- Email: [email protected]
His bundle pacing: Initial experience and lessons learned
Available online at www.sciencedirect.com
ScienceDirect Journal of Electrocardiology 49 (2016) 658 – 663 www.jecgonline.com
Review
His bundle pacing: Initial experience and lessons learned Amrish Deshmukh, MD, a Pramod Deshmukh, MD b,⁎ a
Abstract
Department of Medicine, University of Chicago, 5841 S. Maryland Avenue, MC 6092, Chicago, IL b Arrhythmia Center, Robert Packer Hospital, 1 Guthrie Square, Sayre, PA
Direct His bundle pacing provides the most physiologic means of artificial pacing of the ventricles with a preserved His-Purkinje system and may play a role in patients with a diseased intrinsic conduction system. We describe our initial motivations and experience with permanent direct His bundle pacing and important lessons learned since that time. © 2016 Published by Elsevier Inc.
Motivation and first experience The relationship between the activation sequence of the ventricles and its contractile function was first described by Wiggers in 1925 [1]. In this pioneering study, it was demonstrated that artificial stimulation of the ventricles resulted in altered cardiac activation and impaired systolic function when compared to the rapid multisite excitation coordinated by the native His-Purkinje system [1–3]. That the alteration in the sequence of ventricular activation influences ventricular performance was clearly demonstrated by the experimental study by Kosowsky et al. compared His bundle versus RV apical pacing at different AV intervals. They demonstrated that at any P-R interval, ventricular function (LV peak pressure, LV dp/dt and aortic flow were significant greater with His bundle pacing than with pacing from the RV apex [4]. These differences were well understood by cardiac physiologists and was summarized as such by Drs. N Levy and PJ Martin in their chapter titled “Cardiac excitation and contraction” in their cardiac physiology textbook, edited by Dr. AC Guyton (1974) [5]. They cite numerous other papers to bolster their conclusion and to point out the practical significance of this information to the then “widespread” use of artificial pacemakers. For example, in 1971 a study demonstrated biventricular pacing improved force generation of the ventricles when compared to right ventricular pacing [6]. At the time when we first performed permanent selective or direct His-bundle pacing (DHBP), evidence was also mounting that long term right ventricular pacing induced altered myocardial perfusion and contractile dysfunction [7,8]. In order to avoid the deleterious consequences of right
ventricular pacing, it was our practice to prolong programmed atrioventricular delays and avoid rate responsive pacing so as to minimize ventricular pacing and utilize the native His-Purkinje activation system. However, in patients with atrioventricular nodal disease this approach could compromise atrioventricular synchrony [9]. Pacemaker modes to directly minimize ventricular pacing were only developed several years later [10,11]. Therefore the impetus for avoiding artificial pacing or developing a more physiologic mode of pacing was clear. DHBP clearly qualified as the most physiologic ventricular pacing mode and was first demonstrated in canines by Scherlag et al. [12,13]. Subsequently, temporary transcatheter DHBP was demonstrated in humans and stable models of transcatheter DHBP were developed in canines [14,15]. In our initial experience reported at the Heart Rhythm Society in 1995, we were presented with a patient who had atrial fibrillation and severely decompensated cardiomyopathy. At this time tachycardia induced cardiomyopathy was a well described entity [16,17]. In addition, rate control of AF via AV node ablation and pacemaker placement had been associated with improved functional outcomes and improvement of cardiomyopathy [18–22]. Therefore, DHBP was attempted with AV node ablation in order to achieve rate control with preservation of the native conduction system. The patient had acute improvement in hemodynamic status with liberation from inotropes and had reversal of cardiomyopathy in longer follow up. We subsequently published the first series of permanent DHBP in a cohort of similar patients [23].
Procedural experience ⁎ Corresponding author. E-mail addresses: [email protected], Seck_pat@ guthrie.com http://dx.doi.org/10.1016/j.jelectrocard.2016.07.005 0022-0736/© 2016 Published by Elsevier Inc.
Our initial experience in permanent DHBP was guided by anatomy, prior animal studies, and standard techniques for mapping and temporary pacing of the His bundle. As a single
A. Deshmukh, P. Deshmukh / Journal of Electrocardiology 49 (2016) 658–663
659
tricuspid annulus and position the catheter superior to the AV septum (Fig. 1). Once the His bundle was localized and a pacing site which satisfied the criteria below was identified in proximity to the mapped location, lead placement was performed. In order to optimize anatomic selectivity during lead placement, a “Sweet-Tip” non-retractable screw in lead was utilized. In order to minimize the turns required within the pacing lead, it was preferentially introduced via the right subclavian vein. Targeting of the His bundle was further optimized via modification of a preformed J-stylet in which the short and distal limb of the J was modified with an out of the plane bend oriented superiorly and anteriorly. In patients with an enlarged right atrium, the width of the turn in the J-stylet was widened so as to facilitate placement at the His bundle (Fig. 1). Criteria for DHBP Fig. 1. Fluoroscopic visualization of initial approach to direct His-bundle pacingRight anterior oblique projection of right femoral access hexapolar mapping catheter and right subclavian access permanent pacemaker leadAbbreviations: PPM-L, permanent pacemaker lead; Hx-map, mapping hexapolar catheter; AbL-Cath, ablation catheter.
The criteria developed for DHBP in humans were based on those set out by Scherlag et al. based on studies in canines and the known electrophysiologic properties of the His bundle. [23–25]:
operator and based on the anatomy of the His bundle, access was obtained via right femoral and right subclavian venipuncture. This approach minimizes the need for repositioning the patient and the number of turns made by the pacing lead. Mapping of this His bundle was performed by a hexapolar catheter with 2 mm inter-electrode spacing using the distal electrode pair. Mapping was performed in the right anterior oblique projection to best visualize the
1. His-Purkinje mediated cardiac activation as evidence by a concordance with native QRS and T wave complexes on 12-lead electrocardiogram. 2. An identical pace-ventricular and His-ventricular interval over a wide range of range of pacing rates. 3. All-or-none capture as demonstrated by the absence of QRS widening with sequentially lower pacing output with abrupt loss of capture (Fig. 2).
Fig. 2. Criteria 3 – Direct His-bundle pacing demonstrates all or none capturePacing at the His bundle demonstrates all or none capture. Pacing amplitude is decreased until the 5th stimulus which leads to complete loss of capture.
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The third criteria were added to define DHBP in addition to previously proposed definitions on the basis that the His bundle demonstrates electrical isolation and histological properties similar to nervous tissue which possess all-or-none excitation [24]. Further, as initially described, criteria 1 and 2 lack anatomic specificity – at a given pacing site which satisfies only these criteria, a change in the pacing amplitude, duration or polarity may alter the paced morphology [24,26]. An abrupt loss of capture in modifying these parameters excludes the capture of the His bundle via the atria or ventricles [23,26]. The specificity of these criteria has been validated since our initial experience [26]. Lessons learned Since our initial experience, our group and others have developed several important concepts related to DHBP which are highlighted below: 1. Non-selective His-bundle and para-Hisian pacing: based on the definition of DHBP, the terms para-Hisian pacing and non-selective His-bundle pacing are readily interpretable. So called para-Hisian or pacing refers to pacing with capture of the right ventricle in anatomic proximity to the His bundle [26–28]. Pacing at such anatomic sites may lead to non-selective indirect His bundle capture at high thresholds but will not satisfy criteria 3 (Figs. 2, 3, 4). Indeed at lower thresholds, para-Hisian pacing leads to a wide complex surface EKG and delayed activation of the ventricles [26–28]. We therefore prefer to
avoid the term para-Hisian pacing when referring to non-selective indirect His bundle pacing. Conversely, in patients with DHBP, higher pacing thresholds may lead to indirect capture of the ventricle causing QRS widening (Fig. 3). Since our initial experience it has been confirmed that DHBP in fact anatomically correlates to lead placement at the His bundle via a path on the atrial side of the tricuspid valve [29]. 2. Reversal of bundle branch blocks (BBB) and cardiac resynchronization therapy (CRT) with DHBP: as early as 1978 it had been demonstrated that distal His pacing at increased thresholds could restore a narrow QRS complex in canine models of BBB [30]. These investigators excluded the possibility of indirect ventricular capture via recording ventricular signals in the high septum. Therefore, DHBP may overcome so called functional longitudinal dissociation within the proximal His-Purkinje system or can occur distal to areas of block within the AV node and His bundle which would otherwise result in BBB [30]. In our own initial experience with DHBP we encountered this phenomenon as in Fig. 5 [25]. This finding has since been replicated by multiple authors [31–35]. DHBP may serve as an alternative and potentially superior mode of CRT compared to epicardial left ventricular pacing in patients with proximal His-Purkinje dysfunction. We examined this possibility in a group of patients requiring AV node ablation for persistent atrial fibrillation by directly comparing cardiac function under RV pacing, traditional CRT, and DHBP. DHBP provided the narrowest QRS and greatest improvement in LVEF [36].
Fig. 3. Narrowing of QRS complex and complete loss of capture with direct His bundle pacingAt high pacing thresholds, pacing leads localized to the His bundle may capture the ventricle indirectly. Here, higher pacing thresholds at stimuli 1–4 leads to a widened QRS. In the 5th and 6th stimuli, pacing at a lower threshold results in direct His bundle capture with a QRS similar to the native QRS complex. At an even lower pacing threshold in the 7th stimulus, there is a complete loss of capture.
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Fig. 4. Indirect capture of the His bundle does not demonstrate all or none captureThis is an example of indirect His bundle capture from a site anatomically removed from the His bundle. With decreasing pacing thresholds, the QRS widens (5th stimulus), implying a non-His site of capture.
3. DHBP as an alternative to CRT in patients with obligate ventricular pacing. Based on evidence of the deleterious consequences of right ventricular pacing, concurrent epicardial left ventricular pacing is currently recommended in patients requiring a high burden of ventricular pacing [37]. Our practice has been to perform DHBP in such patients with narrow baseline
QRS with an additional right ventricular lead for ventricular sensing and back up pacing (Fig. 6) [38]. 4. DHBP can be combined with LV epicardial pacing in patients with left BBB. In patients who do not have reversal of their LBBB with DHBP, cardiac resynchronization can still be performed with a combination of DHBP and LV epicardial pacing via the traditional coronary sinus
Fig. 5. Correction of bundle branch blocks with direct His bundle pacingDirect His bundle pacing in this patient leads to partial reversal of a right bundle branch block with a narrowing in the QRS morphologyAbbreviations: RBBB, right bundle branch block; DHBP, direct His bundle pacing.
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Fig. 6. Direct His bundle pacing in a patient with atrioventricular nodal dysfunction allows shortening of the atrioventricular delay without widening of the QRS
lead. This mode of pacing utilizes the native conduction system to the maximum degree. Recent work has demonstrated that DHPB and LV epicardial pacing provide improved systolic function beyond traditional CRT [39]. References [1] Wiggers CJ. The muscular reactions of the mammalian ventricles to artificial surface stimuli. Am J Physiol 1925;73:346–78. [2] Lewis T, Rothschild MA. The excitatory process in the Dog's heart. Part II. The ventricles. Biol Sci 1915;206:181–226. [3] Durrer D, van Dam RT, Freud GE, Janse MJ, Meijler FL, Arzbaecher RC. Total excitation of the isolated human heart. Circulation 1970;41:899–912. [4] Kosowsky BD, Scherlag BJ, Damato AN. Re-evaluation of the atrial contribution to ventricular function: Study using His bundle pacing. Am J Cardiol 1968;21:518–24. [5] Guyton AC. Function of the human body. Saunders; 1974. [6] Gibson DG, Chamberlain DA, Coltart DJ, Mercer J. Effect of changes in ventricular activation on cardiac haemodynamics in man. Comparison of right ventricular, left ventricular, and simultaneous pacing of both ventricles. Br Heart J 1971;33:397–400. [7] Lee MA, Dae MW, Langberg JJ, Griffin JC, Chin MC, Finkbeiner WE, et al. Effects of long-term right ventricular apical pacing on left ventricular perfusion, innervation, function and histology. J Am Coll Cardiol 1994;24:225–32. [8] Tse H-F, Lau C-P. Long-term effect of right ventricular pacing on myocardial perfusion and function. J Am Coll Cardiol 1997;29:744–9, http://dx.doi.org/10.1016/S0735-1097(96)00586-4. [9] Rosenqvist M, Isaaz K, Botvinick EH, Dae MW, Cockrell J, Abbott JA, et al. Relative importance of activation sequence compared to atrioventricular synchrony in left ventricular function. Am J Cardiol 1991;67:148–56. [10] Gillis AM, Pürerfellner H, Israel CW, Sunthorn H, Kacet S, Anelli-Monti M, et al. Reducing unnecessary right ventricular pacing with the managed ventricular pacing mode in patients with sinus node disease and AV block. Pacing Clin Electrophysiol 2006;29:697–705, http://dx.doi.org/ 10.1111/j.1540-8159.2006.00422.x. [11] Sweeney MO, Shea JB, Fox V, Adler S, Nelson L, Mullen TJ, et al. Randomized pilot study of a new atrial-based minimal ventricular pacing mode in dual-chamber implantable cardioverter-defibrillators. Heart Rhythm 2004;1:160–7, http://dx.doi.org/10.1016/j.hrthm.2004.03.059. [12] Scherlag BJ, Kosowsky BD, Damato AN. A technique for ventricular pacing from the His bundle of the intact heart. J Appl Physiol 1967;22:584–7.
[13] Scherlag BJ, Helfant RH, Damato AN. A catheterization technique for His bundle stimulation and recording in the intact dog. J Appl Physiol 1968;25:425–8. [14] Narula OS, Scherlag BJ, Samet P. Pervenous pacing of the specialized conducting system in man: His bundle and A-V nodal stimulation. Circulation 1970;41:77–87, http://dx.doi.org/10.1161/01.CIR.41.1.77. [15] Mabo P, Scherlag BJ, Munsif A, Otomo K, Lazzara R. A technique for stable His-bundle recording and pacing: electrophysiological and hemodynamic correlates. Pacing Clin Electrophysiol 1995;18:1894–901, http:// dx.doi.org/10.1111/j.1540-8159.1995.tb03838.x. [16] Packer DL, Bardy GH, Worley SJ, Smith MS, Cobb FR, Coleman RE, et al. Tachycardia-induced cardiomyopathy: A reversible form of left ventricular dysfunction. Am J Cardiol 1986;57:563–70, http:// dx.doi.org/10.1016/0002-9149(86)90836-2. [17] Lemery R, Brugada P, Cheriex E, Wellens HJ. Reversibility of tachycardia-induced left ventricular dysfunction after closed-chest catheter ablation of the atrioventricular junction for intractable atrial fibrillation. Am J Cardiol 1987;60:1406–8. [18] Kay GN, Bubien RS, Epstein AE, Plumb VJ. Effect of catheter ablation of the atrioventricular junction on quality of life and exercise tolerance in paroxysmal atrial fibrillation. Am J Cardiol 1988;62:741–4. [19] Grogan M, Smith HC, Gersh BJ, Wood DL. Left ventricular dysfunction due to atrial fibrillation in patients initially believed to have idiopathic dilated cardiomyopathy. Am J Cardiol 1992;69:1570–3. [20] Cruz FE, Cheriex EC, Smeets JL, Atié J, Peres AK, Penn OC, et al. Reversibility of tachycardia-induced cardiomyopathy after cure of incessant supraventricular tachycardia. J Am Coll Cardiol 1990;16:739–44. [21] Langberg JJ, Chin MC, Rosenqvist M, Cockrell J, Dullet N, Van Hare G, et al. Catheter ablation of the atrioventricular junction with radiofrequency energy. Circulation 1989;80:1527–35. [22] Fitzpatrick AP, Kourouyan HD, Siu A, Lee RJ, Lesh MD, Epstein LM, et al. Quality of life and outcomes after radiofrequency His-bundle catheter ablation and permanent pacemaker implantation: Impact of treatment in paroxysmal and established atrial fibrillation. Am Heart J 1996;131:499–507. [23] Deshmukh P, Casavant DA, Romanyshyn M, Anderson K. Permanent, direct His-bundle pacing : A novel approach to cardiac pacing in patients with normal His-Purkinje activation. Circulation 2000;101:869–77, http://dx.doi.org/10.1161/01.CIR.101.8.869. [24] Williams DO, Scherlag BJ, Hope RR, El-Sherif N, Lazzara R, Samet P. Selective versus non-selective His bundle pacing. Cardiovasc Res 1976;10:91–100, http://dx.doi.org/10.1093/cvr/10.1.91. [25] Deshmukh PM, Romanyshyn M. Direct His-bundle pacing: present and future. Pacing Clin Electrophysiol 2004;27:862–70, http:// dx.doi.org/10.1111/j.1540-8159.2004.00548.x.
A. Deshmukh, P. Deshmukh / Journal of Electrocardiology 49 (2016) 658–663 [26] Cantù F, De Filippo P, Cardano P, De Luca A, Gavazzi A. Validation of criteria for selective His bundle and Para-hisian permanent pacing. Pacing Clin Electrophysiol 2006;29:1326–33, http://dx.doi.org/ 10.1111/j.1540-8159.2006.00543.x. [27] Strasberg B, Swiryn S, Rosen KM. Endocardial mapping of a Para-hisian PVC. Chest 1982;81:239–41, http://dx.doi.org/10.1378/chest.81.2.239. [28] Hirao K, Otomo K, Wang X, Beckman KJ, McClelland JH, Widman L, et al. Para-hisian pacing: A new method for differentiating retrograde conduction over an accessory AV pathway from conduction over the AV node. Circulation 1996;94:1027–35, http://dx.doi.org/10.1161/01.CIR.94.5.1027. [29] Correa de Sa DD, Hardin NJ, Crespo EM, Nicholas KB, Lustgarten DL. Autopsy analysis of the implantation site of a permanent selective direct his bundle pacing lead. Circ Arrhythm Electrophysiol 2012;5:244–6, http://dx.doi.org/10.1161/CIRCEP.111.968834. [30] El-Sherif N, Amay-Y-Leon F, Schonfield C, Scherlag BJ, Rosen K, Lazzara R, et al. Normalization of bundle branch block patterns by distal His bundle pacing. Clinical and experimental evidence of longitudinal dissociation in the pathologic his bundle. Circulation 1978;57:473–83, http://dx.doi.org/10.1161/01.CIR.57.3.473. [31] Barba-Pichardo R, Manovel Sánchez A, Fernández-Gómez JM, Moriña-Vázquez P, Venegas-Gamero J, Herrera-Carranza M. Ventricular resynchronization therapy by direct His-bundle pacing using an internal cardioverter defibrillator. Europace 2013;15:83–8, http://dx.doi.org/10.1093/europace/eus228. [32] Dabrowski P, Kleinrok A, Kozluk E, Opolski G. Physiologic resynchronization therapy: A case of his bundle pacing reversing physiologic conduction in a patient with CHF and LBBB during 2 years of observation. J Cardiovasc Electrophysiol 2011;22:813–7, http://dx.doi.org/10.1111/j.1540-8167.2010.01949.x.
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[33] Lustgarten DL, Calame S, Crespo EM, Calame J, Lobel R, Spector PS. Electrical resynchronization induced by direct His-bundle pacing. Hear Rhythm 2010, http://dx.doi.org/10.1016/j.hrthm.2009.09.066. [34] Manovel A, Barba-Pichardo R, Tobaruela A. Electrical and mechanical cardiac resynchronisation by novel direct his-bundle pacing in a heart failure patient. Heart Lung Circ 2011;20:769–72, http://dx.doi.org/ 10.1016/j.hlc.2011.05.617. [35] Moriña-Vázquez P, Barba-Pichardo R, Venegas-Gamero J, Herrera-Carranza M. Cardiac resynchronization through selective His bundle pacing in a patient with the so-called InfraHis atrioventricular block. Pacing Clin Electrophysiol 2005;28:726–9, http://dx.doi.org/10.1111/j.15408159.2005.00150.x. [36] Deshmukh P, Deshmukh A, Romanyshyn M, Anderson K, Lahoda D, Lambert P. BZ. Comparison of direct His-bundle and biventricular pacing. Hear Rhythm 2009;6:S362–90, http://dx.doi.org/10.1016/ j.hrthm.2009.03.043. [37] Epstein AE, DiMarco JP, Ellenbogen KA, Estes NAM, Freedman RA, Gettes LS, et al. ACC/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities. Hear Rhythm 2008;5:934–55, http://dx.doi.org/10.1016/j.hrthm.2008.04.015. [38] Deshmukh P, Deshmukh A, Romanyshyn M, Anderson K. Direct His bundle triple site pacing: A novel alternative to biventricular pacing. Hear Rhythm 2009;6:S1–54, http://dx.doi.org/10.1016/ j.hrthm.2009.03.032. [39] Padeletti L, Pieragnoli P, Ricciardi G, Innocenti L, Checchi L, Padeletti M, et al. Simultaneous His bundle and left ventricular pacing for optimal cardiac resynchronization therapy delivery: Acute hemodynamic assessment by pressure-volume loops. Circ Arrhythm Electrophysiol 2016;9, http://dx.doi.org/10.1161/CIRCEP.115.003793.
ScienceDirect Journal of Electrocardiology 49 (2016) 658 – 663 www.jecgonline.com
Review
His bundle pacing: Initial experience and lessons learned Amrish Deshmukh, MD, a Pramod Deshmukh, MD b,⁎ a
Abstract
Department of Medicine, University of Chicago, 5841 S. Maryland Avenue, MC 6092, Chicago, IL b Arrhythmia Center, Robert Packer Hospital, 1 Guthrie Square, Sayre, PA
Direct His bundle pacing provides the most physiologic means of artificial pacing of the ventricles with a preserved His-Purkinje system and may play a role in patients with a diseased intrinsic conduction system. We describe our initial motivations and experience with permanent direct His bundle pacing and important lessons learned since that time. © 2016 Published by Elsevier Inc.
Motivation and first experience The relationship between the activation sequence of the ventricles and its contractile function was first described by Wiggers in 1925 [1]. In this pioneering study, it was demonstrated that artificial stimulation of the ventricles resulted in altered cardiac activation and impaired systolic function when compared to the rapid multisite excitation coordinated by the native His-Purkinje system [1–3]. That the alteration in the sequence of ventricular activation influences ventricular performance was clearly demonstrated by the experimental study by Kosowsky et al. compared His bundle versus RV apical pacing at different AV intervals. They demonstrated that at any P-R interval, ventricular function (LV peak pressure, LV dp/dt and aortic flow were significant greater with His bundle pacing than with pacing from the RV apex [4]. These differences were well understood by cardiac physiologists and was summarized as such by Drs. N Levy and PJ Martin in their chapter titled “Cardiac excitation and contraction” in their cardiac physiology textbook, edited by Dr. AC Guyton (1974) [5]. They cite numerous other papers to bolster their conclusion and to point out the practical significance of this information to the then “widespread” use of artificial pacemakers. For example, in 1971 a study demonstrated biventricular pacing improved force generation of the ventricles when compared to right ventricular pacing [6]. At the time when we first performed permanent selective or direct His-bundle pacing (DHBP), evidence was also mounting that long term right ventricular pacing induced altered myocardial perfusion and contractile dysfunction [7,8]. In order to avoid the deleterious consequences of right
ventricular pacing, it was our practice to prolong programmed atrioventricular delays and avoid rate responsive pacing so as to minimize ventricular pacing and utilize the native His-Purkinje activation system. However, in patients with atrioventricular nodal disease this approach could compromise atrioventricular synchrony [9]. Pacemaker modes to directly minimize ventricular pacing were only developed several years later [10,11]. Therefore the impetus for avoiding artificial pacing or developing a more physiologic mode of pacing was clear. DHBP clearly qualified as the most physiologic ventricular pacing mode and was first demonstrated in canines by Scherlag et al. [12,13]. Subsequently, temporary transcatheter DHBP was demonstrated in humans and stable models of transcatheter DHBP were developed in canines [14,15]. In our initial experience reported at the Heart Rhythm Society in 1995, we were presented with a patient who had atrial fibrillation and severely decompensated cardiomyopathy. At this time tachycardia induced cardiomyopathy was a well described entity [16,17]. In addition, rate control of AF via AV node ablation and pacemaker placement had been associated with improved functional outcomes and improvement of cardiomyopathy [18–22]. Therefore, DHBP was attempted with AV node ablation in order to achieve rate control with preservation of the native conduction system. The patient had acute improvement in hemodynamic status with liberation from inotropes and had reversal of cardiomyopathy in longer follow up. We subsequently published the first series of permanent DHBP in a cohort of similar patients [23].
Procedural experience ⁎ Corresponding author. E-mail addresses: [email protected], Seck_pat@ guthrie.com http://dx.doi.org/10.1016/j.jelectrocard.2016.07.005 0022-0736/© 2016 Published by Elsevier Inc.
Our initial experience in permanent DHBP was guided by anatomy, prior animal studies, and standard techniques for mapping and temporary pacing of the His bundle. As a single
A. Deshmukh, P. Deshmukh / Journal of Electrocardiology 49 (2016) 658–663
659
tricuspid annulus and position the catheter superior to the AV septum (Fig. 1). Once the His bundle was localized and a pacing site which satisfied the criteria below was identified in proximity to the mapped location, lead placement was performed. In order to optimize anatomic selectivity during lead placement, a “Sweet-Tip” non-retractable screw in lead was utilized. In order to minimize the turns required within the pacing lead, it was preferentially introduced via the right subclavian vein. Targeting of the His bundle was further optimized via modification of a preformed J-stylet in which the short and distal limb of the J was modified with an out of the plane bend oriented superiorly and anteriorly. In patients with an enlarged right atrium, the width of the turn in the J-stylet was widened so as to facilitate placement at the His bundle (Fig. 1). Criteria for DHBP Fig. 1. Fluoroscopic visualization of initial approach to direct His-bundle pacingRight anterior oblique projection of right femoral access hexapolar mapping catheter and right subclavian access permanent pacemaker leadAbbreviations: PPM-L, permanent pacemaker lead; Hx-map, mapping hexapolar catheter; AbL-Cath, ablation catheter.
The criteria developed for DHBP in humans were based on those set out by Scherlag et al. based on studies in canines and the known electrophysiologic properties of the His bundle. [23–25]:
operator and based on the anatomy of the His bundle, access was obtained via right femoral and right subclavian venipuncture. This approach minimizes the need for repositioning the patient and the number of turns made by the pacing lead. Mapping of this His bundle was performed by a hexapolar catheter with 2 mm inter-electrode spacing using the distal electrode pair. Mapping was performed in the right anterior oblique projection to best visualize the
1. His-Purkinje mediated cardiac activation as evidence by a concordance with native QRS and T wave complexes on 12-lead electrocardiogram. 2. An identical pace-ventricular and His-ventricular interval over a wide range of range of pacing rates. 3. All-or-none capture as demonstrated by the absence of QRS widening with sequentially lower pacing output with abrupt loss of capture (Fig. 2).
Fig. 2. Criteria 3 – Direct His-bundle pacing demonstrates all or none capturePacing at the His bundle demonstrates all or none capture. Pacing amplitude is decreased until the 5th stimulus which leads to complete loss of capture.
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The third criteria were added to define DHBP in addition to previously proposed definitions on the basis that the His bundle demonstrates electrical isolation and histological properties similar to nervous tissue which possess all-or-none excitation [24]. Further, as initially described, criteria 1 and 2 lack anatomic specificity – at a given pacing site which satisfies only these criteria, a change in the pacing amplitude, duration or polarity may alter the paced morphology [24,26]. An abrupt loss of capture in modifying these parameters excludes the capture of the His bundle via the atria or ventricles [23,26]. The specificity of these criteria has been validated since our initial experience [26]. Lessons learned Since our initial experience, our group and others have developed several important concepts related to DHBP which are highlighted below: 1. Non-selective His-bundle and para-Hisian pacing: based on the definition of DHBP, the terms para-Hisian pacing and non-selective His-bundle pacing are readily interpretable. So called para-Hisian or pacing refers to pacing with capture of the right ventricle in anatomic proximity to the His bundle [26–28]. Pacing at such anatomic sites may lead to non-selective indirect His bundle capture at high thresholds but will not satisfy criteria 3 (Figs. 2, 3, 4). Indeed at lower thresholds, para-Hisian pacing leads to a wide complex surface EKG and delayed activation of the ventricles [26–28]. We therefore prefer to
avoid the term para-Hisian pacing when referring to non-selective indirect His bundle pacing. Conversely, in patients with DHBP, higher pacing thresholds may lead to indirect capture of the ventricle causing QRS widening (Fig. 3). Since our initial experience it has been confirmed that DHBP in fact anatomically correlates to lead placement at the His bundle via a path on the atrial side of the tricuspid valve [29]. 2. Reversal of bundle branch blocks (BBB) and cardiac resynchronization therapy (CRT) with DHBP: as early as 1978 it had been demonstrated that distal His pacing at increased thresholds could restore a narrow QRS complex in canine models of BBB [30]. These investigators excluded the possibility of indirect ventricular capture via recording ventricular signals in the high septum. Therefore, DHBP may overcome so called functional longitudinal dissociation within the proximal His-Purkinje system or can occur distal to areas of block within the AV node and His bundle which would otherwise result in BBB [30]. In our own initial experience with DHBP we encountered this phenomenon as in Fig. 5 [25]. This finding has since been replicated by multiple authors [31–35]. DHBP may serve as an alternative and potentially superior mode of CRT compared to epicardial left ventricular pacing in patients with proximal His-Purkinje dysfunction. We examined this possibility in a group of patients requiring AV node ablation for persistent atrial fibrillation by directly comparing cardiac function under RV pacing, traditional CRT, and DHBP. DHBP provided the narrowest QRS and greatest improvement in LVEF [36].
Fig. 3. Narrowing of QRS complex and complete loss of capture with direct His bundle pacingAt high pacing thresholds, pacing leads localized to the His bundle may capture the ventricle indirectly. Here, higher pacing thresholds at stimuli 1–4 leads to a widened QRS. In the 5th and 6th stimuli, pacing at a lower threshold results in direct His bundle capture with a QRS similar to the native QRS complex. At an even lower pacing threshold in the 7th stimulus, there is a complete loss of capture.
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Fig. 4. Indirect capture of the His bundle does not demonstrate all or none captureThis is an example of indirect His bundle capture from a site anatomically removed from the His bundle. With decreasing pacing thresholds, the QRS widens (5th stimulus), implying a non-His site of capture.
3. DHBP as an alternative to CRT in patients with obligate ventricular pacing. Based on evidence of the deleterious consequences of right ventricular pacing, concurrent epicardial left ventricular pacing is currently recommended in patients requiring a high burden of ventricular pacing [37]. Our practice has been to perform DHBP in such patients with narrow baseline
QRS with an additional right ventricular lead for ventricular sensing and back up pacing (Fig. 6) [38]. 4. DHBP can be combined with LV epicardial pacing in patients with left BBB. In patients who do not have reversal of their LBBB with DHBP, cardiac resynchronization can still be performed with a combination of DHBP and LV epicardial pacing via the traditional coronary sinus
Fig. 5. Correction of bundle branch blocks with direct His bundle pacingDirect His bundle pacing in this patient leads to partial reversal of a right bundle branch block with a narrowing in the QRS morphologyAbbreviations: RBBB, right bundle branch block; DHBP, direct His bundle pacing.
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Fig. 6. Direct His bundle pacing in a patient with atrioventricular nodal dysfunction allows shortening of the atrioventricular delay without widening of the QRS
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