group 2. Fifty percent of group 1 patients had complete abolition of slow pathway conduction. CONCLUSION: Successful cryoablation for treatment of AVNRT is associated with a reduction in PR > or = RR and with decreases in maximal AH with A1A2 pacing or atrial overdrive pacing. Further study is needed to determine the usefulness of these parameters for assessment of ablation efficacy or as proxies for AVNRT inducibility.     

Effect of postganglionic vagal stimulation on the organization of atrioventricular nodal conduction in isolated rabbit heart tissue

Postganglionic stimulation of vagal terminals (PGVS) in the isolated rabbit heart atrioventricular (AV) node was used to study the effects of cholinergic influence on AV nodal conduction. Standard microelectrode techniques were used to record action potentials, predominantly from cells located in the N region of the AV node. In addition, programmed stimulation was used in conjunction with PGVS to initiate or terminate AVN reentry. The introduction of a single short burst of PGVS (total duration 50 to 100 msec, impulse duration 1 msec, and interimpulse interval 6 msec) with subthreshold amplitude for AV node fibers caused reproducible disorganization of the prevailing excitation front. This was manifest as local nonuniform depression of conduction, hump formations in the action potentials, and alteration in the sequence of depolarization. The introduction of repetitive bursts of PGVS revealed a triphasic time course of changes in AV nodal conduction time, representing initial maximal prolongation, relative shortening, and secondary inhibition. It was found that these phases corresponded to vagally induced initial disorganization and a subsequent rebound process. Vagally induced disorganization of the sequence of action potential depolarization was also a triggering mechanism for concealed as well as manifest AV nodal reentry. In the latter case the reentry circuit usually involved the AN region and perinodal atrial tissue. PGVS-induced depression of the N region was also able to block the retrograde wavefront, thereby terminating reentry. The possible relationship of PGVS-induced disorganization of conduction and the inhomogeneous structure of AV node are discussed. The present results provide additional information for better understanding of the AV nodal conduction abnormalities observed clinically and particularly those related to AV node-vagus interaction.     

Preceding His-atrial interval as a determinant of atrioventricular nodal conduction time in the human and rabbit heart

This investigation shows that atrioventricular (A-V) nodal conduction time (A-H interval), both in the human and in the isolated rabbit heart, is determined mainly by the length of the preceding His-atrial (H-A) interval. The A-H intervals obtained during atrial extrasystolic stimulation at different basic rates, during Wenckebach cycles and during both transient and steady state responses to stepwise increases in stimulation frequency were plotted against the corresponding H-A intervals. The A-H intervals were found to have nearly the same duration provided they were preceded by the same H-A interval. The only important difference appeared in the short H-A interval range as a shortening of the A-H interval at faster basic rates. This facilitating effect of frequency, which was found in the majority of cases, is compatible with the similarly frequency-dependent shortening of the functional refractory period of the A-V node.     

Effects of the site and timing of atrioventricular nodal input on atrioventricular conduction in the isolated perfused rabbit heart

Programmed stimulation was used to study patterns of atrioventricular nodal propagation in an isolated rabbit heart preparation. Stimulation was done at the two major atrioventricular nodal input regions, the crista terminalis and interatrial septum, by use of various sequencing protocols. The influence of stimulation input interactions on atrioventricular nodal propagation was then evaluated with the use of simultaneous extracellular and intracellular recordings from the various regions of the atrioventricular node and His bundle. Activation of the atrioventricular node occurred predominantly via the stimulated input site, although perinodal conduction to the opposite input also occurred and could modify the atrioventricular conduction pattern. Engagement patterns of both AN and N fibers were dependent on the sequence of activation at the major input sites, and similar conduction times to the His bundle were often associated with different local activation times, depending on the site of premature stimulation. Conversely, if premature stimulation was timed to produce constant local activation times but the input site varied, then the time to His bundle activation could also vary. Atrioventricular nodal functional and effective refractory periods and conduction patterns were dependent on both the timing and pattern of engagement at the principal inputs to the atrioventricular node as well as the subsequent organization of activation of the various regions of the atrioventricular node. Furthermore, depending on the sequence of stimulation at the crista terminalis and interatrial septum, activation patterns were either organized or inhomogeneous in the AN and N regions of the atrioventricular node, consequently influencing the H-H interval, and in some instances resulting in conduction block to the His bundle. It is concluded that the relative timing of activation at the principal input regions of the atrioventricular node is critical to patterns of atrioventricular nodal propagation and subsequent conduction to the His bundle. Our results emphasize the complexity of atrioventricular nodal propagation during premature stimulation.     

Incidence, determinants and significance of fixed retrograde conduction in the region of the atrioventricular node. Evidence for retrograde atrioventricular nodal bypass tracts.

Of 104 consecutive patients studied in our laboratory with His bundle electrograms, atrial and ventricular pacing and the atrial and ventricular extrastimulus techniques, 18 patients in whom the existence and utilization of ventriculoatrial (V-A) bypass tracts were excluded demonstrated evidence for fixed and rapid retrograde conduction in the region of the atrioventricular node (A-V) as suggested by the following: (1) short (36 +/- 2 msec [mean +/- standard error of mean]) and constant retrograde H2-A2 intervals during retrograde refractory period studies; (2) significantly (P less than 0.025) better V-A than A-V conduction; (3) significantly (P less than 0.025) shorter retrograde functional refractory period of the V-A conducting system than of the A-V conduction system; and (4) the retrograde effective refractory period of the A=V nodal region was not attainable in any of the 18 patients. Fourteen of the 18 patients (77 percent) had a history of palpitations and 10 (51 percent) had documented paroxysmal supraventricular tachycardia; in 13 (72 percent) single echoes or sustained reentrant supraventricular tachycardia, or both, could be induced during atrial pacing or atrial premature stimulation studies, or both. During tachycardia all these 13 patients had a short (37 +/- 2.4 msec) and constant conduction time in the retrograde limb (H-Ae interval) of the reentrant circuit that was identical to the H2-A2 interval. In conclusion, fixed and rapid retrograde conduction in the region of the A-V node (1) is seen in approximately 17 percent of patients, (2) is associated with a large incidence of reentrant paroxysmal supraventricular tachycardia, and (3) suggests the presence of A-V nodal bypass tracts (intranodal or extranodal functioning in retrograde manner).     

Dual atrioventricular nodal pathways associated with a gap phenomenon in atrioventricular nodal conduction

A 67 year old man underwent electrophysiologic study for evaluation of syncope. During atrial pacing at a basic cycle length of 600 ms, atrial premature stimuli were introduced at progressively shorter coupling intervals. The graph of atrial coupling intervals versus corresponding His bundle responses revealed an abrupt increase in atrioventricular (AV) nodal conduction time with coupling intervals from 320 to 340 ms. In an atrial coupling interval of less than 320 ms, conduction was again rapid until the effective refractory period of the atrium was reached. These unique findings are compatible with dual pathways and a gap phenomenon within the AV node.