HYPERTROPHIC CARDIOMYOPATHY IN A DOMESTIC SHORT HAIR CAT

M.A. Nurliyana
Faculty of Veterinary Medicine, Universiti Putra Malaysia, Serdang, Selangor,
Malaysia
SUMMARY
A 3 years old domestic short hair, male cat was presented to University
Veterinary Hospital-University Putra Malaysia (UVHUPM) for the complaint of
respiratory distress. Radiographic findings on the first day revealed pulmonary
oedema. However, it was initially diagnosed as bronchopneumonia. Problems
resolved after furosemide therapy, however, on day-4, the thoracic radiograph
revealed moderate enlargement of the heart with VHS 8.8 and valentine heart
shape. Full diagnostic investigation of the heart was conducted through
echocardiography. A diagnosis of feline hypertrophic cardiomyopathy (HCM) was
made from the echocardiographic evaluations based on the standard criteria by
American College of Veterinary Internal Medicine (ACVIM). Other diagnostic
workouts inclusive the blood pressure level and thyroid function test was
conducted to rule out hyperthyroidism and hypertension as secondary cause of
HCM.
Keywords: Pulmonary Oedema, Bronchopneumonia, Feline, Hypertrophic cardiomyopathy, VHS,
Echocardiography

INTRODUCTION
Hypertrophic cardiomyopathy
(HCM) is one of the most commonly
encountered heart disease in cats.
This disease is characterized by an
abnormal thickening (hypertrophy) of
one or several areas of the walls of
the heart, usually of the left ventricle
(ACVIM, n.d.). HCM was defined as a
diastolic left ventricular (LV) septal or
free wall thickness 6 mm (J.R.
Payne et.al, 2014).

CASE REPORT
Twin, 3 years old domestic
short hair, male cat, weighing 3.4 kg
was referred to University Veterinary
Hospital-Universiti Putra Malaysia
(UVH-UPM)
for
complaint
of
respiratory distress with appetite
bowel and urination are negative.
Upon physical examinations, the

temperature and pulse were within

the normal ranger, however, there
are

*Corresponding author: Nurliyana Meor

Abdullah
(M.A.
Nurliyana)
Email:
160647@student.upm.edu.my

increase in respiratory rate. Twin was

dyspnoeic with abdominal breathing
and
harsh
lung
sound
upon
auscultation.
A result of the complete blood
count
and
serum
biochemistry
analysis results were normal and did
not contribute towards determining
the cause of dyspnoea in this cat.
Thoracic radiograph was taken
on the first day to evaluate the
conditions. On lateral view, there are
loss of cardiac silhouette and
presence of mixed pattern of the
lung density at perihilar region with

bronchial, interstitial and alveolar

pattern. An initial diagnosis of
bronchopneumonia was made based
on the radiographic findings. As the
cat was dyspnoeic, intranasal oxygen
prong was conducted as initial
treatment above all. Other initial
medications that aimed to reduced
bronchopneumonia are administered
inclusive nebulization (NaCl and
gentamycin), Marbofloxacin 2mg/kg
(intravenously,
once
daily),
Aminophylline
5mg/kg
(intravenously,
twice
daily),
Tramadol 3mg/kg (intravenously,
three times daily), Dexamethasone
1mg/kg (intravenously, once daily).
However, the condition of the cat still
worsen and on day 2, the case was
re-diagnosed as pulmonary oedema
and furosemide therapy was started
aimed to reduce to the accumulation
of fluid. Second radiograph was
repeated and the pulmonary oedema
has resolved. However, from the
radiograph, there are moderate
enlargement of the heart with
Vertebral Heart Size (VHS) of 8.8,
bulging of the left atrium and
valentine
heart
shape.
Further
diagnostic investigation on the heart
was
conducted
through
echocardiography
and
revealed
enlargement of the left ventricular or
hypertrophic cardiomyopathy (HCM).
There are also increase in the left
atrium to aorta ratio suggestive of
left atrial enlargement.
From the M-mode evaluation
of the left ventricle, the left
ventricular wall or interventricular
septal thickness at end-diastole are
more than 6mm which indicate HCM.
The diagnosis was made based on
the standard criteria set by ACVIM.
Thyroid function test and blood
pressure parameter was determined
and the result was unremarkable
thus rule out the possibility of

hyperthyroidism and hypertension as

secondary cause of HCM in this case.
Echocardiographic
examination strongly pointed to a
diagnosis of Feline Hypertrophic
Cardiomyopathy. ACE inhibitor or
benazepril hydrochloride 0.5 mg/kg
( tab, orally, twice daily) was
indicated for HCM in this cat.
DISCUSSION
Hypertrophic cardiomyopathy
is the most common cardiac disease
in the cat. A recent study showed
that in a cardiology referral centre,
46% of cats with heart disease
showed no clinical signs of heart
failure, which highlights how difficult
it can be for veterinary nurses to
recognize a cat with severe heart
disease (P. Charlotte, 2013). Similar
to patient in this case, often the cat
when presented, they are already in
CHF state.
Secondary
hypertrophic
diseases of the heart may be caused
by hyperthyroidism or hypertension,
and lead to signs that mimic HCM,
but if addressed early may be
reversible by treating the underlying
condition.
Primary HCM is not
reversible, and has been shown to
have a genetic link, particularly in
Main
Coons.
Unfortunately,
genotyping is not yet available. It is
not yet possible to isolate the gene
that causes HCM in cats, but through
studying family trees, it has been
shown to be an autosomal dominant
gene in some Main Coons and likely
other breeds as well. (J. Andrea,
2007). In Maine Coon (MC) cats the
c.91G > C mutation in the gene
MYBPC3, coding for cardiac myosin
binding protein C (cMyBP-C), is
associated with feline hypertrophic
cardiomyopathy
(fHCM).
The
mutation causes a substitution of an
alanine for a proline at residue 31

(p.A31P) of cMyBP-C (M. Christiansen

et.al, 2011).
Cats with HCM have reduced
left ventricular compliance that is
probably caused by a combination of
chamber
stiffness,
myocardial
fibrosis, impaired relaxation (an
active, oxygen and energy-requiring
process), and myocardial ischemia;
which reduces oxygen delivery
(Stokhof, 1997).
Cat with HCM also have
increased
risk
to
develop
a
devastating
complication
called
arterial thromboembolism (ATE). ATE
has been found in 12% to 28% of
cats
with
hypertrophic
cardiomyopathy (HCM) and 27% of
cats
with
unclassified
cardiomyopathy. In approximately
70% of cases, the embolization is to
the distal aorta (Smith et al., 2003).
Affected cat will experience acute,
painful condition causing cold and
paresis of the back legs.
Patient in this case was
presented
with
dyspnoea
and
abdominal breathing, thus, oxygen
therapy was indicated as a first line
treatment. This was supported by P.
Charlotte (2013) which stated that if
a cat presents to the veterinary
practice in respiratory distress, first
line treatment should include oxygen
therapy,
diuresis
and
minimal
handling.
Electrocardiography,
clinical
laboratory and ancillary studies do
not sufficiently distinguish HCM from
other forms of cardiomyopathy. Thus,
a careful clinical work up, including
high quality cardiac ultrasonography,
is required for definitive diagnosis.
Confirmation of LV hypertrophy,
including
papillary
muscle
thickening, is necessary for diagnosis
(V.L. Fuentes et.al, 2010)

For cats with HCM that are

already in congestive heart failure,
more
aggressive
therapy
is
necessary. Once the cat is stabilized,
other medications may be required.
Cats that are in heart failure and
have fluid accumulation in their
lungs often benefit from having
diuretics administered. (J. Ross,
2006). In this case, Furosemide is
indicated to treat the pulmonary
oedema.
For the treatment of HCM
itself, the choice is either ACE
inhibitor, Beta-blocker, or Calcium
channel blocker. However, none of
this treatment are
proven to
successfully treated HCM, but, it has
been documented to improve and
prolonged the quality of life of
affected cats.
To reduce the chance of a
thrombus forming within the heart,
many cats are given medications
that reduce the bloods ability to clot,
such as Aspirin or Clopidogrel.
CONCLUSION
Not all cats with heart disease
will develop clinical signs. Treatment
goals for feline HCM aimed to
controlling heart rate, alleviating
pulmonary congestion, removing
pleural fluid (if present), and
decreasing
the
likelihood
of
thromboembolism
or
saddle
thrombus. Echocardiography remains
the gold standard for diagnosis of
HCM in cats.
ACKNOWLEDGEMENTS
The authors would like to
thank to Dr. Khor Kuan Hua as the
supervisor,
staff
of
University
Veterinary Hospital, Universiti Putra
Malaysia, and DVM Class of 2015
Universiti Putra Malaysia.
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