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Leading Edge
Cardiac Pacing Site Optimization
Amara Estrada, DVM, DACVIM (Cardiology)
University of Florida
Introduction
The first fully implantable pacemaker was placed in a person in
1958.1 The first artificial pacemaker implantation in a dog was
described by Dr. James Buchanan more than 40 years ago.2 Since
that time, transvenous pacing has become a procedure commonly
performed by veterinary cardiologists in the treatment of complete
atrioventricular (AV) block, high-grade second-degree AV block,
sick sinus syndrome, and atrial standstill. It is a minimally invasive
surgical procedure in which pacing leads are most commonly
advanced into the right ventricular apical endocardium via surgical
cutdown over the jugular vein.
Initially, pacemakers provided asynchronous pacing, with no
sensing of inherent heartbeats and no alteration of the pacing
impulse in response to inherent beats. These early pacemakers simply
paced 100% of the time. Subsequent pacemakers were created to
pace in a ventricular demand mode (VVI pacing): the pacemaker
sensed inherent beats and could either inhibit the pacing impulse
or trigger a pacing impulse within the ventricular myocardium
to allow for ventricular depolarization (FIGURE 1). Although this
mode of ventricular pacing was better, some patients did not respond
well, experiencing continued syncopal or near-syncopal events,
dizziness, and, sometimes, congestive heart failure. The term pacemaker syndrome was coined to refer to a complex of clinical signs
and symptoms related to the potential adverse hemodynamic and
electrophysiologic consequences of ventricular pacing in human
patients. Neurologic symptoms or lethargy and symptoms suggesting
low cardiac output or congestive heart failure may be indicative
of pacemaker syndrome in people; corresponding clinical signs
may lead to suspicion of this syndrome in animals.
demonstrated in a variety of patient groups as well as at different
heart rates.
While single-chamber ventricular pacing prevents bradycardia
and death from ventricular standstill, dual-chamber pacing may
Physiologic Pacing
AV dyssynchrony and lack of rate modulation were initially identified
as causes of pacemaker syndrome. Since the initial descriptions
and development of pacing techniques, technological advances
have enhanced the sophistication of cardiac pacemakers to allow
proper sequencing of atrial and ventricular contraction and
physiologic rate modulation. The restoration of AV synchrony
by pacing was branded early on as physiologic pacing in humans
because it mimics the normal sequence of AV activation. Physiologic rate modulation has allowed patients to have lower heart
rates at rest and higher heart rates with exercise.3 In humans, the
importance of atrial contribution to cardiac output has been
Figure 1. Example of the typical placement of a transvenous permanent pacemaker.
A small venotomy is made over the jugular vein and a lead is placed in the right
ventricular apical endocardium. The lead is then attached to a generator that can
be buried subcutaneously in the neck or over the back. The top electrocardiogram
(ECG) is from a patient with a pacemaker programmed in an asynchronous pacing
mode. In this mode, the pacemaker paces at a constant rate without the ability
to sense inherent beats and prevent pacing on top of them or within vulnerable
periods (ovals and circle). The complexes in these periods are ventricular premature
complexes, and in the ST segment there are pacing spikes followed by ventricular
depolarizations. The bottom ECG is from a patient with a ventricular demand
pacing system in which the pacemaker only paces when needed; it is able to sense
inherent beats and withhold pacing at those times.
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Cardiac Pacing Site Optimization
Figure 2. Example of a patient with sick sinus syndrome and an atrial-based
pacing system. In this situation, the pacemaker delivers an atrial pacing impulse,
causing atrial depolarization. Because the patient has a normal AV node, this atrial
depolarization is then conducted through the normal conduction pathway to cause
ventricular depolarization.
be able to better emulate normal cardiac physiology by restoring
AV synchrony and matching the ventricular pacing rate to the sinus
rate. In patients with sick sinus syndrome, periods of sinus arrest,
and a normally functioning AV node, synchronization between the
atria and ventricles can easily be accomplished by using atrial leads
(FIGURE 2). For patients with AV nodal disease, AV synchrony can be
maintained by using dual-lead systems, in which one lead is placed
in the right atrium and the other lead is placed in the right ventricle
(FIGURE 3). In this situation, both leads are capable of sensing inherent
beats as well as pacing the chamber in which they are located.
Dual-chamber pacing can also be accomplished using a singlelead system that includes a floating atrial electrode in the right
atrium and a ventricular pacing electrode in the right ventricular
apical endocardium (FIGURE 4). This system can sense inherent
sinus node depolarizations (P waves) and deliver ventricular
pacing impulses in response.
Maintenance of AV synchrony by using either dual-chamber
pacing systems or atrial pacing systems has reduced clinical
symptoms and improved quality of life in people with complete
AV block3 and sick sinus syndrome4 and offers significant clinical
improvement compared with single-chamber ventricular pacing.3,4
In short- and long-term studies,3,4 AV synchrony improves stroke
volume, raises systolic blood pressure, reduces right atrial pressure
and pulmonary capillary wedge pressure, and is less likely to elicit
cardioinhibitory reflexes compared with single-chamber ventricular
pacing. Interestingly, studies in humans have not shown reductions
Figure 3. Example of a patient with sick sinus syndrome and AV nodal disease with
a dual-chamber pacing system. There is one lead within the right atrium that can both
pace and sense and a second lead in the right ventricle that can also pace and sense.
in mortality with rate-modulated dual-chamber ventricular pacing
compared with rate-modulated VVI pacing.5–7
Despite the ability to restore physiologic heart rates and maintain
AV synchrony in patients with bradyarrhythmia, current pacing
techniques could still be improved. The drive to improve pacing
practices has pushed human and veterinary electrophysiologists
to rethink what is meant by physiologic pacing. The most common
pacing site, the right ventricular apex (RVA), allows for easy and
secure endocardial lead placement but is considered suboptimal for
pacing by some electrophysiologists.8–12 During normal sinus rhythm
or atrial pacing, impulse activation of the ventricles is characterized
by minimal asynchrony, activation of the left ventricle (LV) before
the right ventricle (RV), and activation of apical myocardial cells
before basal cells. During RVA pacing, the activation sequence
deviates significantly from the physiologic one and is associated
with a considerable depression of LV function,8 a high incidence of
myocardial perfusion defects,13 regional changes in tissue perfusion,14
increases in tissue catecholamine activity,15 disorganization of
myofibers and subcellular elements,16 and cellular alterations
ranging from mitochondrial morphologic changes to degenerative
fibrosis and fatty deposits in human patients.17
Where Is the Ideal Pacing Site?
Methods of maximizing the clinical benefits of pacing therapy
for bradyarrhythmias have traditionally focused solely on the
features of the impulse generator. With renewed appreciation for
the important role that the pacing site may play in patient outcome,
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Cardiac Pacing Site Optimization
Figure 5. Example of a patient with complete heart block and a biventricular (BiV)
pacing system. One lead is in the right atrium; a second lead is in the traditional
location, the RVA; and a third lead has been placed into the coronary sinus (from
the right atrium) and passed through the left lateral coronary vein into a position
overlying the left ventricular free wall. The ECGs to the left show this patient paced
in different lead configurations and the difference in the appearance and width of
the QRS complexes.
Figure 4. Example of a patient with a single-lead, dual-chamber pacing system. This
lead has a floating atrial electrode that is able to sense native P waves. Once P
waves are sensed, a ventricular pacing impulse is delivered and causes ventricular
depolarization in reponse to the underlying sinus rate.
focus is now shifting to identifying the optimal or ideal site for
pacing and delivering leads to that location. The fact that RVA
pacing causes LV dysfunction was recognized as early as 1925.18
During both sinus and atrial pacing, the Purkinje system contributes
significantly to rapid electrical activation of the ventricles, whereas
the impulse from ventricular pacing is almost exclusively conducted
more slowly through myocardium. When Wiggers18 examined a
variety of stimulation sites on the epicardial surface of the canine
heart, he found that the site of stimulation exerted considerable
influence on LV function and postulated that the degree of functional impairment was inversely related to the proximity of the
stimulation site to the His-Purkinje system. The question has
now arisen: if the RVA is unsuitable for long-term ventricular
pacing, what is the alternative?
In an effort to identify the optimal or ideal pacing site that will
not worsen cardiac function, alternate sites in the RV have been
investigated: the outflow tract, septum, and free wall. Studies
evaluating these alternate pacing sites have produced conflicting and
controversial results.19–21 His-bundle pacing has been of theoretical
interest for many years. The idea of delivering a pacing impulse
directly into the cardiac conduction system is attractive because
of the possible hemodynamic benefits that could be obtained by a
normal activation sequence. However, the small size and anatomic
position of the His bundle have made this approach difficult.
Cardiac resynchronization using biventricular pacing is sometimes recommended as a treatment for congestive heart failure in
people. This recommendation is based on the concept that heart
failure can be exacerbated by dyssynchrony within the conduction
system and that resynchronizing the contraction pattern can improve
cardiac function.21,22 In this situation, simultaneous or nearsimultaneous transvenous stimulation pacing of the RV and LV
is possible using traditional pacing sites (the RV and right atrium
[RA]) and a third lead placed within the coronary sinus and into
a left lateral coronary vein overlying the LV free wall (FIGURE 5). Such
a pacing strategy has not yet been shown to protect or improve
LV performance in patients requiring pacing for bradyarrhythmias.
In an ongoing clinical trial, dogs with naturally occurring thirddegree or complete heart block in need of pacing therapy are being
randomly assigned to three treatment groups with differing combinations of long-term pacing leads: (1) dual-chamber RA-RVA
pacing, (2) dual-chamber RA-LV free wall pacing, and (3) dualchamber biventricular pacing. Synchronization is assessed by
electrocardiograms and tissue Doppler imaging, and cardiac
function is assessed by echocardiographic determination of stroke
volume, cardiac output, and ejection fraction. This study is under
way at the University of Florida Veterinary Medical Center. Results
are expected in September 2012.
References
1. Elmqvist R, Senning A. Implantable pacemaker for the heart. In Smyth CN, ed. Medical
Electronics. Springfield, IL: Charles C Thomas; 1960:253.
2. Buchanan JW, Dear MG, Pyle RL, et al. Medical and pacemaker therapy of complete heart
block and congestive heart failure in a dog. J Am Vet Med Assoc 1968;152(8):1099-1109.
3. Ausbel K, Furman S. The pacemaker syndrome. Ann Intern Med 1985;103:420-429.
4. Lamas GS, Lee KL, Sweeney MO, et al. Ventricular pacing or dual chamber pacing for
sinus node dysfunction. N Engl J Med 2002;24:1854-1862.
5. Wong GC, Hadjis T. Single chamber ventricular compared with dual chamber pacing:
a review. Can J Cardiol 2002;18(3):301-307.
6. Toff WD, Camm AJ, Skehan JD. Single-chamber versus dual-chamber pacing for
high grade atrioventricular block. N Engl J Med 2005;353(2):145-155.
7. Connoily SJ, Kerr CR, Gent M, et al. Effect of physiologic pacing versus ventricular
pacing on the risk of stroke and death due to cardiovascular causes. Canadian Trial of
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Cardiac Pacing Site Optimization
Physiologic Pacing Investigators. N Engl J Med 2000;342(19):1385-1391.
8. Prinzen FW, Peschar M. Relation between pacing induced sequence of activation and left
ventricular pump function in animals. Pacing Clin Electrophysiol 2002;25:484-498.
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pacing. Am J Physiol 1986;221:1686-1691.
10. Burkhoff D, Oikawa R, Sagawa K. Influence of pacing site on left ventricular contraction.
Am J Physiol 1986;251:428-435.
11. Rosenqvist M, Bergfeldt L, Haga Y, et al. The effect of ventricular activation sequence on
cardiac performance during pacing. Pacing Clin Electrophysiol 1996;19:1279-1286.
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in the paced heart with MRI tagging. Am J Physiol 1999;276:881-891.
13. Tse H-F, Lau C-P. Long-term effect of right ventricular pacing on myocardial perfusion
and function. J Am Coll Cardiol 1997;29:744-749.
14. Nielsen JC, Boetcher M, Toftegaard Nielsen T, et al. Regional myocardial blood flow in
patients with sick sinus syndrome randomized to long-term single chamber atrial or dual
chamber pacing-effect of pacing mode and rate. J Am Coll Cardiol 2000;35:1453-1461.
15. Lee MA, Dae MW, Langberg JJ, et al. Effects of long-term right ventricular apical pacing
on left ventricular perfusion, innervation, function and histology. J Am Coll Cardiol 1994;
24:225-232.
16. Karpawich PP, Justice CD, Cavitt DL, Chang CH. Developmental sequela of fixed-rate
ventricular pacing in the immature canine heart: an electrophysiologic, hemodynamic,
and histopathologic evaluation. Am Heart J 1990;119:1077-1083.
17. Karpawich PP, Rabah R, Haas JE. Altered cardiac histology following right ventricular
apical pacing in patients with congenital atrioventricular block. Pacing Clin Electrophysiol
1999;22:1372-1377.
18. Wiggers CJ. The muscle reactions of the mammalian ventricles to artificial surface
stimuli. Am J Physiol 1925;73:346-378.
19. Gold MR, Shorofsky SR, Metcalf MD, et al. The acute hemodynamic effect of right
ventricular septal pacing in patients with congestive heart failure secondary to ischemic
or idiopathic dilated cardiomyopathy. Am J Cardiol 1997;79:679-681.
20. Guidici MC, Thornburg GA, Buck DL, et al. Comparison of right ventricular outflow tract
and apical lead permanent pacing on cardiac output. Am J Cardiol 1997;79:209-212.
21. Bistow MR, Saxon LA, Boehmer J, et al. The Comparison of Medical Therapy, Pacing,
and Defibrillation in Heart Failure (COMPANION). Cardiac-resynchronization therapy with
or without an implantable defibrillator in advanced chronic heart failure. N Engl J Med
2004;350:2140-2150.
22. Cleland JGF, Daubert JC, Erdmann E, et al. Cardiac Resynchronization–Heart Failure
(CARE-HF). The effect of cardiac resynchronization on morbidity and mortality in heart
failure. N Engl J Med 2005;352:1539-1549.
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