Competitive Anterograde and Retrograde Atrioventricular Junctional Activation in Atrial Fibrillation

Reset and Cancellation. In eight medically-treated patients with chronic atrial fibrillation and a random ventricular rhythm, we studied the effect of single right ventricular stimuli delivered after each eighth spontaneous R wave during at least 1 hour. The coupling interval of the extrastimulus was fixed and differed marginally from the shortest spontaneous RR interval. The histograms of spontaneous RR intervals and of the “compensatory” pauses following the ventricular extrasystoles were calculated. Analyses of these histograms and simulation of the interaction between anterograde and retrograde impulses in a computer model suggests that in seven of the eight patients the compensatory pause may be caused by two distinctly different mechanism.s: (1) reset of the timing cycle of atrioventricular nodal activation by relatively early retrograde impulses: and (2) interception of anterograde impulses by relatively late ventricular extrasystoles. The finding that early retrograde impulses are not blocked by concealed atrioventricular nodal conduction makes the existence of decremental conduction and extinction of atrial impulses at different levels within the node unlikely. The results of this study support the hypothesis that the distal side of a weakly coupled junctional area inside the AV node behaves as a pacemaker for the ventricular rhythm during atrial fibrillation. ( J Cardiovasc Electrophysiol, Vol. 1. pp. 448–456, October 1990 )     

Atrioventricular Nodal Conduction Rather than Automaticity Determines the Ventricular Rate During Atrial Fibrillation and Atrial Flutter

AV Nodal Conduction During Atrial Fibrillation and Flutter . Introduction: Recent clinical studies have advanced the hypothesis that the atrioventricular (AV) node does not conduct cardiac impulses, but functions as a pacemaker whose discharge rate and rhythm are modulated electrotonically by atrial impulses. Major support for the hypothesis comes from the observation that the short ventricular cycles during atrial fibrillation can be totally eliminated by ventricular pacing at relatively long ventricular cycle lengths. Methods and Results: The hypothesis was tested in ten anesthetized open chest mongrel dogs with sustained atrial fibrillation or atrial flutter (AF). Large differences (> 120 msec) between the ventricular pacing cycle length that achieved > 95% ventricular capture and the shortest spontaneous RR cycle during AF were considered to be consistent with the modulated AV nodal pacemaker hypothesis, while values ≤ 120 msec were not. The results showed that the ventricular pacing cycle length capturing > 95% of ventricular complexes during AF depended on the spontaneous ventricular rate during AF. Short spontaneous RR cycles during AF required short ventricular pacing cycle lengths to achieve > 95% capture, and the difference between the ventricular pacing cycle length and the shortest spontaneous RR cycle length was narrow, i.e., ≤ 120 msec. Slower ventricular rates could be captured at longer ventricular pacing cycle lengths, and the difference between the ventricular pacing cycle length capturing > 95% of the ventricular complexes and the shortest spontaneous RR interval during AF was large, i.e., > 120 msec. A continuum existed, and values ≤ 120 msec could be transformed to values > 120 msec by increasing vagal intensity to slow the ventricular response. We also found in five dogs that we could not achieve overdrive suppression of automaticity of the putative AV nodal pacemaker focus by ventricular pacing at various cycle lengths and durations during atrial fibrillation. Conclusion: In conclusion, data from this study fail to support the modulated AV nodal pacemaker hypothesis and are more consistent with conventional concepts of AV nodal conduction.     

Impulse Formation and Conduction of Excitation in the Atrioventricular Node

AV Nodal Conduction. Meijler et al. have recently challenged the classical concept of AV nodal conduction (the conduction hypothesis) and suggest that the AV node might he controlling ventricular rhythmicity through its automaticity electrotonically modulated In atrial excitation (the modulated pacemaker hypothesis). This article critically evaluates the three major arguments of Meijler: (1) the absence of convincing evidence for conduction of excitation in the AV node; (2) the prevalence of disproportionately short AV intervals in larger animals; and (3) elimination of KR intervals shorter than the cycle length of ventricular pacing during atrial fibrillation, to judge which of these two hypotheses would more satisfactorily explain various experimental and clinical findings accumulated in the past. Previous observations including microelectrode mapping of the rabbit AV junction during regular sinus rhythm as well as second–degree AV block, clinical and experimental studies on concealed conduction, and studies on the ventricular response to atrial fibrillation appear to he compatible with the conduction hypothesis, whereas clearcut evidence for automatic impulse formation in the AV node has not been presented, except in a small number of hearts showing spontaneous AV junctional rhythms. In view of these observations and theoretical considerations based on comparative anatomy of the AV node–His–Purkinje system and on the latest experimental study on the equine AV node, the authors conclude that the conduction hypothesis appears to better explain all the available data, except perhaps in a few cases with second–degree intra–AV nodal block.     

Achieving regular slow rhythm during atrial fibrillation without atrioventricular nodal ablation: selective vagal stimulation plus ventricular pacing.

OBJECTIVES: The aim of this study was to achieve regular slow ventricular rhythm during atrial fibrillation (AF) without destroying the AV node (AVN). BACKGROUND: Recent experimental and clinical studies have demonstrated that selective AVN vagal stimulation (AVN-VS) can be used to slow ventricular rate during AF; however, an irregular rhythm remains. Alternatively, ventricular on-demand (VVI) pacing achieves rate regularization but at rates faster than the already fast intrinsic rate during AF. We hypothesized that AVN-VS combined with VVI pacing would achieve slow, regular rhythm during AF without requiring AVN ablation. METHODS: AF was induced in eight dogs. AVN-VS was applied to the epicardial fat pad that projects vagal nerve fibers to the AVN. A computer-controlled algorithm adjusted AVN-VS intensity to achieve three levels of mean ventricular RR interval: 75%, 100%, or 125% of the spontaneous sinus cycle length. At each of the three levels, concomitant VVI pacing was delivered at a constant cycle length equal to the corresponding target. Hemodynamic measurements were performed during the study to elucidate the advantages of the proposed method. RESULTS: AF resulted in rapid, irregular ventricular rates (RR = 287 +/- 36 ms, or 56% of sinus cycle length). AVN-VS achieved average ventricular rate slowing to the three target levels in all dogs (RR increased to 381 +/- 41, 508 +/- 54, and 632 +/- 68 ms, respectively). At each of the three target rate levels, AVN-VS combined with VVI pacing fully eliminated rate irregularities. The regular slow ventricular rhythms during AF were associated with significant hemodynamic improvement. CONCLUSIONS: A novel approach combining AVN-VS with VVI pacing results in a regular, slow ventricular rhythm during AF that does not necessitate AVN ablation. Rate regularization achieved by this approach was associated with pronounced hemodynamic benefits during AF.     

Selective experimental chelation of calcium in the AV node and His bundle

There are P cells in the human and canine AV (atrioventricular) node which are virtually devoid of gap junctions. All other components of myocardial cellular connections are calcium-dependent except the gap junction. Direct perfusion of disodium EDTA through the AV node artery of 16 anaesthetized dogs produced three immediate effects: complete AV block, a rapid irregular atrial rhythm and a separate rapid irregular ventricular rhythm. The atrial arrhythmia was short in duration and sinus rhythm resumed, initially with complete AV and VA block; both waned until normal AV conduction returned in each dog. In 3 of the 16 dogs there was transient complete AV block during which two independent His potentials were separately associated with the atrial and ventricular complexes. When conducted sinus rhythm resumed, there was initially A-H prolongation (but not H-V). Atropine, propranolol and reserpine had no influence on any electrophysiologic effect of EDTA. Both tachycardias probably originate in P cells of the AV node, the irregularity being attributable to varying enhancement of automaticity plus functional disaggregation of P cells. AV block is attributed to failure of conduction between disaggregated P cells, which in turn must be an obligatory pathway for normal AV conduction, because of their anatomic interposition. The findings further suggest that the AV nodal P cells are the site of the normal 40 ms delay in AV conduction, and that they may be the site of origin of the His potential.     

右侧显性房室旁道合并右后隔慢旁道的电生理特点和消融治疗

报道两例右侧显性房室旁道合并右后隔慢旁道的电生理特点和消融治疗。两例显性预激综合征接受射频消融治疗 ,心房和心室程控刺激评价消融前后电生理变化。心脏标测证实两例病人存在右侧显性房室旁道 ,阻断该旁道后AV间期延长达 16 3和 16 7ms,QRS波群变宽呈完全预激形 ,程控刺激和标测证实为右后隔慢旁道 ,前传速度慢但无递减传导 ,无VA传导 (例 1)或VA递减传导 (例 2 )。消融阻断慢旁道后AV再次延长达 188ms和 2 17ms,心室预激消失 ,QRS波群呈右束支阻滞形 ,心室刺激见VA分离。结论 :两例病人为右侧游离壁显性房室旁道合并右后隔慢旁道 ,前者掩盖后者的前向传导。正常房室传导束 (AVN HPS)的传导速度慢于慢旁道是其显现前传的原因。     

On the role of ventricular conduction time in rate stabilization for atrial fibrillation.

AIM: Ventricular pacing (VP) could stabilize the ventricular rhythm in atrial fibrillation (AF). This study investigates the role of ventricular conduction time (VCT) in rate stabilization for AF. METHODS AND RESULTS: A novel computer model was used to generate various patterns of RR intervals in AF. For each model configuration, the rate stabilization effect of VP was compared with respect to different VCTs. In all tested cases, the ventricular rate in AF could be stabilized at pacing intervals longer than the shortest spontaneous RR intervals. For each model configuration, slightly longer pacing interval (difference <100 ms) was needed to achieve 95% VP when the antegrade/retrograde VCT was increased from 10/10 to 110/110 ms, whereas the VCT had less effect at lower pacing rate. Although longer VCT was associated with increased percentage of ventricular fusion, its role was diminished at higher pacing rate when more retrograde waves could conduct to the atrium. CONCLUSION: Ventricular conduction time has limited effects on rate stabilization, which could be explained by multi-level interactions between antegrade waves induced by AF and retrograde waves induced by VP.     

Temporal organization of atrial activity and irregular ventricular rhythm during spontaneous atrial fibrillation: an in vivo study in the horse

INTRODUCTION: Atrial fibrillation (AF) is common in healthy horses. We studied the temporal organization of AF to test the hypothesis that the arrhythmia is governed by a high degree of periodicity and therefore is not random in the horse. Further, we surmised that concealed conduction of AF impulses in the AV node results in an inverse relationship between AF frequency and ventricular frequency. METHODS AND RESULTS: Fast Fourier transform (FFT) analysis of atrial activity was done on signal-averaged ECGs (n = 11) and atrial electrograms (n = 3) of horses with AF at control (C), after quinidine sulfate (22 mg/kg by mouth every 2 hours) at 50% time to conversion (T50), and immediately before conversion (T90) to sinus rhythm. FFT always revealed a single dominant frequency peak. The mean dominant frequency decreased until conversion (C = 6.84 +/- 0.85 Hz, T50 = 4.87 +/- 1.5 Hz, T90 = 3.41 +/- 1.18 Hz; P < 0.001). Mean AA intervals (n = 500) gradually increased after quinidine. Mean RR intervals (n = 500), standard deviation of the mean (SDM), Poincaré plots, and serial autocorrelograms (SACs) of 500 RR intervals were measured at C and T90 to determine the ventricular response to AF and quinidine-induced changes in the variability of the ventricular response. Mean RR interval and SDM were reduced after quinidine (C = 1431 +/- 266 msec and 695 +/- 23 msec; T90 = 974 +/- 116 msec and 273 +/- 158 msec, respectively; P < 0.01). Poincaré plots and SAC at C and at T90 revealed a significant correlation of consecutive RR intervals typical of a system with a deterministic behavior. At T90, the variability of RR intervals was reduced and the overall periodicity of RR intervals was increased after quinidine administration. CONCLUSION: In the horse, AF is a complex arrhythmia characterized by a high degree of underlying periodicity. The inverse AA-to-RR interval relationship and reduced variability of RR intervals after quinidine suggest that the ventricular response during AF results from rate-dependent concealment of AF wavelets bombarding the AV node, which nevertheless results in a significant degree of short-term predictability of beat-to-beat changes in RR intervals.     

Rate stabilization by right ventricular apex or His bundle pacing in patients with atrial fibrillation.

AIMS: In patients with atrial fibrillation right ventricular pacing can block antegrade conduction at pacing intervals longer than the shortest spontaneous R-R interval, causing the stabilization of ventricular rhythm. In this study the effects of pacing at two sites were compared in order to evaluate the role of conduction times in determining the stabilization of ventricular rhythm. METHODS: In eight patients with permanent atrial fibrillation, the ventricular rate was recorded before and during pacing at the right ventricular apex and the His bundle with different cycle lengths. RESULTS: In all patients, we obtained a reduction in spontaneous QRS complexes with respect to those anticipated at pacing rates slightly above the spontaneous mean rate, and the ventricular rhythm stabilized at pacing intervals longer than the spontaneous shortest R-R intervals. Between pacing sites we did not observe any difference in the reduction in spontaneous beats and the cycle stabilizing the rhythm. Moreover, simulation of the interaction between antegrade and retrograde impulses in a computer model confirmed that results obtained by pacing at the His bundle cannot be readily explained as a consequence of conduction delays. CONCLUSION: This study suggests that the lag introduced by the His-Purkinje conduction cannot explain, as proposed, the stabilization of ventricular rhythm observed in patients with atrial fibrillation and right ventricular pacing.     

Ventricular echo beats during ventricular pacing or junctional bradycardia: studies in the normal canine heart

In 15 adult dogs ventricular echoes were elicited during sinus rhythm by incremental ventricular pacing and during atrioventricular (AV) junctional rhythm by depressing simultaneously AV junctional automaticity and retrograde AV nodal conduction. Concomitant slowing of AV junctional automaticity and conduction was achieved by selective intranodal administration of verapamil. In three dogs incremental pacing from either ventricle failed to retrogradely activate the atria, and in each case the site of block was found to be in the AV node. In two dogs with retrograde atrial capture there was little or no rate-dependency of retrograde ventriculoatrial (VA) conduction. During incremental ventricular pacing a single ventricular echo beat was observed in 10 of the 12 dogs that had atrial capture, and the atrium appears to be an essential link in the production of each ventricular echo. Ventricular echo occurred when the time allotted for retrograde VA conduction amounted to 70 +/- 4% of the duration of the ventricular pacing cycle length. During AV junctional rhythm, a single ventricular echo was elicited in half of the dogs and in each of those cases intranodal verapamil produced a profound depression of retrograde VA conduction. These experiments suggest that retrograde AV nodal longitudinal dissociation occurs in the slow current-dependent cells of the AV node.     

Atrioventricular Nodal Response to Retrograde Activation in Atrial Fibrillation

Atrioventricular Nodal Reset. Retrograde (ventriculoatrial) conduction that reaches the atrioventricular node simultaneous with, or just before an atrial impulse ean facilitate subsequent anterograde conduction. However, a spontaneous or programmed ventricular extrasystule during atrial nbrillation is generally followed by a compensatory pause indicating subsequent delayed anterograde transmission. This characteristic response was used as a model to study the mechanism of atrioventricular nodal behavior during atrial fibrillation. In eight medically-treated patients with chronic atrial fibrillation and a relatively slow but random ventricular response, single premature right ventricular stimuli were delivered after every eighth spontaneous R wave during at least 1 hour. A fixed coupling interval of the ex-trastimulus, considerably shorter than the shortest spontaneous RR interval, was used. The histograms of the postextrasystolic intervals were compared with those of the spontaneous noninterrupted RR intervals. The average postextrasystolic interval was 180 to 300 msec longer than the mean control RR interval, and in six of eight patients, the shape of the histogram of the postextrasystolic cycles was insignificantly different from that of the spontaneous RR intervals. This suggests that In those six patients, the retrograde impulse had reset the random timing cycle of atrioventricular nodal discharge during atrial fibrillation. This observation is compatible with the hypothesis that electrotonically-mediated propagation across a weakly coupled junctional area within the atrioventricular node, rather than decremental conduction and extinction of anterograde atrial impulses at different levels within the node, may be the mechanism of atrioventricular transmission in atrial fibrillation. (J Curdiovasc Electrophysiol, Vol. 1, pp. 437–447, October 1990)     

Circadian Rhythms of Atrioventricular Conduction Properties in Chronic Atrial Fibrillation With and Without Heart Failure

Objectives. We examined the circadian variations in atrioventricular (AV) conduction properties during atrial fibrillation (AF) by a technique based on the Lorenz plot of successive ventricular response (VR) intervals and analyzed their relations with clinical features.Background. The VR interval in chronic AF shows circadian variation, which is attenuated in patients with an increased risk of death. Although the VR interval is determined by the dynamic processes in the AV node randomly stimulated by rapid atrial activity, the circadian variations of the AV conduction properties related to this mechanism are unknown.Methods. In 48 patients with chronic AF, Lorenz plots were generated on overlapping sequential segments of 512 VR intervals in 24-h ambulatory electrocardiograms. For each scatter plot, the 1.0-s intercept of the lower envelope (LE_1.0) of the plot and the degree of scatter above the envelope (root mean square difference from the envelope [scattering index]) were measured for estimating AV node refractoriness and concealed AV conduction, respectively.Results. In all patients, a significant circadian rhythm was observed for the average VR interval, LE_1.0and scattering index, with an acrophase occurring at night. The mesor, amplitude and acrophase of LE_1.0and the scattering index closely and independently correlated with the corresponding rhythm variables of the average VR interval (partial r²0.98, 0.86 and 0.68 for LE_1.0and 0.98, 0.92 and 0.92 for scattering index). The amplitudes of these measures were lower in patients with congestive heart failure (CHF) even after adjustment for the effects of age, duration of AF, medications, left atrial diameter and blood pressure (p < 0.01 for all).Conclusions. These results suggest that 1) both AV node refractoriness and the degree of concealed AV conduction during AF may show a circadian rhythm; 2) the circadian rhythms of these properties may independently contribute to the circadian variation of the VR interval; and 3) these circadian rhythms may be attenuated in patients with CHF.     

Determinants of the ventricular rate during atrial fibrillation

Determinants of the ventricular cycle length during atrial fibrillation were examined in 52 patients. Thirty-three patients had structural heart disease and none had an accessory atrioventricular (AV) connection. The AV node effective and functional refractory periods, the shortest atrial pacing cycle length associated with 1:1 conduction, the AV node conduction time and indexes of concealed conduction in the AV node were measured in the baseline state (36 patients) and after modification of sympathetic tone by infusion of isoproterenol or propranolol (8 patients each). Atrial fibrillation was then induced with rapid atrial pacing, and the mean, shortest and longest ventricular cycle lengths were measured. Variables that correlated most strongly with the mean RR interval during atrial fibrillation were the AV node effective refractory period (r = 0.93; p less than 0.001), AV node functional refractory period (r = 0.87; p less than 0.001) and shortest atrial pacing cycle length associated with 1:1 conduction (r = 0.91; p less than 0.001). The AH interval during sinus rhythm (r = 0.74; p less than 0.001) and during atrial pacing at the shortest cycle length with 1:1 conduction (r = 0.52; p less than 0.001) had weaker correlations. Measures of concealed conduction did not improve the prediction of the mean or longest ventricular cycle length during atrial fibrillation. In conclusion, the refractory periods and conductivity of the AV node are the best indicators of the potential of the node to transmit atrial impulses to the ventricles during atrial fibrillation. The degree of concealed conduction in the AV node is a less important determinant of the mean ventricular rate during atrial fibrillation.     

Atrioventricular nodal fast pathway modification: mechanism for lack of ventricular rate slowing in atrial fibrillation

OBJECTIVES: Atrioventricular node (AVN) modification is one of the alternatives for ventricular rate control in patients with drug refractory atrial fibrillation (AF). However, the underlying mechanisms, and in particular the role of the dual pathway electrophysiology is not clear. By using a novel index, His electrogram (HE) alternans, we have previously demonstrated in rabbits that both the slow (SP) and the fast pathways (FP) are involved in AVN conduction during AF. This electrophysiological-morphological study was designed to address the role of selective FP ablation on AVN conduction during AF. METHODS AND RESULTS: In 12 rabbit AVN preparations dual pathway conduction was confirmed by HE alternans during A1A2 pacing protocol, as well as during AF. On average 48% of the conducted beats during AF utilized the FP. Selective FP ablation (n=12) guided by HE alternans resulted in only-SP conduction, with longer AVN conduction time at basic beats, but without change of AVN effective refractory period (ERP). Interestingly, despite elimination of all FP-conducted beats during AF, the selective FP ablation allowed previously concealed SP beats to be conducted, resulting in little net effect on the ventricular rate (average His-His interval 199+/-10 ms before versus 201+/-13 ms after FP ablation, p>0.05). Morphological evidence indicated that FP ablation created lesions within the transitional cells of the superior approaches at the junction between the central fibrous body and the AVN. However, extension of FP ablation lesion into the compact AVN domain resulted in non-selective AVN modification and slowing of ventricular rate during AF. CONCLUSIONS: Despite its longer ERP, FP is responsible for a substantial number of ventricular beats during AF. However, selective FP ablation has a minor effect on ventricular rate. The most likely mechanism for this phenomenon is that FP ablation allows previously concealed SP beats to be conducted. On the other hand, ventricular rate slowdown could be achieved if FP ablations caused collateral damage in the compact node. This study highlights the usefulness of HE alternans as a novel tool to monitor dual pathway conduction during AF and to guide AVN modification.     

The Elusive Extracellular AV Nodal Potential: Studies from the Canine Heart, Ex Vivo

Various forms of extracellular recordings from the AV node (AVN) have been reported. However, lack of consistent validation have precluded the use of such recordings in experimental and clinical studies. In 14 Langendorff perfused dog hearts, the triangle of Koch (TOK) was exposed and an octapolar electrode catheter (2 mm rings, 2 mm spacing) was inserted under the endocardium so that the bipolar pairs recorded electrograms from the apex to the base of the TOK. All recording were filtered between 0.05 and 250 Hz, except for a His bundle (Hb) recording (30–250 Hz) made from another bipolar electrode catheter placed in the aortic root. Transmembrane action potentials (AP) were recorded close to the sites of extracellular electrograms. Pin electrodes at the periphery of the bath were arranged to register two ECG leads from the volume conductor. During recovery of electrical activity 11 of 14 preparations developed a junctional rhythm that initially manifested only an AV nodal extracellular and corresponding intracellular AV nodal potentials followed gradually by conduction to the Hb and ventricles but no retrograde atrial activation; 3 preparations initially produced Hb rhythms based on extracellular and transmembrane AP recordings from the AVN and Hb. The amplitude and duration of the AVN extracellular potentials (average: 97 ± 26 V and 92 ± 25 msec, respectively) during AVN rhythms, significantly differed from those during atrial pacing (262 ± 185 V and 78 ± 26 msec, p < 0.05). Histologic sections of the sites underlying the electrodes recording AVN potentials showed AVN tissue throughout. We conclude that extracellular AV nodal potentials are independent waveforms with specific qualitative and quantitative characteristics that distinguish them from adjacent atrial, transitional, Hb or ventricular potentials.     

Bundle branch block on alternate beats during atrial fibrillation

This article reports a case of tachycardia-dependent right bundle branch block (RBBB) occurring during atrial fibrillation. In some sections of the recording, an alternans occurs between complexes with a complete RBBB pattern and complexes showing normal intraventricular conduction or incomplete RBBB. Alternans is frequently observed during phases of fast and nearly regular rhythm, but it occurs even in the presence of a markedly irregular ventricular response. The RBBB alternans associated with short and regular RR intervals is likely to represent a manifestation of 2:1 bundle branch supernormal conduction, whereas alternans occurring with irregular cycles expresses a complex interaction between the RR cycle length and some mechanisms affecting intraventricular conduction, such as tachycardia-dependent bundle branch block, supernormal conduction and concealed retrograde activation of the anterogradely blocked bundle branch (the so-called "linking" phenomenon).     

Deterioration of interatrial conduction in patients with paroxysmal atrial fibrillation: Electroanatomic mapping of the right atrium and coronary sinus

OBJECTIVES: The purpose of this study was to analyze the velocities across the coronary sinus ostium (cross-CSo) and within the coronary sinus (intra-CS) in patients with and without paroxysmal atrial (AF) fibrillation and to estimate the interatrial conduction deterioration area in AF patients. BACKGROUND: Interatrial conduction delay in AF patients has been reported. However, localization of the interatrial conduction delay still is not clear. METHODS: Thirteen patients with paroxysmal AF and 10 control patients with AV nodal reentrant tachycardia or ectopic atrial tachycardia were enrolled in the study. Right atrial and CS mapping were performed using the CARTO electroanatomic mapping system during sinus rhythm and during distal CS pacing. The activation times and spatial distances of cross-CSo and intra-CS were measured between paired sites, from which the activation velocities of cross-CSo and intra-CS were obtained. RESULTS: During sinus rhythm, the activation velocities of cross-CSo in the AF group (1.2 +/- 0.2 m/s) were significantly slower than those in the control group (2.9 +/- 1.6 m/s, P < .05). During distal CS pacing, the cross-CSo velocities of the AF group (1.0 +/- 0.5 m/s) also appeared slower than those in the control group (1.4 +/- 0.2 m/s, P = .07). However, no difference was found in intra-CS activation velocities between the two groups (2.8 +/- 1.9 vs 3.2 +/- 2.2 m/s and 1.5 +/- 0.3 vs 1.4 +/- 0.3 m/s, P > .05 during sinus rhythm and distal CS pacing, respectively). CONCLUSIONS: Interatrial conduction at the posteroparaseptal region across the CS ostium was significantly slower in patients with paroxysmal AF than in control patients, further supporting the link between interatrial conduction deterioration and paroxysmal AF.     

Ventricular response to atrial fibrillation: role of atrioventricular conduction pathways

Irregularity of the ventricular rhythm is a hallmark of patients with atrial fibrillation, yet the genesis of the irregularity is not yet fully understood. The role of the atrioventricular (AV) node in determining the irregularity of the ventricular response to atrial fibrillation was investigated by comparing the frequency distributions of the atrial (AA) and the ventricular (RR) intervals. Atrial electrograms and surface electrocardiographic leads were recorded during sustained atrial fibrillation in 12 patients with conduction over the AV node. The scaling factor (mean RR interval/mean AA interval) quantified the ability of the conduction pathway to scale the atrial input to a slower ventricular response and ranged from 2.55 to 5.92 (mean +/- SD 3.77 +/- 0.92). The coefficient of variation (SD/mean) measured the relative variability of the AA and RR interval distributions. The atrial and ventricular coefficients of variation were not significantly different (0.20 +/- 0.04 versus 0.21 +/- 0.03, p greater than 0.27). Similar recordings were analyzed in six patients with conduction over a accessory AV pathway. The scaling factor ranged from 1.54 to 2.46 (2.02 +/- 0.39) and, as was the case for patients with conduction over the AV node, the atrial and ventricular coefficients of variation did not significantly differ (0.24 +/- 0.08 versus 0.27 +/- 0.10, p greater than 0.6). For both groups of patients, ventricular variability and the maximal RR intervals were predicted by the product of the scaling factor and either atrial variability or maximal AA intervals, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Mechanism of tachycardia-dependent appearance of ventricular extrasystoles in concealed bigeminy

A case of concealed ventricular bigeminy is reported in which the number of sinus QRS complexes intervening between two successive noninter-polated extrasystoles was always uneven. Coupling intervals of manifest extrasystoles to the preceding sinus QRS complexes were almost fixed and much longer than sinus QT intervals. Bradycardia-dependent disappearance of manifest bigeminy and tachycardia-dependent appearance of extrasystoles occurred in this case. Apparently, 2:1 block of sinus impulses occurred in the reentrant pathway, with markedly depressed conductivity. Concealed electrotonic conduction of blocked sinus impulses in the pathway of extrasystoles may have favored the appearance of the subsequent manifest extrasystoles without concealed conduction owing to two-level block. A possible explanation for the mechanism of such concealed bigeminy is presented, which uses the concepts of longitudinal dissociation and electrotonic inhibition in the reentrant pathway with markedly depressed conductivity.     

The hemodynamic consequences of cardiac arrhythmias: Evaluation of the relative roles of abnormal atrioventricular sequencing,irregularity of ventricular rhythm and atrial fibrillation in a canine model

To evaluate the hemodynamic consequences of various cardiac arrhythmias, hemodynamic and angiographic studies were performed on 20 open-chest, atrioventricular (AV) heart-blocked dogs during various programmed pacing protocols. Protocols included AV pacing at intervals of 100 msec and ?100 msec, ventricular (V) pacing during AV dissocation, and V pacing during atrial fibrillation (AF). In addition, the effects of regular versus irregular V pacing were also evaluated. During regular V pacing, cardiac output was optimal at an AV interval of 100 msec, but decreased by 25% at AV ?100 msec and by 18% during both AV dissociation and AF. During irregular V cycles, cardiac output decreased further (e.g., by an additional 7% during AF). Pulmonary venous regurgitation was observed only during AV dissociation and during regular pacing at AV ?100 msec. Notably, mitral valvular regurgitation was observed only during irregular V cycles, but not during regular V pacing, even in the presence of AV dissociation or AF. Using these methods it was possible to resolve some previously reported controversies regarding the relative importance of AV sequencing, atrial systole versus AF, regular versus irregular rhythms, as well as the possible contribution of mitral and/or pulmonary venous regurgitation to the adverse hemodynamics of various cardiac arrhythmias.