Septal His-Purkinje Ventricular Pacing in Canines: A New Endocardial Electrode Approach

Septal His-Purkinje Ventricular Pacing in Canines: A New Endocardial Electrode Approach PETER P. KARPAWICH, JAMES GATES, and KENNETH B. STOKES From the Section of Cardiology, Children's Hospital of Michigan, and the Wayne State University School of Medicine, Detroit, Michigan KARPAWICH, P.P., ET AL.: Septal His-Purkinje Ventricular Pacing in Canines: A New Endocardial Elec-

trode Approach. Ventricular activation sequences and cardiac performance are influenced hy pacing sites. Stimulation of or close to the specialized atrioventricuJar (AV) conduction system optimizes paced ventricular /unction compared to alternative epi- or endocardial muscle conduction sites. This study reports a new endocardia] electrode impJant approach to approximate septal His-Purkinje ventricular pacing. Five 6-month-oId beagles were used. A custom, platinum-iridium, exposed heJicaJ screw electrode (Medtronic, Inc.], 4.5-mm long, with a 17.8-mm^ surface area, was designed with a polyurethane covered 4 /i]ar MP35N niclde conducfor Jead. An 8 French sheath (USCI, Inc.] was modified as introducer to permit simultaneous implant intracardiac pressure and electrogram recordings. Following a thoracotomy, the introducer was inserted through the right atrial appendage and advanced to record optimal Hisbundle electrogram while maintaining atrial pressure along the septal tricuspid valve annulus. After electrode implant, ECG demonstrated narrow paced QRS morphology. Mean implant values showed sensed R wave 6.3 mV, slew rate 0.65 V/sec, pacing impedance 319 ohms, and threshold 0.9 Vf3.3 mA at 0.5-msec output. Necropsy showed implant above (he tricuspid annulus with electrode extension into and contained within Ihe proximal ventricular septum. This study demonstrates that an endocardia! seplal approach to His-Purkinje ventricular pacing fo optimize paced ventricular/unction is feasible with a new electrode design and precise septa! implant technique. Alternative introducer designs may permit tranvenous application of this approach. (PACE, Vol. 15, November, Part U 1992) His-Purkinje, pacing, septum, electrode, implant

Introduction Compared with atrial pacing, cardiac performance with ventricular stimulation is limited by lack of any consistent atrial contribution to ventricular filling and asynchronous left and right chamber contraction. Ventricular stimulation utilizing the septal His-Purkinje specialized conduction system improves cardiac function hy permitting nearly simultaneous biventricular activation and normal muscle contraction sequences.'"**

Address for reprints: Peter P. Karpawich. M.D., Pediatric Cardiology, Children's Hospital of Michigan. 3901 BeauhienBlvd., Detroit, MI 48201.

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Electrical excitation from alternative cardiac muscle pacing sites produces abnormal contraction patterns that decrease normal ventricular synchrony and results in altered myocardial blood flow, segmental wall shortening, inefficient work, and histopathological changes.^"^^ These effects may contribute to the adverse hemodynamics reported with chronic single-chamber [VVWVI,R) pacing.'^'^^ We have previously reported an epicardial approach to direct septal His-Purkinje pacing that normalizes ventricular contraction sequences, improves hemodynamics, and maintains normal cellular morphology.^"^ This current study introduces a new, potentially more clinically-applicable, endocardial electrode implant approach for septal His-Purkinje pacing.

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Materials and Methods Electrode/Introducer Design

A new active-fixation electrode (Medtronic, Inc., Minneapolis, MN, USA) was designed to permit deeper penetration into the proximal membranous ventricular septum from the tricuspid annulus endocardial surface than possible with currently available electrodes. The helical screw electrode was composed of a platinum-iridium alloy, 4.5 mm in length with a macroscopic surface area of 17.8 mm^. The lead was an 80A polyurethane covered 4 filar MP35N nickle conductor coil construction. This electrode implant concept is schematically illustrated in Figure 1. The electrode diameter permitted insertion into a standard 8 French Hemaquet catheter sheath [USCI, C.R. Bard, Tewksbury, MA, USA), which was modified to serve as a lead introducer by the addition of bipolar mapping electrodes at the tip. This modification permitted simultaneous recording of intracardiac pressures and electrocardiograms during electrode manipulation along the septal tricuspid leaflet annulus. Implant Technique Five 6-month-old beagles (mean weight 12 kg) were utilized. All animal handling and procedures were in accordance with established guidelines of the Animal Investigation Committee of Wayne

HIS-PURKINJE PACING ELECTRODE IMPLANT CONCEPT

State University. Following anesthesia and standard surgical techniques, a thoracotomy was performed and the pericardial sac incised to expose the right atrial appendage. A 6 French quadripalar electrode catheter was inserted into the femoral vein and advanced under fluoroscopic guidance across the tricuspid annulus to record optimal Kisbundle potentials. The mapping introducer v/as inserted into the right atrial cavity through a pursestring incision and advanced along the atrial siiptal/tricuspid valve annulus region of the right fibrous trigone to approximate the transvenous electrode pair recording optimal His potentials and confirmed by two-dimensional echocardiography. Simultaneous intracardiac pressures, electrograms, and surface ECG were continuously monitored on an AR-6 physiological recorder (Electronics for Medicine, Pleasantville, NY, USA).

Results Optimal electrode implant positioning along the specialized AV conduction system was confirmed by persistent His-bundle impulse recordings as the special introducer was manipulated from right ventricle to atrium with monitoring of intracardiac pressures [Fig. 2). The electrode was then inserted into the introducer, actively secured at the site of optimal His potential, and the introducer removed. Implant pacing and sensing measurements were performed with a Model 5311 pacing system analyzer (Medtronic, Inc.) and listed in Table I. In

RtOHT ATRIUM

TRICUSPttrWLVE

Table I. Electrode Implant Values LEFT VENTRICLE

RIGHT VENTRICLE

Figure 1. Schematic representation of the right atrial insertion of the septa] lead above the tricuspid valve annulus. The helical screw electrode extends into and is contained within the proximai muscuJar ventricular septum, approximating the conduction system.

2012

Impedance (ohms)

Threshold (0.5 msec) (V/mA)

Dog

Sensed R (mV)

Slew Rate (V/sec)

1 2 3 4 5

7.0 6.8 6.2 5.4 6.3

0.39 0.33 1.58 0.32 0.65

203 233 281 561 320

1,0/4.6 1.0/4.O C.8/1.4 C.9/3.3 C.8/3.2

Mean

6.3 0.3

0.65

319 82

0,9/3.3 0,1/0.8

SEM

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1

111

111

1

III

1111

1 M 11 M 1'.II

1 1 M' M

Ii

tll|llll|

Figure 2. Simultaneous surface ECG lead II and infracardiac recordings of atrial (A) and persistent His-bundle fHJ electrograms with pressure recordings during puJi-back of the introducer from right ventricle fRV) to right atrium (RAJ. Pressure scale 10 mmHg, paper speed 100 mm/ sec.

all instances, ventricular pacing resulted in narrow surface QRS complexes comparable to intrinsic rhythms (Fig. 3). Proper electrode positioning in the proximal intraventricular septum was confirmed by two-dimensional echocardiography. Doppler studies showed normal tricuspid and aortic valve flow patterns. At necropsy, electrode implant positioning was above the tricuspid annulus in the anterior atrial septum. Electrode extension continued into the middle of and was contained within the proximal ventricular septum (Fig. 4).

Discussion Utilization of the normal septal His-Purkinje specialized conduction system during ventricular pacing has been advocated since the early work of Wiggers,^ which demonstrated that altered myocardial electrical excitation results in asynchronous left and right ventricular contraction and depresses myocardial function, when compared with normal septal excitation. He recommended pacing as close to the Purkinje system as possible. This early work has since been expanded by subsequent authors who have demonstrated hemodynamic, metabolic, and histoiogic benefits of maintenance of normalized excitation.

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Regional myocardial blood flow contributes to optimal muscle function. In a recent report by Prinzen,'' substantiating previous works of pacinginduced unequal septal and posterior wall thickening and perfusion, asynchronous chamber activation with ventricular pacing caused a redistribution of myocardial fiber strain and a 60% alteration in blood flow between early and late activated regions. Derangements of wall motion, demonstrated by paradoxical systolic bulging and diastolic shortening have also been reported with ventricular pacing.^-^ Such inherent hemodynamic changes decrease effective muscle mass and limit cardiac performance, irrespective of any lack of atrial contribution to ventricular filling. In this manner, rate responsive atrial pacing (AAI,R) with normal intrinsic ventricular conduction has been shown to significantly improve hemodynamics over comparable rate, dual chamber (DDD,R) pacing.^^ Although this concept of altered stress and contraction patterns has recently been applied^^ to improve cardiac performance in patients with inherent left ventricular outflow tract cardiomyopathy, the normally structured heart undergoes compensatory adverse histological changes.^"^^ The AV portion of the right atrial septum has membranous and muscular components with the tricuspid valve annulus attached to the membra-

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HRA

HBE

Figure 3. Simultaneous surface ECG lead II with intracardiac electrograms recorded from right atrium (HRA) and His-bundle (HBE) during septal pacing (left] and at termination of pacing. There is little distortion of the paced surface QRS compared with normal. Following pacing, the His-bundle recording is readily visualized between low atrial and ventricular septal electrograms confirming proper pacing electrode positioning. Paper speed 100 mm/sec.

Figure 4. Cross-section appearance of proper septaJ electrode insertion viewed from beJow. Cardiac structures include right ventricle (RV), orifices of tricuspid (T) and mitral (MJ vaJves, and aortic outflow (Ao). The septal lead is visible on the atrial side of the tricuspid valve with electrode tip (arrow) extending into the middle of the intraventricuJar septum. 2014

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nous ventricular septum. In this manner, the specialized AV conduction system and ventricular septum can be approached through a properly placed atrial electrode. This concept permits normalized initiation of ventricular pacing with the potential to avoid implant trauma or chronic fibrosis to tricuspid valve leaflets and chordae associated with ventricular insertion. This current study was designed to demonstrate that septal His-Purkinje pacing is technically feasible with potential clinical application. Such an approach would have its greatest application in the young patient in whom ventricular pac-

ing may be anticipated to be extended longer than in the elderly, postinfarct adult. In the former, prevention of valve damage and adverse compensatory histoiogic changes while maintaining normalized hemodynamics may be desirable. In the latter, initiation of ventricular pacing to approximate normal septal conduction, even in the presence of postinfarct bundle branch block may improve hemodynamics. An appropriately designed introducer would permit a transvenous approach.

AcJcnowJedgment; The authors wish to thank Cheryl Justice, BCS. for technical assistance.

References 1. Rosenqvist M, Brand J, Schuller H. Atrial versus ventricular pacing in sinus node disease: A treatment comparison study. Am Heart J 1986; 111: 292-297. 2. Wiggers CJ. The muscular reactions of the mammalian ventricles to artificial surface stimuli. Am J Physiol 1925; 73:346-378. 3. Raichlen JS, Campbell FW, Edie RN, et al. The effect of the site of placement of temporary epicardial-pacemakers on ventricular function in patients undergoing cardiac surgery. Circulation 1984; 70: I118-I123. 4. Karpawich PP, Perry BL, Farooki ZQ, et al. Pacing in children and young adults with nonsurgical atrioventricular block: Comparison of single-rate ventricular and dual chamber modes. Am Heart J 1987; 113:316-321. 5. Bedotto JB, Crayburn PA, Black WH, et al. Alterations in left ventricular relaxation during atrioventricular pacing in humans. J Am Coll Cardiol 1990; 15:658-664. 6. Heyndrickx GR, Vilaine JP, Knight DR, et al. Effects of altered site of electrical activation on myocardial performance during inotropic stimulation. Circulation 1985; 71:1010-1016. 7. Prinzen FW, Augustijn TA, Allessie MA, et al. Redistribution of myocardial fiber strain and hlood flow by asynchronous activation. Am J Physiol 1990; 259:H300-H308. 8. Burkhoff D, Oikawa RY, Sagawa K. Influence of pacing site on canine left ventricular contraction. Am J Physiol 1986; 251:H428-H435.

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9. Adomian GE, Beazell J. Myofibrillar disarray produced in normal hearts hy chronic electrical pacing. Am Heart ] 1986; 112:79-83. 10. Karpawich PP, Justice CD, Cavitt DL, et al. Developmental sequelae of fixed-rate ventricular pacing in the immature canine heart: An electrophysiologic, hemodynamic, and histopathologic evaluation. Am Heart J 1990; 119:1077-1083. 11. Karpawich PP, Chang CH, Cavitt DL. Ventricular pacing-induced histopathology in the young with congenital heart block, (abstract) J Am Cloll Cardiol 1992; 19:326A. 12. Kruse I, Amman K, Conradson T, et al. Acomparison of the acute and long-term hemodynamic effects of ventricular inhibited and atrial synchronous ventricular inhibited pacing. Circulation 1982; 65:846-855. 13. Karpawich PP, Paridon SM, Pinsky WW. Failure of rate responsive ventricular pacing to improve physiologic performance in the univentricular heart. PACE 1991; 14:2058-2061. 14. Karpawich PP, Justice CD, Chang CH, et al. Septal ventricular pacing in the immature canine heart: Anew perspective. Am Heart J1991; 121:827-833. 15. Leclerq C. Mabo P, Le Helloco A. et al. The importance of preserving normal intrinsic conduction in permanent cardiac pacing, (abstract) PACE 1992; 15:511. 16. Jeanrenaud X, Voght P, Goy JJ, et al. Permanent pacemaker therapy for hypertrophic obstuctive cardiomyopathy. (abstract) J Am Coll Cardiol 1992; 19:325A.

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