In a retrospective study of 104 dogs that underwent pacemaker implantation: - Over 90% of dogs showed resolution of clinical signs such as collapse. One-, three-, and five-year survival estimates post-implantation were 86%, 65%, and 39%, respectively. - The most common breeds that underwent the procedure were Labrador Retrievers, West Highland White Terriers, and Springer Spaniels. - Major complications occurred in 15 dogs and minor complications in 23 dogs, with 3 of the major complications resulting in fatalities. However, the procedure successfully reduced or eliminated clinical signs in over 90% of cases.

1. PAPER
Results of pacemaker
implantation in 104 dogs
OBJECTIVES: To document the outcome, survival and complications
involved in pacemaker implantation in dogs in a retrospective study.
METHODS: Case records for all dogs in which pacemaker implantation
was performed were reviewed.
RESULTS: A total of 104 dogs underwent pacemaker implantation.
Dogs were presented with atrioventricular (AV) block (71), sick
sinus syndrome (25) or vasovagal syncope (eight). Age at
presentation varied from six months to 13 years with a median age of
seven years and two months. The Labrador was the most commonly
represented breed (17 cases). All but one dog survived pacemaker
implantation, with 93 showing resolution of their clinical signs while
10 dogs showed intermittent residual signs. One-, three- and five-
year survival estimates were 86, 65 and 39 per cent, respectively.
Major complications after implantation were documented in 15 dogs
and three of these led to fatalities. Minor complications were noted
in 23 dogs. Sudden death occurred in six dogs three to 55 months
following successful pacemaker implantation.
CLINICAL SIGNIFICANCE: Transvenous pacemaker implantation was
successful in reducing or eliminating clinical signs in over 90 per
cent of dogs with third-degree atrioventricular (AV) block or sick
sinus syndrome. In dogs with vasovagal syncope, six of eight dogs
had greatly reduced frequency of collapse and two became
asymptomatic. Although the procedure was associated with
complications, these were rarely life threatening and good survival
was documented in the majority of cases.
M. S. JOHNSON, M. W. S. MARTIN
AND W. HENLEY*
Journal of Small Animal Practice (2007)
48, 4–11
DOI: 10.1111/j.1748-5827.2006.00190.x
INTRODUCTION
Pacemaker implantation is used in the
treatment of symptomatic bradycardia in
dogs. This technique was first utilised in
a dog with congestive heart failure (CHF)
due to complete (third degree) atrioven-
tricular (AV) block in 1967 (Buchanan
2003). The technique is now widely avail-
able at referral centres, being chiefly used
in dogs with third-degree AV block and
sick sinus syndrome.
Several studies have documented the
success of implantation in groups of dogs,
the largest of which was by Oyama and
others of 154 dogs in 2001. Major com-
plications, considered to be life threaten-
ing or leading to loss of pacemaker or
lead function, were documented in 33
per cent of dogs while minor complica-
tions were noted in 31 per cent (Oyama
and others 2001). However, in this study,
implantations were performed by multiple
operators (with variable experience) and at
multiple referral centres.
In this retrospective study, we sought
to document how our results (in which
pacing was performed at one centre) com-
pared with that of Oyama and others
(2001). In the study by Oyama and others
(2001), complications appeared to be rel-
atively high in comparison with our own
experience. This study also documents the
signalment and clinical presentation of
a UK population of dogs that were pre-
sented with symptomatic bradyarrhyth-
mias. These results document interesting
differences to the findings of Oyama
and others (2001). We also wished to doc-
ument the results of pacemaker implanta-
tion in dogs with vasovagal syncope. This
topic has not been previously published to
the authors’ knowledge.
MATERIALS AND METHODS
The records of all dogs referred to the
Veterinary Cardiorespiratory Centre for
pacemaker implantation over a 12-year
period between May 1993 and May 2005
were reviewed. Records were examined
for the results of physical examination, elec-
trocardiography (ECG), thoracic radiogra-
phy, echocardiography and blood profile
including basal thyroxine. Signalment,
presenting signs, electrocardiographic
diagnosis and presence of concurrent
structural cardiac disease were noted.
Some dogs underwent long-term elec-
trocardiographic monitoring using 24-
hour Holter recorders (Tracker or Lifecard;
Reynolds), owner-activated event recorders
(Cardiobeeper; Numed) or implantable
loop recorders (Reveal device; Medtronic).
Vasovagal syncope (neurocardiogenic,
vasodepressor syncope) was defined as
Veterinary Cardiorespiratory Centre, 43 Waverley
Road, Kenilworth, Warwickshire CV8 1JL
*School of Mathematics and Statistics,
University of Plymouth, Drake Circus, Plymouth
PL4 8AA
4 Journal of Small Animal Practice Vol 48 January 2007 Ó 2006 British Small Animal Veterinary Association

2. syncope following a predictable behaviour
pattern, which involved excitement or
coughing in dogs in this series. Dogs
affected with vasovagal syncope may show
sinus rhythm or sinus tachycardia fol-
lowed by sinus bradycardia, hypotension
or both, leading to syncope. A gradual
return to normal sinus rhythm follows.
In this series, a diagnosis was made by
ambulatory ECG monitoring or ausculta-
tion at the time of syncope which docu-
mented bradycardia during syncopal
episodes. Blood pressure was not recorded
at the time of collapse.
Dogs that were presented with CHF
were stabilised with diuretics and angio-
tensin converting enzyme inhibitors
(ACEI) before pacemaker implantation.
Since 2001, temporary pacing was
performed following sedation with acetyl-
promazine (ACP injection; Novartis) and
morphine (morphine sulphate injection;
Martindale Pharmaceuticals) before in-
duction of general anaesthesia. Temporary
pacing wires were usually inserted via the
lateral saphenous vein or, if this was
technically unfeasible, via the contralateral
jugular vein. Temporary pacing using an
external temporary pacing unit was set
at a fixed rate, usually 80 to 100/minute
before induction of anaesthesia.
General anaesthesia was induced using
thiopentone (Thiovet; Novartis) or
propofol (Rapinovet injection; Schering-
Plough) intravenously followed by main-
tenance with an oxygen/nitrous oxide/
halothane mixture. The left jugular was
exposed by a cut-down technique, except
in dogs with a persistent left cranial vena
cava when the right jugular was utilised. A
single unipolar or bipolar lead was then
inserted into the right ventricular apex
under fluoroscopic guidance using either
passive or active fixation leads.
In a small number of cases, dual-cham-
ber pacing was performed utilising two
leads, with one lead actively implanted
in the right atrium and a second implanted
passively in the right ventricle. In a minor-
ity of additional cases, dual-chamber sens-
ing with ventricular pacing (VDR mode)
using a single tripolar lead (containing an
atrial sensor) was used.
The pacemaker generator, either new or
used, was inserted into the subcutaneous
tissues of the dorsal neck in all cases.
Non-absorbable sutures were used when
suturing both pacemaker and leads.
Antibiotics, usually ampicillin (Amfipen;
Intervet) were provided for seven to 10
days postoperatively. Dogs were hospital-
ised for a minimum of three days before
discharge. Sutures were removed in 10
to 12 days by the referring veterinarian.
The neck was bandaged for a minimum
of 10 days after surgery.
Records were examined for method of
lead fixation (active or passive), whether
a new or used pacemaker was implanted
and the pacing mode. In the case of used
pacemakers, confirmation of adequate
battery life was undertaken before implan-
tation. This was assessed by a pacing
technician, ensuring a minimum residual
battery life of at least four years in all cases.
Pacemaker programming by a pacing
technician was performed three to four
months postimplantation followed by
annual rechecks. Parameters such as pacing
rate, amplitude and sensitivity, pulse dura-
tion and width, lead impedance, threshold
and battery voltage and life were assessed.
Follow-up was based on revisits at these
times plus telephone contact with the
owner of cases that died in the interim.
Survival and outcome were assessed.
Records of any cases dying or undergoing
euthanasia were examined for cause of
death, whether pacemaker related, due to
heart failure or other non-cardiac disease.
Complications were recorded and classi-
fied as either major or minor. Major com-
plications, as defined in the study by
Oyama and others (2001), were defined as
either life threatening or those necessitat-
ing pacemaker and/or lead replacement.
Minor complications did not necessitate
repeat surgery to reimplant either pace-
maker or lead andwereoften self-resolving.
Median survival times and estimated
survival probabilities were obtained using
the product-limit estimator of the survivor
function (Kaplan and Meier 1958). Cox
regression models were fitted to assess
the associations between time to death
from cardiac-related causes and potential
risk factors (Cox 1972). Dogs were
censored if they were lost to follow-up,
alive at the end of the study or died from
non-cardiac-related causes. Variables were
selected for inclusion in the multivariable
model by first screening univariable mod-
els; variables with P,02 were considered
for inclusion in subsequent models. The
multivariable model was constructed
using a backwards elimination procedure
with variables retained in the model if they
significantly improved the fit (likelihood
ratio chi-squared P,005). The goodness
of fit of the selected model was checked by
plotting deviance residuals against time to
identify poorly fitting points (Dohoo and
others 2003). The proportional hazards
assumption was assessed by adding inter-
actions between time and the risk factors
into the selected multivariable model
(Dohoo and others 2003). All analyses
were carried out using SAS/STAT (SAS
version 8; SAS Institute).
RESULTS
A total of 104 dogs underwent pacemaker
implantation. Age at presentation varied
from six months to 13 years with a median
age of seven years and two months. Breeds
most commonly represented are summar-
ised in Fig 1. The Labrador was most
commonly represented (17 cases) followed
by the West Highland white terrier (13
cases), springer spaniel (11 cases), boxer
(seven cases), crossbreed (six cases) and
cavalier King Charles spaniel (five cases).
Fifty-nine were female (49 neutered) while
45 were male (17 neutered).
A majority of cases (81) were evaluated
for collapse with a further four having
presyncopal episodes alone, involving
transient weakness, ataxia and disorienta-
tion. Fifteen had a history of lethargy and
exercise intolerance while two were
reported to exhibit no clinical signs, with
bradycardia detected during routine
examination by the referring veterinarians.
Two dogs presented with clinical signs
of acute onset of left heart failure with
pulmonary oedema.
The electrocardiographic diagnosis was
third-degree AV block in 67 dogs, sick sinus
syndrome with sinus arrest in 25, vasovagal
syncope in eight and second-degree AV
block in four. Dogs with vasovagal syncope
demonstrated marked bradycardia after
excitement (seven cases) or after coughing
on exertion (one case). The ECG diagnosis
for the most commonly presented breeds is
presented in Fig 2.
Journal of Small Animal Practice Vol 48 January 2007 Ó 2006 British Small Animal Veterinary Association 5
Pacemaker implantation in dogs

3. Fifty per cent of dogs underwent
temporary pacing before general anaes-
thesia for pacemaker implantation while
50 per cent did not. Temporary leads were
inserted via the lateral saphenous vein in
46 dogs (Fig 3). In small dogs, when
saphenous access was not possible, jugular
access was used (six cases). Passive leads
were inserted in 71 dogs, active in 23
and tripolar in five. In five dogs, dual-
chamber pacemakers were used.
In all the cases, the permanent pacing
lead was inserted transvenously via the
jugular veins. One dog with a persistent
left cranial vena cava was successfully
implanted via the left jugular vein, involv-
ing a circuitous route into the right
atrium. One dog developed fibrosarcoma
at the pacemaker site, necessitating epicar-
dial lead implantation with the new pace-
maker located in the abdomen.
Thirty-nine new and 65 used (ex-
hospital) pacemakers were implanted.
The used units were confirmed for ade-
quate battery life before implantation.
Fixed rate pacing usually set at a fixed
rate of 80 or 100 bpm (VVI mode) was
utilised in 39 dogs. Rate responsive units
capable of increasing the rate depending
on the level of activity (VVIR, usually
set at a range of 60 to 160 bpm) were
inserted in a further 55 dogs. Five dogs
had dual-chamber pacemakers implanted.
Five had a single tripolar passive lead
inserted into the right ventricle (VDR
or VDI mode).
Twenty-six dogs were presented with
concurrent cardiac disease. Eighteen dogs
had moderate to marked mitral and/or
tricuspid regurgitation. Five dogs were
presented with additional arrhythmias –
two had episodes of ventricular tachycar-
dia, two had ventricular premature beats
and one had supraventricular premature
beats. Congenital defects were noted in
two cases (one had mild aortic stenosis
and one mild pulmonic stenosis) while
one had dilated cardiomyopathy.
Outcome
Of 104 dogs undergoing pacemaker
implantation, one dog (that was presented
with CHF) died during reimplantation of
the ventricular lead following lead dis-
lodgement one day after initial surgery.
The remaining 103 dogs survived anaes-
thesia and implantation and 90 per cent
showed resolution or marked improve-
ment in their clinical signs. Six dogs con-
tinued to collapse, albeit infrequently after
implantation. Four of these six dogs had
vasovagal syncope, one had third-degree
AV block and one had sick sinus syn-
drome. Pacing function was normal in
these six cases. Four dogs continued to
exhibit intermittent presyncope (two with
vasovagal syncope, two with sick sinus
syndrome). This was infrequent and no
action was taken. Pacing function appeared
normal in all four cases.
Two dogs were presented with left heart
failure and two with right heart failure. All
had resolution of heart failure after pacing
and ongoing heart failure therapy was not
necessary.
One dog developed lone atrial fibrilla-
tion 33 months after implantation. The
initial VDDR mode was then switched
to VVIR.
Survival
The survival probability estimates for
death from any cause at one, three and five
years postimplantation were 86, 65 and
39 per cent, respectively. Fifty-one cases
were alive at the conclusion of this study
while 48 died or were euthanased (Fig 4).
The median follow-up period for all dogs
was 28 months. Five were lost to follow-
up but all were known to have survived
and were asymptomatic one year after
implantation.
FIG 2. Chart showing the numbers of dogs affected by different bradyarrhythmias. 3AVB
Third-degree AV block, 2AVB Second-degree AV block, SSS Sick sinus syndrome
FIG 1. Graph showing the most commonly affected breeds and the arrhythmia at presentation.
Labradors presented chiefly with AVB, WHWT with SSS and boxers with vasovagal collapse.
AVB AV block, WHWT West Highland white terriers, SSS sick sinus syndrome,
CKCS Cavalier King Charles spaniel
6 Journal of Small Animal Practice Vol 48 January 2007 Ó 2006 British Small Animal Veterinary Association
M. S. Johnson and others

4. A total of 27 dogs died of non-cardiac-
related causes (Fig 4), with an estimated
median survival time for non-cardiac
deaths of five years nine months post-
implantation (95 per cent confidence
interval [CI] five years to seven years six
months). The median age at death was
12 years (95 per cent CI 11 years to 12
years six months). The estimated survival
probabilities for non-cardiac-related deaths
at three years and five years postimplanta-
tion were 80 and 64 per cent, respectively.
The most common cause of death was
non-cardiac neoplasia in 10 cases.
Cardiac-related deaths occurred in 21
dogs (Fig 4). The median postimplanta-
tion survival time for cardiac-related
deaths was estimated as seven years five
months (95 per cent CI lower limit of four
years nine months but no upper limit)
with the median age at death non-estima-
ble (due to the survival curve remaining
above 50 per cent until after the last death
time at 12 years four months). The esti-
mated survival probabilities for cardiac-
related deaths at three years and five years
postimplantation were 81 and 61 per cent,
respectively.
Twelve dogs were eventually eutha-
nased due to CHF at periods ranging from
seven to 78 months (mean 33 months)
postimplantation. CHF had not been
present at the time of pacemaker implan-
tation. Of these 12 dogs, four developed
dilated cardiomyopathy. These included
two springer spaniels, one Labrador and
one boxer. Two of these four dogs had
arrhythmias at presentation – one had pre-
mature ventricular complexes and one had
paroxysmal ventricular tachycardia (boxer)
while the remaining two had no heart
disease identified at the time of pre-
sentation. The boxer presenting with ven-
tricular tachycardia had short episodes of
non-sustained tachycardia but collapse
was due to profound bradycardia due to
third-degree AV block.
Eight of the 12 dogs were eventually
euthanased due to severe mitral or tricus-
pid regurgitation. Four of these had mild
to moderate mitral or tricuspid regurgita-
tion at presentation, one of these also had
moderate left atrial enlargement. Four of
the 12 dogs developed marked valvular
regurgitation despite having no evidence
of valvular regurgitation or other abnor-
mality on initial echocardiography.
Sudden death occurred in six dogs at
three to 55 months postimplantation.
These included one basset hound, one
Jack Russell terrier, one cavalier King
Charles spaniel, one bearded collie and
two West Highland white terriers. Both
the West Highland white terriers had pre-
sented with sick sinus syndrome while the
other four dogs had third-degree AV block
at presentation. Four dogs had used pace-
makers and two dogs had new pace-
makers. Four were in VVIR mode and
two in VVI. In all cases, no sensing prob-
lems had been detected at the most recent
annual pacing check, which was current.
One dog with third-degree AV block
was euthanased due to renewed collapses
at 14 years of age, three years after im-
plantation. Pacemaker function appeared
normal and the reason for the collapses
was not apparent.
Cox regression analysis identified an
association between the choice of a
FIG 3 Radiograph showing the temporary pacing wire placed via the saphenous vein (before
removal) following placement of the permanent pacing lead via the jugular vein
FIG 4. Chart showing the final outcomes of the 104 cases, with an overall median follow-up period of
28 months
Journal of Small Animal Practice Vol 48 January 2007 Ó 2006 British Small Animal Veterinary Association 7
Pacemaker implantation in dogs

5. new/used pacemaker and the risk of a
cardiac-related death: re-using old pace-
makers was associated with a three-fold
increase in the hazard rate compared with
using a new pacemaker (heart rate [HR]
from multivariable model 32; 95 per cent
CI 10 to 110; P=003). The other risk
factor in the selected multivariable model
was the presence of concurrent heart dis-
ease at implantation which was associated
with a five-fold increase in the hazard rate
(HR 49; 95 per cent CI 21 to 119;
P=0001). Figures 5 and 6 contain esti-
mated survival curves illustrating the
reduced survival rates for dogs given a
second-hand pacemaker or suffering
from concurrent heart disease at implanta-
tion. Age, sex, neutered status, pacing
mode and clinical signs at implantation
were not significantly associated with
survival time (P=013, 057, 033, 009
and 083, respectively).
Major complications
Major complications were noted in 15
cases and fatalities occurred in three
(Table 1). Complications included lead
dislodgement (five), pacemaker failure of
unknown cause (two), lead damage (two),
twiddlers syndrome (two), looping of
the lead (one), perioperative mortality
(one), endocarditis (one) and neoplasia
at the pacemaker site (one).
Lead dislodgement occurred in five
dogs – two dislodged after one and four
days (passive leads) and three after three,
eight (passive leads) and 24 months (active
lead) postimplantation. In all cases, either
a new replacement lead was inserted or the-
original lead was repositioned. The dog in
which dislodgement occurred after one day
underwent repeat general anaesthesia for
lead reinsertion but died under anaesthesia.
Pacemaker failure developed in two
dogs after five and 18 months, necessitat-
ing implantation of a new pacemaker in
each case. In both the dogs, used pace-
makers were implanted initially. The cause
of failure was not known but battery life
had been assessed by a pacing technician
and found to be adequate within six
months of failure in both cases.
Two dogs sustained trauma leading to
lead damage after 14 and 15 months. In
both the dogs, a new lead was inserted.
In one of these dogs after a further four
months, a dog bite over the pacemaker
site led to infection in this region. A new
pacemaker and lead were implanted at
this time.
Two dogs presented with twiddlers syn-
drome after five and 18 months, leading to
recurrence of clinical signs (Fig 7). Exces-
sive coiling of the lead had resulted from
scratching of the neck or rolling on the
back. Uncoiling of the lead was necessary
in both dogs.
One dog developed a murmur three
years after implantation due to looping of
the lead in the pulmonary artery, which
caused obstruction to pulmonary flow.
The lead was straightened and no further
complications arose.
One dog developed persistent pyrexia
due to endocarditis adjacent to the pacing
lead after 20 months, leading eventually to
euthanasia.
In one case, fibrosarcoma developed at
the pacemaker generator site, 30 months
after implantation. Both pacemaker
generator and lead were removed. A new
pacemaker generator was inserted into the
abdomen and an epicardial lead was
screwed into the apex of the heart. Despite
intervention by a surgical oncologist to re-
move the sarcoma, pulmonary metastasis
FIG 5. Kaplan-Meier survival curves comparing time to death from cardiac-related causes for
dogs implanted with new and used pacemakers. The crosses represent censoring times (that is, the
times at which dogs were lost to follow-up or died of other causes)
FIG 6. Kaplan-Meier survival curves comparing time to death from cardiac-related causes for
dogs with and without concurrent heart disease at implantation. The crosses represent censoring
times (that is, the times at which dogs were lost to follow-up or died of other causes)
8 Journal of Small Animal Practice Vol 48 January 2007 Ó 2006 British Small Animal Veterinary Association
M. S. Johnson and others

6. necessitating euthanasia occurred one
month later.
Minor complications
Minor complications arose in 23 dogs
(Table 2). Seroma, which was self-
resolving, around either the pacemaker
or lead site or both was the most common
complication and was seen in 17 cases
within 10 days of surgery. One additional
case developed seroma after 24 months
and this originated from migration of
the plastic sleeve around the lead due to
suture breakdown, causing a foreign body
reaction.
Wound breakdown occurred after 10
days in one case. Resuturing of the wound
was necessary.
Migration of the tip of one passive lead
into a new site at the right ventricular apex
occurred. Another lead formed a loop
in the right atrium. In both the cases,
normal pacing continued and no action
was necessary.
One dog was re-presented after two
months with recurrence of syncope and
third-degree AV block. Failure to capture
was documented on ECG. Interrogation
of the pacing generator did not reveal
abnormalities in battery and output
settings. Lead displacement was not ap-
parent. Capture was restored on in-
creasing the pacing output amplitude.
Exit block around the (active) lead tip
was suspected.
In one dog, implanted with a dual-
chamber pacemaker (DDD), DDD func-
tion failed initially. A VVIR mode was
utilised until the problem was rectified
by a pacing technician.
Vasovagal syncope
Eight dogs were diagnosed with vasovagal
syncope. Five were young boxers (two
were one to two years old and three were
three to four years old) and three terrier
crossbreeds (one, five and 10 years old).
All collapsed frequently after excitement.
One terrier coughed predictably on excite-
ment and then collapsed. The cause of the
cough was not apparent but coughing was
only evident when excited. In four dogs
the diagnosis was made using a Cardio-
beeper event recorder, one with a Reveal
device and one by Holter monitoring.
In the remaining two dogs, excitement
when greeting the owners caused collapse
and marked pallor. Auscultation disclosed
bradycardia followed by gradual return to
tachycardia at these times.
In two dogs, collapse ceased after pace-
maker implantation. Four continued to
exhibit occasional syncope and presyncope
while two demonstrated presyncopal signs
alone. Presyncopal signs included tran-
sient weakness, ataxia or disorientation.
In all six dogs, signs were judged by the
owner to be much less frequent after
implantation.
DISCUSSION
Pacemaker implantation is a worthwhile
therapy intervention for the management
of symptomatic bradyarrhythmias, with
the majority of dogs (90 per cent) showing
a resolution of clinical signs. The overall
survival estimates at one, three and five
years were 86, 65 and 39 per cent, respec-
tively; this compares with a three-year sur-
vival of 45 per cent in the study by Oyama
and others (2001).
Labradors, springer spaniels and West
Highland white terriers were the most com-
monly affected breeds in this series. Both
Labradors and West Highland white terriers
were commonly represented in another
large study (Oyama and others 2001), with
another study documenting the frequency
of sick sinus syndrome in the West High-
land white terrier (Moneva-Jordan and
others 2001). The large numbers of springer
spaniels documented in this study may rep-
resent a difference in presentation in the UK.
The most common reason for pace-
maker implantation was third-degree AV
block followed by sick sinus syndrome,
as documented in previous reports (Bona-
gura and others 1983, Darke and others
1989, Sisson and others 1991, Oyama
and others 2001).
Pacemaker implantation was successful
in eliminating or reducing clinical signs
Table 1. List of major complications encountered in 15 dogs
Major complication Number of cases
Lead dislodgement 5
Pacemaker generator failure 2
Pacemaker-related death
(endocarditis, neoplasia) 2
Perioperative mortality 1
Lead damage 2
Twiddlers syndrome 2
Looping of lead, requiring repositioning 1
FIG 7. Radiograph showing the twisted pacing lead due to twiddlers syndrome in a dog
Journal of Small Animal Practice Vol 48 January 2007 Ó 2006 British Small Animal Veterinary Association 9
Pacemaker implantation in dogs

7. in dogs with frequent vasovagal syncope.
However, in only two of eight affected
dogs did signs resolve completely after
pacing. In the remaining six dogs, clinical
signs reduced markedly but did not cease.
The success of pacing human beings with
vasovagal syncope has been described in
one large study (Connolly and others
1999). Syncope reduced markedly in fre-
quency after pacing while presyncope was
unaffected. This is likely due to the co-
existence of hypotension and bradycardia
as a cause of syncope. Pacing can amelio-
rate bradycardia but not hypotension at
the time of collapse (Connolly and others
1999). Pacing is probably only advisable
in affected dogs, which show frequent
clinical signs and documented evidence
of profound bradycardia at the time of
syncope. In the eight affected dogs in this
series, it seems unlikely that clinical signs
would have resolved spontaneously as all
cases were presented with a chronic history
of frequent, predictable syncope after
excitement or coughing. Owner satisfac-
tion with this population of dogs post-
implantation was high, given the marked
clinical improvement apparent.
Temporary pacing before anaesthesia
was performed in 50 per cent of dogs,
which had been adopted since 2000 in this
centre. This was readily performed in most
dogs from the lateral saphenous vein,
which has been previously documented
in the literature (Kienle 1998). Occasion-
ally this involved some manipulation of
the temporary lead where the vein courses
around the stifle joint, in which location,
the lead tended to catch in branches of the
saphenous vein. This approach was not
possible in every small dog, in which case,
the jugular vein was utilised instead. One
of the advantages of pacing from the
saphenous rather than the jugular vein
was that the dog could be kept in the same
lateral position for both temporary and
permanent pacing. In addition, removal
of the temporary lead was remote from
the sterile surgical site and direct visual-
isation of any haemorrhage following
removal could be easily observed and
controlled.
Early studies of pacemaker implan-
tation in dogs documented high com-
plication rates using epicardial leads
(Bonagura and others 1983) or transve-
nous untined leads, leading to a high rate
of lead migration (Sisson and others
1991). Later reports of the use of transve-
nously implanted tined leads gave more
encouraging results (Darke and others
1989). With familiarity in the implanta-
tion procedure, the complication rate
has been greatly reduced. In the study
by Oyama and others (2001), the overall
major complication rate was high at 33 per
cent. In the study by Oyama and others
(2001), however, the major complication
rate for experienced operators (17 per
cent) was much lower than that of less
experienced operators and this is similar
to the 14 per cent recorded in this study.
Human studies have also documented
similar complications after pacing (Kivi-
nieme and others 1999).
Although major complications occurred
in 15 dogs, either pacemaker and/or lead
reimplantation was successful in correct-
ing the problem in 12 of 15 cases, with
three fatalities. While 23 dogs had minor
complications, these were readily resolved.
New pacemakers were associated with
a decreased risk of cardiac-related deaths.
The reason for this is unclear at this time as
all second-hand units were rechecked
annually and found to be functioning
satisfactorily and to have adequate battery
life. Allocation of new and used pace-
makers was not random, so this effect
may be confounded with disease status
at implantation. We attempted to remove
any confounding effect of disease status by
adjusting the Cox regression model for the
presence of concurrent heart disease at
implantation. However, the possibility
remains that the estimated effect of using
a new pacemaker is a consequence of other
unmeasured differences in baseline disease
status between those dogs given new and
second-hand pacemakers. It would be
interesting to compare this result with
those of other centres to ascertain whether
new pacemakers provide better survival in
the long term.
Pacemaker implantation is possible via
the left jugular vein in cases of persistent
left cranial vena cava. This was performed
in one case in this study. However, the
approach to the right atrium is more dif-
ficult and time consuming. In the medi-
cal literature, one report advised using a
wire stylet to shape the pacing lead into
a pigtail conformation to facilitate pas-
sage from right atrium to right ventricle
(Zerbe and others 1992). Alternatively,
routine use of the right jugular for
implantation would avoid this possible
complication.
One dog developed fibrosarcoma
around the pacemaker site 30 months after
implantation. It is not known whether an
implant can induce neoplasia. In the med-
ical literature, there are several reports of
malignancy at the pacemaker site. These
have involved both sarcomas and carcino-
mas (Biran and others 1979, Fraedrich
and others 1984, Bhandarkaar and others
1993, Carpentier and others 2000). There
is no overall consensus on whether the
implant is the cause of the neoplasms or
whether their occurrence was coincidental.
Even if neoplasia proves to be related to
the presence of a pacemaker, this compli-
cation would appear to be rare in animals,
given the absence of published reports.
In this study, bradycardia-induced
heart failure was documented at presenta-
tion in four dogs but resolved in all
cases after pacing. Therefore CHF, once
controlled, does not appear to be a con-
tra-indication to pacing. Several previous
veterinary studies have documented the
resolution of heart failure after pacing
alone without the necessity of chronic
Table 2. List of minor complications encountered in 23 dogs
Minor complication Number of cases
Seroma formation 17
Suture sleeve reaction 1
Wound breakdown 1
Lead displacement 1
Looping of lead, not
requiring repositioning
1
Exit block 1
Temporary failure of proper
DDD pacing
1
10 Journal of Small Animal Practice Vol 48 January 2007 Ó 2006 British Small Animal Veterinary Association
M. S. Johnson and others

8. heart failure medication (Lombard and
others 1981, Bonagura and others 1983,
Darke and others 1989, Oyama and others
2001, Buchanan 2003).
Sudden death was noted in six dogs
three to 55 months after pacemaker im-
plantation. These cases had not shown
evidence of presyncope or syncope before
unexpected death. None of the affected
breeds are prone to dilated cardiomyo-
pathy. Pacemaker failure seemed an un-
likely cause as all pacemakers had been
regularly interrogated and found to have
been working satisfactorily with adequate
battery life remaining. Several veterinary
studies have referred to eventual sudden
death after pacing in dogs with seven of
154 sudden deaths in one study (Oyama
and others 2001), two of 19 in another
(Darke and others 1989) and five of
40 in a third study (Sisson and others
1991). As discussed in an article by
Zehender and others (1992), this has been
well documented in human beings where
sudden death appears to occur chiefly due
to an adverse reaction between intrinsic
(usually ectopic) and paced beats. Such
an occurrence was suspected in these six
dogs but could not be verified.
In human beings, pacemaker implanta-
tion in young adults without structural
heart disease can lead to a survival similar
to that of an age-matched control popula-
tion (Mayosi and others 1999). In older
human beings, survival may be much
more limited due to deaths from either
non-cardiac disease or structural heart dis-
ease not related to pacing. (Suvarna and
others 1999, Flaker and others 2003).
Similarly, many implanted dogs eventu-
ally die or are euthanased due to non-
cardiac illness or structural heart disease
not related to pacing. Insufficient numbers
of young dogs have been studied long term
to ascertain whether their survival after
implantation could be similar to that of
a control age-matched population.
The medical literature also documents
the advantages of dual-chamber pacing
such as the DDD mode versus single-
chamber pacing such as VVI or VVIR
(Nahlawi and others 2004). Dual-chamber
pacing is more physiological with sensing
of the intrinsic beats triggering activation
of the ventricles in the correct sequence
and after an appropriate interval. This
pacing mode can therefore increase the
quality of lifeand activity ofpatients (Sulke
and others 1992). Some studies also docu-
mentimprovedsurvivalwithdual-chamber
pacing (Hesselson and others 1992) while
others do not (Montanez and others
2003). Only small numbers of dogs have
been documented as undergoing dual-
chamber or tripolar pacing, including five
from each category in this study. These
numbers are insufficient to prove a mean-
ingful comparison of outcome and survival
between single chamber, dual chamber and
tripolar modes of pacing. It would be inter-
estingtofollowmuchlargernumbersinthe
future to assess whether dogs undergoing
such pacing modes show similar added
beneficial effects to those documented in
human beings.
Overall results for single-chamber pac-
ing are encouraging, adding further evi-
dence that pacing is clinically effective,
safe and practicable, providing a good sur-
vival in the majority of cases.
Acknowledgements
We would like to thank the referring vet-
erinarians and our dedicated staff. Med-
tronic and Sorin Biomedica performed
the pacemaker programming in the major-
ity of these cases and their assistance is
greatly appreciated.
References
BHANDARKAAR, D. S., BEWU, A. D. TAYLOR, T. V. (1993)
Carcinoma of the breast at the site of migrated
pacemaker generators. Postgraduate Medical
Journal 69, 883-885
BIRAN, S., KEREN, A., FARKAS, T. STERN, S. (1979)
Development of carcinoma of the breast at the
site of an implanted pacemaker in two patients.
Journal of Surgical Oncology 11, 7-11
BONAGURA, J. D., HELPHREY, M. L. MUIR, W. W. (1983)
Complications associated with permanent pace-
maker implantation in the dog. Journal of the
American Veterinary Medical Association 182,
149-155
BUCHANAN, J. W. (2003) First pacemaker in a dog:
a historical note. Journal of Veterinary Internal
Medicine 17, 713-714
CARPENTIER, O., DUBOST-BRAMA, A., MARTIN DE LASSALLE,
E., PIETTE, F. DALAPORTE, E. (2000) Rhabdomyo-
sarcoma at site of pacemaker implantation.
Annales de Dermatologie de Venerelogie 127,
837-840
CONNOLLY, S. J., SHELDON, R., ROBERTS, R. S. GENT, M.
(1999) The North American vasovagal pacemaker
study. A randomised trial of permanent cardiac
pacing for the prevention of vasovagal syncope.
Journal of the American College of Cardiology
33, 16-20
COX, D. R. (1972) Regression models and life tables
(with discussion). Journal of the Royal Statistical
Society B 74, 187-220
DARKE, P. G. G., MCAREAVEY, D. BEEN, M. (1989)
Transvenous cardiac pacing in 19 dogs and one
cat. Journal of Small Animal Practice 39, 491-499
DOHOO, I., MARTIN, W. STRYHN, H. (2003) Veterinary
Epidemiologic Research: AVC Inc. Charlottetown,
Prince Edwards Island, Canada
FLAKER, G., GREENSPON, A., TARDIFF, B., SCHRON, E., GOLD-
MAN, L., HELLKAMP, A., LEE, K. LAMAS, G. (2003)
Death in patients with permanent pacemakers
for sick sinus syndrome. American Heart Journal
146, 887-893
FRAEDRICH, G., KRACHT, J., SCHELD, H. H., JUNDT, G.
MULCH, J. (1984) Sarcoma of the lung in a pace-
maker pocket – simple coincidence or oncotaxis?
Thoracic Cardiovascular Surgery 32, 67-69
HESSELSON, A. B., PARSONNET, V., BERNSTEIN, A. D.
BONAVITA, G. J. (1992) Deleterious effects of
long-term single-chamber ventricular pacing in
patients with sick sinus syndrome: the hidden
benefits of dual-chamber pacing. Journal of the
American College of Cardiology 19, 1542-1549
KAPLAN, E. L. MEIER, P. (1958) Nonparametric
estimation from incomplete observations. Journal
of the American Statistical Association 53,
457-481
KIENLE, R. D. (1998) Interventional anti arrhythmic
therapy. In: Small Animal Cardiovascular Medi-
cine. Eds M. D. Kittleson and R. D. Kienle. Mosby,
St Louis, MO, USA. pp 525-539
KIVINIEME, M. S., PIRNES, M. A., ERANEN, H. J. K.,
KETTUNEN, R. V. J. HARTIKAINEN, J. E. K. (1999)
Complications related to permanent pacemaker
therapy. Pace 22, 711-720
LOMBARD, C. W., TILLEY, L. P. YOSHIOKA, M. (1981)
Pacemaker implantation in the dog: survey and lit-
erature review. Journal of the American Hospital
Association 17, 751-758
MAYOSI, B. M., LITTLE, F. MILLAR, R. N. S. (1999)
Long-term survival after permanent pacemaker
implantation in young adults: 30 year experience.
Pace 22, 407-412
MONEVA-JORDAN, A., CORCORAN, B. M., FRENCH, A., DUKES-
MCEWAN, J., MARTIN, M. W., LUIS FUENTES, V., HITCH-
COCK, L. S. BONAGURA, J. D. (2001) Sick sinus
syndrome in nine West Highland white terriers.
Veterinary Record 148, 142-147
MONTANEZ, A., HENNEKENS, C. H., ZEBEDE, J. LAMAS,
G. A. (2003) Pacemaker mode selection: the
evidence from randomized trials. Pacing Clinical
Electrophysiology 26, 1270-1282
NAHLAWI, M., WALIGORA, M., SPIES, S. M., BONOW, R. O.,
KADISH, A. H. GOLDBERGER, J. J. (2004) Left ventric-
ular function during and after right ventricular pac-
ing. Journal of the American College of Cardiology
44, 1883-1888
OYAMA, M. A., SISSON, D. D. LEMKUHL, L. B. (2001)
Practices and outcome of artificial cardiac pacing
in 154 dogs. Journal of Veterinary Internal Medi-
cine 15, 229-239
SISSON, D., THOMAS, W. P., WOODFIELD, J., PION, P. D.,
LUETHY, M. DE LELLIS, L. A. (1991) Permanent
transvenous pacemaker implantation in forty
dogs. Journal of Veterinary Internal Medicine 5,
322-331
SULKE, N., DRITSAS, A., BOSTOCK, J., WELLS, A., MORRIS,
R. SOWTON, E. (1992) Subclinical pacemaker
syndrome: a randomised study of symptom free
patients with ventricular demand (VVI) pace-
makers upgraded to dual chamber devices. British
Heart Journal 67, 57-64
SUVARNA, S. K., START, R. D. TAYLER, D. I. (1999) A
prospective audit of pacemaker function, implant
lifetime and cause of death in the patient. Journal
of Clinical Pathology 52, 677-680
ZEHENDER, M., BUCHNER, C., MEINERTZ, T. JUST, H.
(1992) Prevalence, circumstances, mechanisms
and risk stratification of sudden cardiac death
in unipolar single-chamber ventricular pacing.
Circulation 85, 596-606
ZERBE, F., BORNAKOWSKI, J. SARNOWSKI, W. (1992)
Pacemaker electrode implantation in patients
with persistent left superior vena cava. British
Heart Journal 67, 65-66
Journal of Small Animal Practice Vol 48 January 2007 Ó 2006 British Small Animal Veterinary Association 11
Pacemaker implantation in dogs