429645

2012
JFM14410.1177/1098612X11429645Hambrook and BennettJournal of Feline Medicine and Surgery

Original Article

Journal of Feline Medicine and Surgery

Effect of pimobendan on the clinical 14(4) 233­–239

© ISFM and AAFP 2012
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DOI: 10.1177/1098612X11429645

non-taurine responsive dilated jfms.com

cardiomyopathy

Lydia E Hambrook and Peter F Bennett

Abstract
This retrospective study was designed to assess the effect of pimobendan on the median survival time (MST) of
cats with non-taurine responsive dilated cardiomyopathy (DCM). Thirty-two client-owned cats with a left ventricular
internal dimension at end systole (LVIDs) >14 mm, a fractional shortening (FS) <28% and a lack of response to
taurine therapy were included over a 9-year period (2001–2010). These cats were divided into pimobendan (n=16)
and non-pimobendan (n=16) treatment groups. All cats received standard treatment with frusemide, taurine and
benazepril or enalapril. Nine cats in the non-pimobendan group also received digoxin. The MST of the pimobendan
group (49 days; range 1 to >502 days) was four times that of the non-pimobendan group (12 days; 1 to 244 days).
The difference in survival between the two groups was statistically significant (P = 0.048). Hypothermia and FS
<20% were associated with a poor prognosis. No adverse effects to pimobendan were noted.

Accepted: 22 August 2011

Dilated cardiomyopathy (DCM) is an uncommon condi-
tion in cats that can result in congestive heart failure
(CHF), aortic thromboembolism (ATE), arrhythmias and
sudden death. In 1987 taurine deficiency was identified
as a major cause of feline DCM.1 Subsequent supplemen-
tation of commercial cat food with taurine has drasti-
cally reduced, but not eliminated, the incidence of
feline DCM.2 Other proposed aetiological factors include
myocardial dysfunction secondary to toxic insult, infec-
tious myocarditis, metabolic errors, immune-mediated
disease, infiltrative disease, chronic volume overload,
chronic tachyarrhythmias, end-stage hypertrophic cardi-
omyopathy and microvascular injury. Genetic links have
also been proposed in cats and established in humans,
mice and Portuguese Water dogs.3–5 Non-taurine respon-
sive feline DCM is often referred to as idiopathic as the
cause of the myocardial dysfunction is rarely apparent at
the time of diagnosis. The aetiology of DCM may also be
multifactorial, given that experimental induction of tau-
rine deficiency in cats failed to result in overt DCM.1,6,7
The prognosis of feline DCM depends on the response
to taurine supplementation. Predicting whether an indi-
vidual is likely to respond to taurine is problematic.
Taurine deficient diets may be difficult to identify as bio-
availability may vary with heat processing, potassium
depletion and acidification.8 Whole blood taurine assays
are thought to be more reliable than plasma taurine
concentrations; however, false positive results may still
be obtained with prolonged fasting or anorexia, and
false negative results may be obtained with postpran-
dial sampling, a recent dietary change or recent throm-
boembolism.2,9,10 Myocardial taurine concentrations also
fail to correlate with the development of overt DCM.7
Concurrent central retinal degeneration (secondary to
taurine deficiency) is an inconsistent finding.2,10
Given the limitations of the tests used to identify
taurine deficiency, taurine supplementation is recom-
mended in all cats with DCM regardless of the whole
blood (or plasma) taurine concentration.2,10,11 Assessment
of the response to taurine supplementation appears to
be the most reliable method of identifying taurine defi-
ciency. Clinical improvement is typically observed
within 2 weeks, however, significant echocardiographic
Melbourne Veterinary Specialist Centre, Glen Waverley, Victoria,
Australia
Corresponding author:
Lydia E Hambrook BVSc, MACVSc (Small Animal Medicine),
Melbourne Veterinary Specialist Centre, Medicine Department,
70 Blackburn Rd, Glen Waverley, VIC, 3150, Australia
Email: lhambrook@melbvet.com.au; red_lyds@yahoo.com.au

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234 Journal of Feline Medicine and Surgery 14(4)
improvement is not usually detected until after the first
4 weeks of treatment.10,11 Those cats which respond to
taurine supplementation and survive greater than 30
days, have a favourable prognosis as a complete recov-
ery is anticipated.1,10,11 The prognosis for non-taurine
responsive cats is grave, with a median survival time
(MST) of just 11 days.12
Historically, treatment options for non-taurine
responsive DCM cats have been limited. Congestive
signs are controlled via diuretics and angiotensin con-
verting enzymes (ACE) inhibitors. Thoracocentesis and
oxygen supplementation may also be required. Digoxin,
a positive inotrope, may have a small, but significant,
positive impact on left ventricular (LV) systolic function,
but it does not appear to have a beneficial effect on sur-
vival.11,13 Pimobendan, a calcium sensitiser and phos-
phodiesterase inhibitor with positive inotropic, lusitropic
and vasodilatory effects, significantly improves survival
times in dogs with DCM.14,15 While several abstracts
have reported that pimobendan therapy is well tolerated
in cats, studies evaluating the effect of pimobendan on
survival are lacking.16,17 The purpose of this study is to
assess the effect of pimobendan on the survival of cats
with non-taurine responsive DCM.
Materials and methods
The medical records of client-owned cats diagnosed with
overt DCM between February 2001 and July 2010 at
the Melbourne Veterinary Specialist Centre, Melbourne,
Australia were retrospectively reviewed. Inclusion crite-
ria included M-mode echocardiographic evidence of LV
dilation (LV internal dimension at end systole, LVIDs >14
mm) and systolic dysfunction (fractional shortening, FS
<28%),2,11,12 clinical signs attributable to DCM (including
CHF and/or ATE) and an intention to treat. Exclusion cri-
teria included a clinical or echocardiographic response to
taurine therapy, prior treatment with pimobendan, evi-
dence of congenital heart disease and a lack of follow-up.
Diagnostic evaluation
The signalment, history and clinical findings were
reviewed in all cats along with haematological, radio-
graphic and electrocardiographic (ECG) findings where
available. Echocardiography was performed by one of
three internal medicine specialists (Drs D Merrett BVSc,
MVS, FACVSc, R Labuc BVSC, MVS, FACVSc and co-
author P Bennett, BVSc, FACVSc, DACVIM) using one of
two ultrasound machines (GE Healthcare LOGIQ5 Pro or
Toshiba Corevision). Standard echocardiography using
2D, M-mode, colour flow and pulse wave Doppler was
performed.18 Between 2001 and 2005, left atrial (LA) and
aortic outflow (AO) Dimensions were measured in the
right parasternal short axis M mode view, but from 2005
onwards these parameters were measured in the right
parasternal long axis 2D view with the image optimised
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for LA and LV outflow tract respectively.18,19 LV dimen-
sions were measured from the right parasternal short axis
view in M mode at the level of the chordae tendineae. An
average of at least three leading edge measurements was
recorded. If sedation was required to facilitate echocardi-
ography, a combination of butorphanol (Dolorex;
Intervet), acepromazine (ACP 2; Delvet), diazepam
(Pamlin; Parnell) and/or ketamine (Ketamine; Parnell)
was administered to effect.
Treatment and outcome
Treatment methods were also reviewed. All cats received
standard therapy with oral frusemide (Lasix-M; Sanofi-
Aventis), taurine (Taurine powder; Musashi) and either
benazepril (Fortekor; Novartis) or enalapril (Enalfor;
Merial). Pimobendan (Vetmedin; Boehringer Ingelheim)
was administered to 80% of cats diagnosed after 2005.
As pimobendan is not registered for use in cats, it was
administered with the informed consent of the owners.
Some cats in the non-pimobendan group also received
digoxin (Lanoxin-BG; Sigma Pharmaceuticals) as a posi-
tive inotrope. Response to treatment and outcome was
determined by a review of patient records and phone
communication with owners. Survival times were calcu-
lated from the time of diagnosis to the time of death.
Statistical analysis
The comparisons of survival times, prognostic factors
and differences between the groups at the time of diag-
nosis were statistically assessed using a commercially
available software program (Statsdirect statistical soft-
ware version 2.7.0). To assess differences between the
groups prior to treatment, Mann Whitney U tests were
performed on the parametric data and Fisher’s exact
tests were used for dichotomous data. Survival data
were collated using Kaplan Meier plots. Median survival
times and Brookmeyer-Crowley 95% confidence inter-
vals (95% CI) were determined. Given that the propor-
tional hazards assumption was satisfied, differences in
survival were assessed using the log-rank test with right
censoring. Statistical significance was indicated by a
P value <0.05.
Results
A search of the medical records between 2001 and 2010
revealed 35 cats that met the inclusion criteria. Three cats
were subsequently excluded because of a clinical and
echocardiographic response to taurine (n = 2) and a lack
of follow-up (one). None of the assessed cats had any
evidence of congenital heart disease. Of the 32 cats
included in the study, 16 were treated with pimobendan.
Signalment
The majority of cats were mixed breeds (15 domestic short-
hair, five domestic longhair, two domestic mediumhair),
Hambrook and Bennett 235
but Burmese (four), Siamese (two), British Shorthair (one),
Somali (one), Russian Blue (one) and Ragdoll (one) were
also represented. Two-thirds were male (20 neutered, one
intact), the remainder were de-sexed females. Median age
was 10 years (range 3–16). Weight ranged from 2.8–7.75 kg
with a median of 4.7 kg.
History
All cats were being fed a wide range of commercial cat
foods and home-cooked diets. Most cats had indoor and
outdoor access. A range of pre-existing medical condi-
tions were identified including; feline idiopathic cystitis
(n = 4), prior hyperthyroidism treated with radioactive
iodine (two), trauma (two), bronchitis (two), chronic
low-grade renal disease (one) and herpes keratitis (one).
None of the cats had any prior history of cardiac disease.
All cats were euthyroid at the time of presentation.
Presenting signs
All cats presented with clinical signs attributable to
DCM including an increase in respiratory effort (n = 28),
ATE (three), ascites (two) and collapse (one). The median
heart rate (HR) was 180 bpm (range 116–250). Thoracic
auscultation revealed abnormalities in 31/32 cats (96.9%)
including a gallop sound (n = 23), systolic murmur (11),
muffled heart sounds (one) and an arrhythmia (nine).
The median respiratory rate was 40 bpm (range 18–80).
Diagnostic investigation
Eighteen cats required sedation to facilitate echocar-
diography. Valvular insufficiency was evident in
22 cats (11 mitral and tricuspid, 10 mitral, one tricus-
pid). Spontaneous echogenic contrast (smoke) was visi-
ble within the left atrium of three cats. A pleural effusion
was evident in 22 cats. Pericardial effusion (n = 4) and
ascites (three) were also observed. Radiographic find-
ings included cardiomegaly in 13 cats and pulmonary
oedema in 11 cats. Of nine cats with audible arrhythmias,
seven had ECGs performed. These revealed ventricular
premature contractions (n = 3), paroxysmal ventricular
tachycardia (one), atrial premature contractions (one)
and supraventricular tachycardia (two).
Treatment
All cats received frusemide (5–20 mg PO q8–12h as
needed, median dose 1.9 mg/kg; range 0.9–3 mg/kg
q8–12h), taurine (250 mg PO q12h) and either benazepril
(n = 31) or enalapril (n = 1) therapy (1.25–5 mg PO q24h,
median dose 0.48 mg/kg; range 0.32–0.89 mg/kg).
Two cats also received spironolactone (Aldactone; Pfizer:
12.5 mg PO q24h, range 2.6–3.5 mg/kg) and aspirin
(Aspirin; Mayne Pharma International: 25 mg PO q72h,
range 4.4–6.8 mg/kg). Fifteen cats required thoracocente-
sis and 11 required oxygen therapy. Sixteen cats received
pimobendan (0.65–1.25 mg PO q12h, 1 h before food,
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median dose 0.26 mg/kg q12h; range 0.16–0.37 mg/kg)
and nine cats received digoxin (31.25 µg PO q24h, median
7 µg/kg; range 4.85–11.1 µg/kg). Seven cats did not
receive a positive inotrope. None of the cats receiving
pimobendan received digoxin. Prior to presentation at
the specialist centre, 17 cats (eight cats in the pimobendan
group and nine cats in the non-pimobendan group)
received frusemide therapy for 1–5 days (median 2 days)
and four cats (one in the pimobendan group and three in
the non-pimobendan group) received an ACE inhibitor
for 2–4 days (median 2 days).
Differences between the non-pimobendan and
pimobendan groups
Assessment of variance between the pimobendan and
non-pimobendan groups revealed a significant increase in
the LA and LA:AO in the pimobendan group at the time
of diagnosis (median 24.3 vs 20.6, P = 0.038 and median
3.21 vs 2.76, P = 0.007, respectively). Fourteen cats in the
pimobendan group had echocardiographic evidence of
valvular insufficiency compared to eight in the non-
pimobendan group (P = 0.03). No other variables were
statistically different between the two groups (Table 1).
Outcomes
Each of the 32 cats demonstrated persistent/recurrent
clinical signs and/or echocardiographic evidence of DCM
despite medical treatment. In the non-pimobendan group,
all 16 of the cats died. A total of seven episodes of ATE
were recorded in four cats (two at the time of diagnosis
and five following the instigation of treatment). Twelve
were euthanased due to refractory CHF (8/16) or ATE
(4/16) and four died suddenly (presumed to be cardiac
related). The survival times ranged from 1 day to 244 days
with a MST of 12 days (95% CI; 4–33 days, see Figure 1).
Of the 16 cats in the pimobendan group 15 died. One
cat remained alive at the time of writing (502 days after
diagnosis) and it was censored from the outcome analy-
sis. Two episodes of ATE were reported. One cat demon-
strated clinical evidence of ATE within 24 h of diagnosis
and a second cat developed an ATE 111 days into treat-
ment. Eight cats were euthanased due to refractory CHF
(n = 5), ATE (two) and seizure activity (one). Sudden
death was observed in seven cats (presumed cardiac
related). The survival times ranged from 1 day to >502
days. The median survival time of the pimobendan
group was 49 days (95% CI; 11–164 days). The differ-
ence in survival between the pimobendan and non-
pimobendan groups was statistically significant (P =
0.048). No adverse effects were reported.
Prognostic indicators
Clinical and echocardiographic variables were com-
pared to survival in an attempt to identify prognostic
indicators. Hypothermia at presentation (<37.2°C) was
236 Journal of Feline Medicine and Surgery 14(4)

Table 1  Comparison of the baseline clinical variables between the non-pimobendan and pimobendan treatment groups

Variable Non-pimobendan group Pimobendan group P value

Median (range) Median (range)

LVIDs 17.55 (14.0–22.4) 17.6 (14.3–26) 0.48

LVIDd 20.65 (15.6–25.7) 22.15 (17.7–28.5) 0.26
IVSd 3.4 (2.5–5.7) 4.15 (2.7–5.4) 0.19
LVFWd 4.6 (2.6–6.2) 4.5 (1.9–5.4) 0.33
FS 14.35 (3–26) 16.9 (7–27) 0.23
LA 20.4 (11–27.5) 24.3 (15–31.4) 0.038*
LA/AO 2.77 (1.6–3.35) 3.21 (2.24–5.24) 0.007*
ATE 2 1 0.61
Heart rate 180 (116–200) 200 (120–250) 0.17
Temperature 37.6 (34.1–39.8) 37.7 (33–39.3) 0.56
Bodyweight 4.38 (2.8–6.44) 4.83 (3.4–7.75) 0.36
Age 10 (4–15) 10 (3–18) 0.72
Female 7 4 0.30
Male 9 12 0.30
Valvular insufficiency 8 14 0.03*
Gallop 14 9 0.06

*Denotes P values <0.05

LVIDs = left ventricular internal dimension at end systole, LVIDd = left ventricular internal dimension at end diastole, IVSd = interventricular sep-
tal thickness at end diastole, LVFWd = left ventricular free wall thickness at end diastole, FS = fractional shortening, LA = left atrial dimension,
AO = aortic outflow, ATE = aortic thromboembolism

Discussion
1.00
Pimobendan appears to have a positive effect on the sur-
Pimobendan vival of cats with non-taurine responsive DCM. While
Non- the MST of cats in the non-pimobendan group was con-
0.75
Pimobendan sistent with that of previous studies (12 days), a four-
Survival fraction

fold increase in the MST of cats in the pimobendan group

0.50
0.25
0.00
0 200 400
Time (days)
Figure 1  Survival times of cats treated with (n = 16) and
without (n = 16) pimobendan. Cats in the pimobendan group
had a significantly longer survival (P = 0.048) than those in
the non-pimobendan group
associated with reduced survival (P = 0.0081). A low
fractional shortening (<20%) at presentation was also
associated with a reduced survival (P = 0.0045). Other
variables (including LVIDs, LVIDd, IVSd, LVFWd, LA,
LA:AO, ATE, BW, age, sex, HR, digoxin and pimobendan
dose) were also assessed, but none had a statistically sig-
nificant effect on survival.
(49 days) was observed.12 Similar to previous studies,
digoxin did not appear to have a significant effect on
survival.11,13
As it currently stands, this is the largest study of non-
taurine responsive, feline DCM.12 Unfortunately, the rar-
ity of DCM in cats prevents the accumulation of large
sample numbers, and post hoc analysis of the power
600 of this study was low (0.22). The retrospective nature of
this study led to a lack of blinding, standardisation and
randomisation of the treatment groups and, as a conse-
quence, the results should be interpreted with caution.
While 80% (16/20) of the cats diagnosed after 2005 were
included in the pimobendan group, it appears unlikely
that their improved survival is a function of advances
in supportive care and/or monitoring over the study
period because cats in the non-pimobendan group that
were also diagnosed after 2008 had poor survival times
(MST of 6.5 days).
Significant differences were evident between the two
treatment groups at the time of diagnosis. LA and LA:AO
were increased in the pimobendan group when com-
pared to the non-pimobendan group. The significance of

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Hambrook and Bennett 237
this difference is difficult to interpret because the method
of measuring the LA and AO changed in 2005 from
the right parasternal short axis M mode to the right
parasternal long axis 2D view. While this change in
methodology may artificially increase the LA:AO ratio
in cats assessed after 2005 (80% of these cats were in
the pimobendan group), LA measurements tend to be
smaller when measured in the long axis 2D view.
Consequently, the change in methodology should not
have lead to an increase in both LA:AO and LA unless a
genuine increase in LA dilation was observed.19
As DCM progresses, dilation of the atrioventricu-
lar annulus can also lead to valvular insufficiency.12,20
Fourteen (87.5%) of the pimobendan cats had echocar-
diographic evidence of valvular insufficiency, compared
to eight (47%) in the non-pimobendan group. While this
difference may have reflected improved echocardio-
graphic detection of valvular insufficiency via the use of
a more advanced ultrasound and improved technique in
the second half of this study, the concurrent increase in
LA:AO suggests an increased incidence rather than
enhanced detection. While none of these variables had
an adverse effect on survival, the increase in LA, LA:AO
and valvular insufficiency in the pimobendan group
may suggest that these cats had more advanced disease
(with annular dilation). None of the affected cats had a
history of a pre-existing heart murmur or echocardio-
graphic evidence of valvular pathology to suggest that
the valvular insufficiency and DCM were secondary to
chronic valvular disease (eg, dysplasia or endocardio-
sis), although this remains a differential.
While the degree of LA dilation was not a prognostic
indicator in this study, a positive correlation between
the incidence of ATE and the degree of LA dilation
has previously been reported.21 Despite the apparent
increase in LA dimension in the pimobendan group, the
incidence of ATE was reduced (n = 2) compared to
the non-pimobendan group (n = 5), but this difference
was not statistically significant. In vitro studies using
feline platelet rich plasma, have demonstrated that
pimobendan exerts an anti-platelet aggregation effect
(thought to be mediated by inhibition of thromboxane
A2).22 Pimobendan may also theoretically reduce the risk
of thrombus formation by improving LA functional indi-
ces (including LA appendage inflow/outflow veloci-
ties).23 Unfortunately, the low numbers of ATE observed
in this study prevented assessment of the effect of
pimobendan on the incidence of ATE in cats with DCM.
Aspirin was administered to two cats in the non-
pimobendan group. Both of these cats presented with
ATE at the time of diagnosis and both experienced recur-
rent ATE despite aspirin therapy. Prophylactic aspirin
therapy was not administered to any other cats because of
a distinct lack of clinical data to support its routine use in
feline cardiomyopathy.24 While ATE has been associated
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with reduced survival in studies of cats with hypertrophic
cardiomyopathy and dilated cardiomyopathy, ATE did
not have an adverse effect on survival in this study.11,21,24,25
Hypothermia at the time of presentation was associ-
ated with reduced survival, which is consistent with
previous studies of cats, dogs and humans with heart
disease.11,15 Severe systolic dysfunction (FS <20%) was
also identified as a negative prognostic indicator. While
reduced FS has been associated with a poor outcome in
humans with DCM, this finding has not been previously
reported in cats.26 Right ventricular internal dimension
at diastole (RVIDd), hospitalisation and concurrent
hyperthyroidism have been previously identified as
prognostic indicators in feline DCM, but these factors
were not assessed in this study.11 In dogs with DCM,
ascites, atrial fibrillation and a young age at presentation
have also been identified as negative prognostic indica-
tors.27, 28 While none of the cats assessed in this study had
atrial fibrillation, the presence of a dysrhythmia was not
associated with reduced survival. Age and the presence
of ascites did not affect outcome. While previous studies
have indicated that body weight correlates with survival
in cats, dogs and humans with heart disease, this trend
was not observed in this study.29
Where possible thoracic radiographs were per-
formed post thoracocentesis. While 22 cats had evidence
of a pleural effusion on ultrasound, 14 had evidence of
residual pleural effusion on thoracic radiographs. Five of
the cats with low volume residual pleural effusion had
radiographic evidence of concurrent cardiomegaly and
pulmonary oedema. The presence of a moderate volume
pleural effusion in the remaining nine cats prevented
accurate radiographic assessment, and consequently the
true incidence of cardiomegaly and pulmonary oedema
could have been higher than previously stated.
While diets were not standardised, all cats received
taurine supplements throughout their treatment. Primary
taurine deficiency appears unlikely in this population of
cats given that all cats continued to exhibit congestive
signs, died suddenly or were euthanased due to car-
diac related issues despite taurine supplementation.
Cats which demonstrated a clinical and/or echocar-
diographic response to taurine supplementation were
excluded from this study. Follow-up echocardiography
was not routinely performed and consequently a partial
taurine response cannot be excluded. Interpretation of
follow-up echocardiography may have been difficult
because improvement may be due to either pimobendan
or taurine therapy. Unfortunately, the poor prognosis of
these cats meant that there was not enough time to trial
taurine therapy prior to the introduction of pimobendan.
Strict inclusion criteria were applied to enable com-
parison with previous survival studies.2,11,12 While echo-
cardiography was performed using sedation in 19 cats,
previous studies have indicated that, while sedation
238 Journal of Feline Medicine and Surgery 14(4)
may decrease FS, LVIDs is unaffected. Consequently
sedation should not lead to incorrect diagnosis of DCM
when two strict criteria (LVIDs >14 mm and FS <28%)
are applied concurrently.30–32 Echocardiographic error
was also minimised by recording an average of at least
three measurements.
While 22/32 cats in this study had echocardiographic
evidence of valvular insufficiency, 2/32 cats had tach-
yarrhythmias and 1/32 cats had evidence of mild, focal
hypertrophy of the left ventricular free wall (6.2 mm,
IVSDd 5.6 mm), it is not known whether these changes
relate to the cause or effect of DCM.33 Given that post-
mortem examinations were not performed, the inciting
cause of DCM and cause of death were not confirmed.
An increased incidence of DCM has previously been
reported in DSH, Siamese, Persians, Himalayans and
Abyssinians, but no breed predisposition was observed
in this study.2,34 The percentage of domestic mixed breed
(68.75%), Burmese (12.5%) and Siamese (6.25%) cats with
DCM was similar to that of the general population pre-
senting to this referral centre (66%, 7% and 4%, respec-
tively). More male than female cats were included in this
study, but the proportion is not statistically different to
the hospital population (P = 0.18).
Pimobendan has demonstrated positive inotropic and
balanced vasodilatory effects in cats during experimen-
tal studies.32 In dogs, pimobendan is thought to have a
very rapid onset of action (<2 h) following oral adminis-
tration and consequently, it is indicated for used for
acute stabilisation of decompensated heart failure.36 An
abstract presented at the European College of Veterinary
Internal Medicine (ECVIM) 2010 reported that the phar-
macokinetics of pimobendan in healthy cats following a
single oral dose (0.23–0.35 mg/kg) was very similar to
that previously reported in dogs, although the maxi-
mum plasma concentration was substantially higher
and the elimination phase was approximately three
times as long.37 Given that such a rapid onset of action is
anticipated with pimobendan therapy, survival data was
collected on the basis of an intention to treat.
In this study, the dose of pimobendan therapy was
extrapolated from the canine dose range and limited by
the available tablet/capsule size.38 Compliance was
improved via the administration of the chewable tablets
rather than the capsules (which tended to adhere to the
roof of the mouth).
Pimobendan use in cats with perceived systolic dys-
function has been only previously been reported in
abstract format. The first abstract (ECVIM 2007), cited
pimobendan use in 11 cats (1.25 mg/cat q12h) with con-
gestive heart failure secondary to dilated (n = 7), hyper-
trophic (three) and restrictive (one) cardiomyopathy.16
No adverse effects were noted and reported survival
times ranged from 9­­­­–585 days. A second abstract pre-
sented at ACVIM 2010, reported mild adverse responses
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in 5/161 cats treated with pimobendan (0.08–0.42 mg/
kg q 12 h) in combination with a range of other medica-
tions (including frusemide, ACE inhibitors and anti-
thrombolytic agents).17 These adverse effects included
agitation (n = 2), anorexia (n = 1), vomiting (n = 1) and
constipation (n = 1). The treated cats were reported to
have congestive heart failure secondary to hypertrophic
(n = 62), unclassified (55) and dilated (27) cardiomyopa-
thy but the diagnostic criteria were not specified. The
median survival time of all cats treated with pimobendan
was 102 days (range 9–870 days). Survival benefit could
not be assessed in these abstracts due to the inclusion
of a range of cardiomyopathies and a lack of a control
population, however, both reports concluded that
pimobendan therapy was well tolerated in cats. No
adverse effects were observed during this study.
Conclusions
Pimobendan therapy appears to improve the survival
of cats with non-taurine responsive DCM. While
pimobendan therapy appears to be well tolerated in cats,
determination of the pharmacokinetics of pimobendan in
cats is also needed to ensure that the dose and dose fre-
quency used in this study is adequate. Further investiga-
tion of the effect of pimobendan on the incidence of ATE
and the survival of cats with DCM is also warranted.
Funding  This research received no specific grant from any
funding agency in the public, commercial, or not-for-profit
sectors.
Conflict of interest  The authors declare that there is no con-
flict of interest.
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