Overdrive suppression of conduction at the canine Purkinje-muscle junction

We have shown previously that overdrive suppression of conduction in depolarized His-Purkinje tissue requires conduction asymmetry. In this study we examined whether overdrive suppression of conduction can occur at the Purkinje-muscle junction, where natural asymmetry of conduction exists. Canine Purkinje-muscle preparations were superfused with hyperkalemic Tyrode's solution (KCl 8 to 12 mM), and action potentials were recorded from Purkinje, junctional, and muscle cells. Initially, the Purkinje fiber was paced at the shortest cycle length at which 1:1 anterograde Purkinje-muscle conduction occurred. The papillary muscle then was paced for 10 to 50 beats at shorter cycle lengths during which, because of conduction asymmetry at the Purkinje-muscle junction, 1:1 retrograde muscle-Purkinje conduction also occurred. After overdrive papillary muscle pacing, Purkinje fiber pacing at the same cycle length that previously resulted in 1:1 conduction now produced transient Purkinje-muscle conduction block (overdrive suppression of conduction). The degree and duration of overdrive suppression of conduction were proportional to the rate and duration of overdrive pacing. After overdrive pacing, Purkinje cell action potential amplitude and Vmax recovered within 300 msec, yet conduction block persisted for up to 7 sec. In contrast, excitability in papillary muscle cells near the Purkinje-muscle junction increased continuously after overdrive pacing. These data suggest that rapid activation of Purkinje cells during overdrive pacing was not required for overdrive suppression of conduction and that restoration of conduction after overdrive pacing was determined primarily by recovery of excitability in papillary muscle cells. Transient Purkinje-muscle conduction block after periods of rapid ventricular rates might account for overdrive-induced conduction disturbances normally attributed to bundle branch block.     

Isolated atrial segment pacing: an alternative to His bundle pacing after atrioventricular junctional ablation.

OBJECTIVES: This study was designed to investigate a practical alternative to His bundle pacing after atrioventricular (AV) junctional ablation by pacing a small area of isolated atrial tissue surrounding the AV node. BACKGROUND: His bundle pacing is preferred after AV junctional ablation in patients with refractory atrial fibrillation. However, it is technically difficult and not clinically useful at the present time. METHODS: This study was conducted in an isolated working swine heart model (n = 5), with real-time imaging capabilities. A small area of atrial tissue surrounding the AV node and the His bundle was isolated using sequential radiofrequency ablation lesions. RESULTS: Complete AV block created by segmental atrial isolation was achieved in 5 of 5 experiments. The isolated atrial segment was bordered by the ablation lines, the tricuspid annulus, and the AV node-His bundle. The AV conduction was characterized using a pacing electrode implanted into the isolated atrial segment. Pacing from the atria, the ventricles, and the isolated atrial segment at different rates confirmed complete bidirectional block between the atria and isolated area, whereas antegrade and retrograde AV nodal conduction between the isolated atrial segment and the ventricles remained intact. Pacing from the isolated area produced minimal changes in systolic left ventricular pressure compared with baseline sinus rhythm (mean -2 mm Hg). CONCLUSIONS: Isolation of a small area of atrial tissue surrounding the AV node is feasible by transcatheter radiofrequency ablation. This procedure may be a useful alternative to conventional AV junctional ablation because it can create complete AV block, while in effect permitting the equivalent of His bundle pacing after AV junctional ablation.     

His bundle recordings in right bundle-branch block coexisting with iatrogenic right ventricular pre-excitation

Iatrogenic right ventricular pre-excitation failed to abolish right bundle-branch block in two patients. When `exclusive' His bundle pacing was performed, the QRS complexes, St-V, and St-LVE intervals were similar to the ventricular deflections, H-V, and V-LVE (intervals) recorded during sinus rhythm. `Exclusive' pacing of the ordinary muscle at the right ventricular inflow tract produced a complete left bundle-branch block pattern without abnormal left axis deviation. Pacing of both His bundle and ordinary muscle yielded combination complexes in which the right bundle-branch block pattern persisted.     

The significance of dissociation of conduction in the canine His bundle. Electrophysiological studies in vivo and in vitro

Fractionated His bundle potentials were induced by ischemia or trauma in 30 anesthetized dogs, in vivo. Functional dissociation, i.e., alteration of the activation sequence of portions of these His bundle potentials was demonstrated in vivo as well as in 10 in vitro preparations of the His-Purkinje system. In vivo, plunge wire and electrode catheters were utilized to record from portions of the His bundle. During vagal-induced slowing of the heart rate, atrial pacing or His bundle pacing, His-Purkinje conduction as measured by the H-V interval was constant over a wide range of heart rates, 50–300/min. One or two hours after anterior septal artery ligation, His bundle damage manifested as split His bundle potentials (H, H′). Atrial pacing or proximal His bundle pacing induced H-H′ delays with concomitant right or left bundle branch block patterns in ECG leads. However distal His bundle pacing at comparable or even higher rates produced normal QRS complexes. In other cases, during atrial pacing or with progressive ischemia at a constant rate, H′ progressively delayed during the H-V interval or even disappeared into the QRS complex with a concomitant occurrence of right or left bundle branch block. In vitro, a dissected septal preparation was studied containing the His bundle, proximal and distal right bundle and left bundle branches. Normal conduction throughout the His-Purkinje system was observed at pacing rates of 30–220/min. Punctate lesions, anatomically placed above the branching His bundle caused tachycardia-dependent, complete bundle branch block with concurrent temporal reversal of proximal and distal His bundle action potentials.These data suggest that ischemic or traumatic lesions in the His bundle may manifest on the electrocardiogram as bundle branch block patterns. From a clinical point of view, a critical site of lesion would markedly increase the liability for A-V block although the electrocardiogram alone would not indicate the actual site of lesion. Predestination of fiber tracts and alternative proposals to the predestination theory are considered to explain QRS aberration due to exclusive His bundle lesions.     

左束支区域起搏的现状和展望

希氏束和左束支区域的生理性起搏较右室心尖部起搏明显改善心脏的电机械同步性,改善心功能。希氏束起搏是最生理的起搏方式,而且可纠正大部分的完全性左束支传导阻滞,改善心脏再同步化,但也存在起搏阈值高、R波振幅低和潜在的希氏束远端病变风险。左束支呈扇形分布左室间隔内膜面下,起搏阈值和R波振幅同右室心尖部相似,而且左束支近端起搏可纠正病变于希氏束的左束支传导阻滞,可作为心脏再同步化治疗的备选方案。现就左束支的解剖、左束支区域起搏的电生理特点和左束支区域起搏的临床应用进行综述。     

Permanent pacing of the bundle of His after radiofrequency atrioventricular node ablation in patients with suprahisian conduction disturbances]

INTRODUCTION AND OBJECTIVES: The asynchronic contraction of the left ventricle due to left bundle branch block or right ventricular pacing is inferior from a hemodynamic point of view to the synchronic contraction through the conduction system. Several authors have reported some cases of pump failure and deterioration of mitral regurgitation after AV nodal ablation. Alternative sites of pacing such as the right ventricular outflow tract pacing have been proposed in order to avoid these complications. Direct His bundle pacing might be a new alternative for permanent pacing, however, it has not been extensively evaluated in humans yet. Our aim is to prove the feasibility of permanent His pacing in terms of stability, thresholds and pump function. PATIENTS AND METHOD: Population: patients without structural heart disease, selected for AV nodal ablation due to uncontrolled paroxysmal atrial fibrillation, or for pacemaker implantation due to supraHis conduction disturbance, with normal conduction system. An active fixation permanent lead was placed in His position using an steering guidewire and a diagnostic catheter as an anatomical reference. We also implanted a lead in the right atrial appendage and both were connected to a DDDR generator. Pacing thresholds and ecocardiographic ventricular function parameters were evaluated (ejection fraction, cavity size, mitral regurgitation). RESULTS: 12 patients met the inclusion criteria. Successful His pacing was achieved in 8 out of 12 cases (66%) with acceptable thresholds at implantation (1.24 +/- 0.13 volts at 0.5 ms) and during follow up at 3 months (1.31 +/- 0.20 volts at 0.5 ms). Neither a significant change in the ecocardiographic parameters not a deterioration in the clinical status caused by ablation or stimulation was evidenced. CONCLUSION: The His bundle may be the site of choice for long term pacing in patients with AV block and normal infraHis conduction system.     

His Bundle pacing for congenital complete AV block: An attempt to fix a broken heart?

Congenital complete atrioventricular block (CCAVB) is usually due to failure of atrioventricular nodal conduction with preservation of the His‐Purkinje system. Most patients with CCAVB ultimately require pacemaker therapy to restore physiologic heart rates, dealing with the detrimental effects of chronic right ventricular (RV) pacing on cardiac structure and function. The ideal stimulation pattern aims to mimic the normal conduction to restore electromechanical coupling, preventing the harmful effects of lack of atrioventricular and inter‐intraventricular synchrony. This can be done through conduction system pacing. Using His bundle pacing (HBP) for cardiac resynchronization therapy in two complete congenital atrioventricular block patients, we have reported better exercise tolerance and echocardiographic improvements related to reversible left ventricular dysfunction that can be corrected by restoration of the normal activation pathway via the His‐Purkinje network.     

Selective versus non-selective His bundle pacing.

His bundle pacing was achieved in 10 anaesthetized open chest dogs by stimulation from bipolar electrode catheters positioned in the aortic root and right heart. Recordings were taken directly through plunge wires from the right atrium, high ventricular septum, and epicardial sites on the right and left ventricles. Six types of response were seen during A-V junctional stimulation: (1) low atrial pacing; (2) combined atrial and His bundle pacing; (3) His bundle pacing; (4) combined atrial, ventricular septal, and His bundle pacing; (5) combined septal and His bundle pacing; and (6) ventricular pacing. Pacing of the His bundle in combination with the atrium and/or ventricular septum is designated as non-selective, whereas stimulation of the His bundle alone is considered selective pacing. Non-selective His bundle pacing can be recognized from the surface leads by changes in onset and amplitude of the QRS with appreciable T-wave alterations. Although electrode position was an important determinant of the type of pacing achieved, a variety of patterns of stimulation resulted from variation in the modalities of the pacing stimulus, ie, polarity, intensity, and duration. Unless these factors are considered, selective His bundle pacing may not be achieved.     

Novel mechanism of postinfarction ventricular tachycardia originating in surviving left posterior Purkinje fibers

BACKGROUND: Other than bundle branch reentry and interfascicular reentry, monomorphic postmyocardial infarction (post-MI) reentrant ventricular tachycardia (VT) including the His-Purkinje system has not been reported. Verapamil-sensitive idiopathic left VT includes the left posterior Purkinje fibers but develops in patients without structural heart disease. OBJECTIVES: The purpose of this study was to describe a novel mechanism of reentrant VT arising from the left posterior Purkinje fibers in patients with a prior MI. METHODS: The study consisted of four patients with a prior MI and symptomatic heart failure who underwent electrophysiologic study and catheter ablation for VT showing right bundle branch block (n = 3) or atypical left bundle branch block (n = 1) morphology with superior axis. In two patients, the VT frequently emerged during the acute phase of MI and required emergency catheter ablation. RESULTS: Clinical VT was reproducibly induced by programmed stimulation. In three patients, both diastolic and presystolic Purkinje potentials were sequentially recorded along the left ventricular posterior septum during the VT, whereas in the fourth patient, only presystolic Purkinje potentials were observed. During entrainment pacing from the right atrium, diastolic Purkinje potentials were captured orthodromically and demonstrated decremental conduction properties, whereas presystolic Purkinje potentials were captured antidromically and appeared between the His and QRS complex. Radiofrequency energy delivered at the site exhibiting a Purkinje-QRS interval of 58 +/- 26 ms successfully eliminated the VTs without provoking any conduction disturbances. CONCLUSION: Reentrant monomorphic VT originating from the left posterior Purkinje fibers, which is analogous to idiopathic left VT, can develop in the acute or chronic phase of MI. Catheter ablation is highly effective in eliminating this VT without affecting left ventricular conduction.     

Coexisting intra- and subnodal block: an unusual abnormality of atrioventricular conduction

The presence of A-V block occurring at two levels of the conducting system was demonstrated in an asymptomatic patient by means of the His bundle recordings. During sinus rhythm, first degree A-V block with complete left bundle branch block was noted, suggesting the presence of bilateral bundle branch block. His bundle recordings demonstrated the coexistence of intranodal (Wenckebach periods, Mobitz Type I) and subnodal (Mobitz Type II) block. The evidence of block below the proximal His bundle offered confirmatory evidence of bilateral bundle branch block. In spite of the abnormal antegrade conduction, there was 1:1 V-A conduction during right ventricular pacing at 110 per minute. With more rapid (130 per minute) ventricular pacing, retrograde Wenckebach periods were observed, suggesting that there was, in addition, possible impairment in retrograde conduction. This report serves to demonstrate (1) the limitations of the body surface ECG in the assessment of A-V conduction and (2) that His bundle electrograms make it possible to detect the presence of coincidental lesions at two levels of the A-V conducting system.     

Region of slow conduction in sustained ventricular tachycardia: direct endocardial recordings and functional characterization in humans

Direct endocardial recording from a discrete region of slow conduction in the left ventricle was performed in a patient during sustained ventricular tachycardia. The tachycardia had a right bundle branch block and superior axis configuration with the earliest site of endocardial activation in the posterolateral left ventricle. At this site, the left ventricular electrogram during the tachycardia displayed two deflections with distinctly different responses to rapid pacing. During rapid pacing from the right ventricular apex, one deflection was transiently entrained, representing activation of the ventricle distal to a region of slow conduction in the reentrant circuit. However, the other deflection was not entrained and arose from activation proximal to this region. At a critically rapid pacing rate, interruption of the tachycardia was associated with conduction block in the region of slow conduction, as demonstrated by dissociation of the two deflections on the posterolateral left ventricular electrogram. At pacing rates that transiently entrained but did not terminate the tachycardia, decremental properties of conduction were demonstrated in the region of slow conduction, but not in the rest of the reentrant circuit. These responses of the posterolateral left ventricular electrogram to pacing during ventricular tachycardia strongly suggest that the recordings bracketed a discrete region of slow conduction in the left ventricle that was critical for the maintenance of ventricular tachycardia. Furthermore, these data demonstrate that this region of slow conduction in the left ventricle had decremental conduction properties and was the site of block during rapid pacing at rates sufficient to interrupt the tachycardia.     

Second degree His-Purkinje block during his bundle pacing

This report presents, for the first time, clear evidence supporting the occurrence of Wenckebach and 2:1 H-V block during His bundle pacing. The simultaneous recording of various intracardiac electrograms, as well as the comparison of the effects produced by selective His bundle pacing and high right atrial pacing at the same rates, permitted the identification of conduction disturbances located distal to the paced His bundle site. This could be done although one criterion usually required to diagnose selective His bundle pacing (namely, stimulus-V intervals of constant duration) was not present.     

Manejo de la insuficiencia cardiaca con estimulación hisiana en bloqueo de rama derecha: reporte de caso

Cardiac resynchronization therapy has proven to be an effective therapy in patients with left bundle branch block and heart failure. Male, 47 years old, heart failure with a left ventricle ejection fraction of 17%, idiopathic heart failure. ECG with sinus rhythm, 1^st degree AV block, PR 400 ms, complete right bundle branch block, anterior hemi-fascicle of the left bundle of His, and QRS duration 200 ms. We decided to perform a selective His bundle pacing. In patients with right bundle branch block the biventricular cardiac resynchronization is not indicated due to low treatment response. His bundle pacing allows recruiting the blocked branch and restoring conduction throughout it, therefore, in the absence of necrosis the biventricular synchrony is achieved. We presented a case of His bundle pacing with recruitment of the right bundle branch, which reestablish biventricular synchrony measured by speckle tracking, and with a significant increase of the left ventricle ejection fraction from 17 to 36.6%, with an absolute increase of 19.6%.Key words: Cardiac resynchronization, Right bundle branch block, His bundle pacing, Heart failure, México     

Ventricular resynchronization by implementation of direct his bundle pacing in a patient with congenital complete AV block and newly diagnosed cardiomyopathy

Congenital complete atrioventricular block (CCAVB) is usually due to failure of AV nodal conduction with preservation of the His Purkinje system, typically present at birth. While most patients with CCAVB ultimately require pacemaker therapy to restore physiologic heart rates, recent studies have suggested that chronic right ventricular (RV) pacing in patients with CCAVB can have detrimental effects on cardiac structure and function, and may account for a 7-10% incidence of congestive heart failure in these patients. Since the His Purkinje system is preserved in CCAVB, this patient population could be uniquely well served by direct His bundle pacing (DHBP) which would be expected to restore physiologic activation of both ventricles. We present a case of a young woman who presented with RV pacing-induced cardiomyopathy who responded dramatically to DHBP.     

Linking: a dynamic electrophysiologic phenomenon in macroreentry circuits

The term "linking" has been used specifically to describe the mechanism for perpetuation of functional anterograde bundle branch block: namely, repetitive transseptal retrograde concealed penetration by impulses propagating along the contralateral bundle. We present selected examples that demonstrate tht linking-type phenomena actually have a wide spectrum of expression in human macroreentry circuits, particularly those incorporating either the bundle branches and His bundle or the normal pathway and Kent bundle. The examples presented are as follows: (1) persistent retrograde functional conduction delays in the His-Purkinje system during right ventricular pacing, (2) anterograde Kent bundle condution at rapid rates, dependent on prior block in the normal pathway, (3) persistent anterograde functional infra-His block of atrial impulses during rapid ventricular pacing in the presence of a retrogradely conducting accessory pathway, and (4) transient advancement of His activation with ventricular fusion complexes during overdrive ventricular pacing of bundle branch reentrant tachycardia. Based on these examples, we characterize linking as a generalized electrophysiologic phenomenon in which each successive impulse entering a macroreentry circuit propagates preferentially along one limb because of functional block in the contralateral limb resulting from the effects of the prior impulse. It is proposed that such functional block may be dynamically maintained either by repetitive impulse interference, which perpetuates local refractoriness (examples No. 1 to 3), or by repetitive impulse collision (example No. 4). The general conceptual scheme outlined can be applied to specific electrophysiologic phenomena associated with a wide variety of reentry circuits in man.     

Mechanisms by which discharge modulates diastolic depolarization in sheep and dog Purkinje fibers

For reasons unknown, a fast drive is prone to induce overdrive excitation in sheep Purkinje fibers under conditions that still induce overdrive suppression in dog Purkinje fibers. Our aim was to study by means of a microelectrode technique diastolic depolarization (DD) and its changes with overdrive in sheep and dog Purkinje fibers perfused in vitro under identical conditions. The major results are: (a) At a slow rate, diastolic depolarization is much faster and larger in sheep than in dog Purkinje fibers. (b) Faster rates increase DD slope and amplitude in sheep and decrease them in dog Purkinje fibers. (c) DD slope and amplitude increase in sheep and decrease in dog if the same number of action potentials are separated by a shorter diastole. (d) The change in DD slope and amplitude induced by a fast drive persists after a subsequent slow drive of approximately 20 s. (e) The fastest drives can induce an oscillatory potential superimposed on early DD in sheep. (f) In both species, high [Ca(2+)](o) increases and low [Ca(2+)](o) decreases DD slope and amplitude. (g) Neither high nor low [Ca(2+)](o) change the DD rate-dependence patterns peculiar to either species. (h) DD amplitude in dog in high [Ca(2+)](o) is still smaller than that in sheep in Tyrode solution. (i) Caffeine prevents the steepening of early DD by drive, but not the subsequent increase which can lead to overdrive excitation in both species. (j) TTX decreases DD slope and amplitude in both species. (k) Cs(+) markedly reduces DD slope and amplitude and more so at faster rates, especially in the sheep. We conclude that the differences in diastolic depolarization and the different behavior of DD with overdrive in the two species account for the propensity of sheep Purkinje fibers to develop overdrive excitation and for that of dog Purkinje fibers to develop overdrive suppression.     

Atrioventricular and intraventricular conduction in hyperkalemia

Twelve patients exhibited electrocardiographic evidence of fascicular block during hyperkalemia. Isolated left posterior hemiblock occurred in four, isolated left anterior hemiblock in two, right bundle branch block with left anterior hemiblock in two, right bundle branch block with left posterior hemiblock in one, left bundle branch block with abnormal left axis deviation in two and advanced atrioventricular block in one. In all seven patients with sinus rhythm the P-R interval shortened after correction of hyperkalemia. Electrophysiologic studies using His bundle recording and atrial pacing in one patient revealed intraatrial conduction delay and marked prolongation of conduction time in the His-Purkinje system. It is concluded that conduction defects in the specialized intraventricular conduction system are common in hyperkalemia and result in electrocardiographic patterns of fascicular block.     

Tachycardia- and bradycardia-dependent atrioventricular block: observations regarding the mechanism of block

A case of paroxysmal bradycardia- and tachycardia-dependent atrioventricular (AV) block is described in a patient with right bundle branch block. The His bundle recordings demonstrated the site of the AV block to be distal to the His bundle recording site (probably in the left bundle branch). Whereas AV block distal to the His bundle occurred at an atrial paced cycle length of 700 ms, intact ventriculoatrial (VA) conduction was present up to a ventricular paced cycle length of 400 ms. Resumption of AV conduction was dependent on a critical HH or RH (in case of escapes) interval. These findings suggest that the bradycardia-dependent block is related to a time-dependent decrease in the amplitude of the current intensity of the proximal segment during late diastole. Spontaneous diastolic depolarization during late diastole resulted in impaired anterograde (AV) conduction but facilitated retrograde (VA) conduction. These findings are consistent with experimental "in vitro" observation in the sucrose gap model of AV block.     

Wolff-Parkinson-White syndrome type B and left bundle-branch block: electrophysiologic and radionuclide study

Coinciding left bundle-branch block and Wolff-Parkinson-White syndrome type B, a very rare electrocardiographic occurrence, was found in a patient with dilated cardiomyopathy. Electrophysiologic study revealed eccentric retrograde atrial activation during ventricular pacing, suggesting right-sided accessory pathway. At programmed atrial pacing, effective refractory period of the accessory pathway was 310 ms; at shorter pacing coupling intervals, normal atrioventricular conduction with left bundle-branch block was seen. Left bundle-branch block was seen also with His bundle pacing. Radionuclide phase imaging demonstrated right ventricular phase advance and left ventricular phase delay; both right and left ventricular phase images revealed broad phase distribution histograms. Combined electrophysiologic and radionuclide investigations are useful to disclose complex conduction abnormalities and their mechanical correlates.     

Studies on overdrive stimulation of canine cardiac Purkinje fibers: maximal diastolic potential as a determinant of the response

The effects of overdrive stimulation were studied on preparations of isolated canine cardiac Purkinje fibers using standard microelectrode techniques. Preparations were made from false tendons, the subendocardial right bundle branch and 24 hour infarct zone Purkinje fibers. Three types of automaticity were recognized: high potential automaticity occurred in fibers with maximal diastolic potentials greater than -70 mV, intermediate potential automaticity occurred in fibers with maximal diastolic potentials between -61 and -70 mV and low potential automaticity occurred in fibers with maximal diastolic potentials less than -60 mV. Short periods of overdrive (15 seconds or 30 beats) resulted in marked suppression of high potential automaticity, slight suppression of intermediate potential automaticity and little or no suppression of low potential automaticity. The extent of postoverdrive suppression of intermediate potential automaticity was related to the rate and duration of the overdrive train and the amount of hyperpolarization that occurred in the pacemaker fiber. Finally, in three experiments on Purkinje fibers from 24 hour infarct zones, delayed afterdepolarizations occurred. In two of these preparations, overdrive stimulation resulted in biphasic responses (postoverdrive enhancement followed by postoverdrive suppression). The results of this study suggest that it may be possible to design simple electrophysiologic tests to determine whether an automatic arrhythmia is being caused by normal or partially depolarized ectopic pacemakers.