Europace (2000) 2, 93–98
doi:10.1053/eupc.2000.0081, available online at http://www.idealibrary.com on
Alternative right ventricular pacing sites — where are we
For over 40 years, since the advent of permanent cardiac
pacing, the right ventricular apex (RVA) has been the
routine site for placement of the ventricular pacing lead,
although interestingly the first reported endocardial elec-
trode placements were, in fact, in the right ventricular
outflow tract (RVOT). Evidence has existed for many
years, however, to suggest that the RVA may not be the
most suitable position for ventricular stimulation. In a
series of elegant experiments in 1925, Wiggers demon-
strated that electrical stimuli applied to ventricular
muscle will cause a deterioration in function over the
long term; it has been shown subsequently that these
effects arise from abnormalities provoked at the cellular
level[4,5]. Further studies have shown that apical pacing
has adverse effects on volume, pressure and inotropic
state[6–10], with thinning of the myocardial wall around
the activation siteand the development of regional
hypertrophy in the long term. This also leads to
perfusion defects[12,13]which are associated with apical
wall motion abnormalities and impaired global left
ventricular function, a situation which progresses with
time. In combination these studies all suggest that,
whilst apical pacing is sufficient to treat the initial
arrhythmia and offers lead stability by means of the
trabeculae, it may introduce the potential for future
A disturbing finding that begins to reinforce the
suggestion that RVA pacing is potentially detrimental
is evident in work by Rosenqvist et al.. In a retro-
spective study of 168 patients comparing VVI vs AAI
implants for sinus node disease (SND) (undertaken at
separate hospitals), they found an increased incidence of
congestive heart failure in those patients treated with a
ventricular device. They concluded that pacing the RVA
for SND predisposed this group to developing heart
failure more than pacing in the atrium alone, and that
this must result, at least in part, as a consequence of
pacing in the RVA. Of additional importance was the
high incidence of atrial fibrillation in the VVI group.
These findings were confirmed ten years later by Nielsen
et al.who also demonstrated this same link between
pacing mode and progression to heart failure. Bedotto
et al. summed up the clinical implications of ventricular
pacing in 1990; prior to 1990, 40–50% of total world-
wide pacemaker implants were for SND in patients with
intact AV nodal conduction and many of these were
ventricular devices, even though the safety and efficacy
of atrial-based pacing in this cohort had already been
proven and the associated effects of pacing mode on
mortality identified[17,18]. Although it is difficult to
separate the potential contribution of the increased
incidence of atrial fibrillation in these patients, these
data began to emphasize the number of patients who are
exposed to an increased risk of developing cardiac
dysfunction in the long term and subsequent studies
have concurred with these initial findings.
In his original paper, Wiggers postulated that the
degree of functional impairment was inversely propor-
tional to the proximity of the stimulation site to the
His-Purkinje system, and hence that the activation
sequence is more important than synchrony of acti-
vation. Thus it is not unreasonable to assume that a
more physiological approach, by positioning the pacing
lead as near to the His-Purkinje system as possible, may
limit the potential damage caused by RVA pacing. It has
been suggested that this is of greatest importance in
young patients receiving first implants as juveniles.
The immature heart can accommodate changes in vol-
ume and pressure readily, but this ability to adapt will
diminish with age and could potentially lead to the
genesis of heart failure in young to middle age. Also,
restoration of more normalized activation and contrac-
tion sequences may be beneficial in producing optimal
haemodynamics for patients with concomitant struc-
tural heart disease, for whom cardiovascular reserve
may be limited and maintenance of AV synchrony
Interest in His bundle pacing was shown as early as
1967 in work by Scherlag et al. as a means of allow-
ing the ventricles to depolarize in a more normalized
fashion. This study demonstrated little difference in
QRS duration and indices of pressure recorded during
intrinsically conducted sinus rhythm, atrial pacing,
and His Bundle pacing. Subsequent studies have made
similar comparisons of His bundle, atrial, and RVA
pacing[5,21,23]and confirmed that the temporal relation-
ship between atrial and ventricular contraction and the
Manuscript submitted 5 January 2000, and accepted 9 January
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Europace, Vol. 2, April 2000