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Feline cardiomyopathy







luca Ferasin














three years as assistant professor
at the University of Padova,
Italy, he moved to the University
of Bristol and taught feline and
Cardiomyopathy is the most common form of heart disease observed in
cats and patients present with a wide spectrum of structural and functional
cardiac abnormalities. Although several attempts have been made to
standardise the classification of the various forms of cardiomyopathy,
substantial disagreement still exists among cardiologists since classification
criteria are often subjective and are continuously evolving as the aetiology
of myocardial disease becomes better understood. This article describes the
current classification of cardiomyopathies, as well as the pathophysiology,
clinical findings and treatment of the disease in feline patients.
canine cardiorespiratory medicine.
In 2006 he was appointed
associate professor in veterinary
cardiology at the University of
Minnesota, USA. He returned to
the UK in 2008 and is currently a
visiting cardiology consultant in
southern England and northern
Italy. He holds the RCVS certificate
in cardiology, the certificate in
teaching and learning in higher
education, and the European
College of Veterinary Internal
Medicine diploma in cardiology.
He is an RCVS recognised specialist
in veterinary cardiology.
Traditional classification

According to the World Health Organization, cardio-
myopathy is defined as a disease of myocardium
associated with cardiac dysfunction (Richardson
and others 1996). Currently, its classification is pri-
marily based on echocardiographic examination
(Table 1), although there is a substantial phenotypic
variability within the same form of cardiomyopathy
(Fig 1) and this often causes subjective interpretations
of echocardiographic diagnosis, especially by inexpe-
rienced ultrasonographers. Pathological investigation
is an alternative approach, but this is less relevant to
practical clinical considerations.

Hypertrophic cardiomyopathy
Hypertrophic cardiomyopathy (HCM) represents the
most common myocardial disease in cats. It is charac-
terised by increased cardiac mass associated with left
ventricular hypertrophy (LVH), which can affect differ-
ent portions of the interventricular septum (IVS) and/
or left ventricular free wall (LVFW). These lesions can
be accompanied by left atrial dilation, aneurismal thin-
ning of the left ventricle (LV) apex, right ventricular
hypertrophy and right atrial enlargement.
Hypertrophic obstructive cardiomyopathy is a
form of HCM that is associated with dynamic outflow
obstruction (see systolic anterior motion, p 209).

Restrictive cardiomyopathy
Restrictive cardiomyopathy (RCM) is characterised by
myocardial stiffness and diastolic dysfunction (restric-
tive pathophysiology), and is the second most common
form of cardiomyopathy in cats (approximately 20 per
cent of referred feline cardiomyopathy cases [Ferasin
and others 2003]). The spectrum of phenotypes in
RCM is even wider than that observed in HCM. In
the human literature, RCM has both myocardial and
endomyocardial forms (Hare 2008), and this classi-
fication has also been used to describe RCM in cats
(Fox 2004). The myocardial form of feline RCM
is characterised by restrictive filling, a normal or mildly
thickened LVFW or IVS, apparently preserved systolic
function and severe atrial (often bi-atrial) enlarge-


Table 1: Criteria used for the traditional classification of feline cardiomyopathy











doi:10.1136/inp.e2271
Provenance: Commissioned
and peer-reviewed

Modified from Ferasin (2009a)
LVH Left ventricular hypertrophy, RVH Right ventricular hypertrophy, LV Left ventricle, RV Right ventricle
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a B C




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iVS

iVS




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Fig 1: Echocardiographic B-mode and M-mode images showing the wide
spectrum of feline cardiomyopathy. (a) Hypertrophic cardiomyopathy
(HCM) with diffuse and substantial concentric left ventricular
hypertrophy (LVH). (b) HCM with segmental LVH. (c) HCM with diffuse
and substantial asymmetric LVH affecting primarily the interventricular
septum (IVS). (d) HCM with diffuse and substantial asymmetric LVH
affecting primarily the left ventricular free wall (LVFW). (e) Myocardial
form of restrictive cardiomyopathy (RCM). (f) Endomyocardial form
of RCM with an extensive fibrotic bridge crossing the left ventricular
lumen. (g) Dilated right ventricle and thinning of the right ventricular
free wall (RVFW) in arrhythmogenic right ventricular cardiomyopathy.
(h) Dilated left ventricle (LV) and thinning of the LVFW in dilated
cardiomyopathy. (i,j) Echocardiographic M-mode images of the LV at the
level of the papillary muscles showing regional hypocontractility and
hyperechogenicity of the LVFW (i) and IVS (j) secondary to myocardial
ischaemia. LA Left atrium

ment. The endomyocardial form of feline RCM dif-
fers from the myocardial form due to the presence of
extensive reparative fibrotic lesions, which affect pri-
marily the LV and can present as large scars bridging
the ventricular lumen.

Dilated cardiomyopathy
A severely dilated LV chamber and hypocontractile
myocardium represent the main features of dilated
cardiomyopathy (DCM). This used to be one of the
most common forms of feline cardiac disease until Pion
and others (1987) reported the association between
taurine deficiency and DCM. This cardiomyopathy is
reversible if oral taurine supplementation is promptly
instituted. Based on this discovery, food companies
increased taurine concentration in commercial feline
diets with a dramatic reduction of the risk of taurine
deficiency in the following years. Nevertheless, some
rare cases of DCM that occur secondarily to taurine
deficiency are still observed, although they are nor-
mally related to a non-conventional diet (ie, vegetar-
ian/vegan diets or canine diets). Conversely, some
cases of DCM diagnosed in non-taurine-deficient
cats may be a manifestation of an end-stage form of
another cardiac disease such as HCM, atrioventricular
(AV) valvular dysplasia, ischaemic myocardial disease,
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may appear s c on c c r r c
they may r from ff r
s r sc c or r
s s s because the s r c r r
of cr s r r r r s r
r r s the r heart c rs
can appear as the affected r s ck
rr c r r c r c r
sustained rapid tachycardia (tachycardiomyopathy) or
unrecognised episodes of toxicity or viral infection.

Arrhythmogenic right ventricular
cardiomyopathy
Arrhythmogenic right ventricular cardiomyopathy
(ARVC) is characterised by markedly enlarged right
chambers with a thin and hypokinetic myocardial free
wall, while the left chambers are minimally involved.
ARVC is one of the major causes of sudden cardiac
death in young people due to the presence of malig-
nant arrhythmias (Hare 2008). Similarly, cats with
ARVC may present with a variety of arrhythmias and
conduction disturbances (Harvey and others 2005).

Unclassified cardiomyopathy
A significant number of feline myocardial diseases show
features that are not typical of any other commonly
recognised cardiomyopathy and are therefore described
as unclassified, although they are likely to be an evolu-
tionary phase of another recognised form of cardiomy-
opathy, (eg, an early or end-stage HCM or myocardial
infarction) rather than an individual pathological entity
(Cesta and others 2005, Ferasin 2009a) (Box 1).


Box 1: Phenotypic classification: does it really matter?

The classic differentiation of cardiomyopathy as
hypertrophic, restrictive or dilated mixes structural
changes (eg, hypertrophy and dilation) with functional
abnormalities (eg, a restrictive pattern of ventricular
filling). Consequently, confusion may arise because the
same disease could appear in two categories, forcing
many clinicians to consider an additional category called
unclassified cardiomyopathy. Although some lesions

and compensatory mechanisms may be similar, even if
they are initiated by different pathologies. Moreover,
rhythmic disturbances and enhanced arrhythmogenicity
also participate in heart remodelling
(tachycardiomyopathy) and should be considered in the
current classification of cardiomyopathy. During the
natural course of the disease, myocardial lesions may
initially affect the left ventricle and subsequently, as a







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a B




rVFW


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C D
Echocardiographic appearance may vary during the progression of myocardial disease. These
echocardiographic images are from a 13-year old female neutered domestic shorthair cat presented initially
for sudden-onset dyspnoea. All images are obtained from the right parasternal short-axis view. (a) Diffuse
and substantial asymmetric hypertrophy affecting the left ventricular free wall (LVFW) and part of the
interventricular septum (IVS). The right ventricle (RV) appears normal. (b) Significant dilation of the left atrium
(LA) and left auricle (LAu). The echocardiographic features in (a) and (b) would be consistent with a diagnosis
of hypertrophic cardiomyopathy. (c,d) The same patient when presented nine months later for follow-up. The
left side of the heart seems normalised while the RV and right atrium (RA) appear dilated. There is flattening
of the IVS secondary to RV pressure/volume overload. These findings could mimic a form of arrhythmogenic
right ventricular cardiomyopathy. This case demonstrates how the same myocardial abnormality can present
with different phenotypes during the natural course of the disease. RVFW Right ventricular free wall,
Ao Aorta, RVOT Right ventricular outflow tract
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i
c
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fr




or W M-mode, r r s r s r - s


or W M-mode, r r s r s r - s





or W

or W
- r r s r s r - s

- r r s r s r - s










iVS




lVFW

a
g 2: (a) M-mode and (b) B-mode
hocardiographic images of the
ft ventricle of a cat showing
false tendon (arrows), which
uld easily be included in the
terventricular septum (IVS)
easurement, especially when
suboptimal imaging setting is
ed. Both images are obtained
om the right parasternal short-
is view. LVFW Left ventricular
e wall
B


iVS







lVFW
Myocardial hypertrophy
There is no consensus on criteria to define LVH.
Wagner and others (2010) compared different defi-
nitions of LVH (Table 2) and concluded that differ-
ent criteria for LVH yield different diagnoses and
that there is limited agreement between M-mode and
B-mode measurements. Furthermore, false positive
results may be generated by M-mode measurements
due to the presence of false tendons (Fig 2), which are
often difficult to identify with this technique and can
be easily and erroneously included in the measurement
of the IVS thickness.


Aetiology and epidemiology

Different studies report different median ages of cats
diagnosed with cardiomyopathy, which may be due
to varying feline populations at different veterinary
institutions. However, with some exceptions, cats
affected by cardiomyopathy are generally mature indi-
viduals, although cardiomyopathy can be recognised
in younger animals. Male cats seem to be more affected
Other causes of myocardial hypertrophy are given
in Table 3.


Pathophysiology

Several cardiac functional abnormalities are observed
in cats that are affected by cardiomyopathy.

Diastolic dysfunction
Feline cardiomyopathy is inevitably accompanied by
reduced ventricular relaxation, which can be second-
ary to myocardial hypertrophy, interstitial fibrosis,


Table 2: Different classification criteria to determine left ventricular
hypertrophy on echocardiographic examination in cats
method Definition type of echocardiographic assessment
than females. Some Maine coon, ragdoll, Norwegian
forest, Persian and Burmese cats may be genetically
predisposed, but the majority of cardiomyopathy cases
in practice are in domestic shorthair cats.
LVH
50%
>50 per cent of one wall
segment or 25 per cent
of two neighbouring wall
segments 6 0 mm
Modified from Wagner and others (2010)

B-mode, LV in right parasternal short- or
long-axis view
The primary aetiology of feline cardiomyopathy is
not fully understood, although familial HCM has been
described in different breeds (eg, Maine coon, ragdoll
and British shorthair cats). A causative mutation for
HCM has been identified in the sarcomeric gene for
the cardiac myosin binding protein C (MYBPC3) both
in Maine coons (Meurs and others 2005) and ragdolls
(Meurs and others 2007), although this mutation
is located in different regions of the same gene in
each breed. Not all cats with this mutation go on to
LVH Left ventricular hypertrophy, IVSd Interventricular septum in diastole, LVFWd Left ventricular
free wall in diastole, LV Left ventricle

Table 3: Potential causes of myocardial lesions to consider before
making a diagnosis of primary cardiomyopathy
potential cause of myocardial hypertrophy potential myocardial lesion observed

Systemic hypertension Concentric LVH
Left or right outflow obstruction Concentric LVH or RVH
Acromegaly Concentric LVH
develop HCM and, similarly, HCM can be diagnosed
in cats that appear negative on genetic testing. It is
Myocardial tumours (eg, lymphomas,
mesotheliomas)
Concentric symmetric or asymmetric LVH
and hypokinesis
therefore possible that other mutations play a role in Hyperthyroidism Modest septal hypertrophy
the phenotypical expression of HCM, and not just at
a sarcomeric level.
Dystrophin-deficient hypertrophic feline
muscular dystrophy
Concentric LVH and hypokinesis, hyperechoic
endocardium
Primary HCM needs to be differentiated from sec-
ondary LVH caused by LV pressure overload (ie, LV
outflow obstruction, systemic hypertension), hyper-
somatotropism and hyperthyroidism. However, it
has been observed that hyperthyroid cats present
with only a modest septal hypertrophy (Connolly and
others 2005).
Myocardial ischaemia Depressed and hypokinetic myocardial areas,
ventricular chamber dilation
Mitral/tricuspid dysplasia LV/RV dilation and LA /RA enlargement
Myocarditis Concentric or asymmetric LVH or RVH
Modified from Ferasin (2009a)
LVH Left ventricular hypertrophy, RVH Right ventricular hypertrophy, LV Left ventricle,
RV Right ventricle, LA Left atrium, RA Right atrium
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typical of i l c to i l
c c or k in the left atrial cavity (
thrombi. (d) c i in the left ic
a form of ic i c i by the pr
A auricle, RA Right atrium, Ao Aorta, Right
i (c) c c i ic of
ws), a risk of of i c i
ular (arrows). cat was i
of an i c i i
tricular c















a B

Fig 3: (a) Eleven-year-old male neutered domestic shorthair cat presented with sudden-onset pain and hindlimb
paresis caused by an arterial thromboembolism. (b) The cats skin in the metatarsal region is dark blue, which is








lau


rVot
ra

ao

la

la


lau

C D

loss of cellular architecture or a combination of these
mechanisms. An increased heart rate may also exac-
erbate the diastolic dysfunction by reducing the time
available for ventricular filling and for coronary blood
flow, which may lead to myocardial ischaemia. The
diastolic dysfunction causes an increase in the LV and
left atrium (LA) filling pressure, resulting in pulmo-
nary venous hypertension and eventually pulmonary
oedema and/or pleural effusion (congestive heart
failure [CHF]).

Systolic dysfunction
Although reduced myocardial contractility is a pre-
dominant feature of DCM and ARVC, systolic dys-
function has also been demonstrated in cats with HCM
by pulsed tissue Doppler imaging (TDI) techniques
(Koffas and others 2006). Systolic impairment can
appear in all forms of cardiomyopathy accompanied
by ischaemia and replacement fibrosis, and systolic
dysfunction will result in increased ventricular filling
pressure and CHF.

Arterial thromboembolism
An altered blood flow or blood stasis within the car-
diac chambers can increase the risk of red blood cell
aggregation and intracavitary thrombus formation,
especially at the level of an abnormally enlarged left
auricle. When a thrombus or a fragment of it dislodges
and moves into the systemic circulation via the aorta, it
can block one of the major arteries causing limb paresis/
paralysis, renal infarction or sudden death. Although
not all patients with echocardiographic evidence of
intracavitary thrombi develop an arterial thrombo-
embolism (ATE), this finding usually represents a
severe risk of haemodynamic complication (Fig 3).

Arrhythmias
Unpublished studies by the author based on 24-hour
ECG Holter recordings (Fig 4) show that almost all
cats affected by cardiomyopathy suffer from significant



Fig 4: Twenty-four-hour ECG (Holter) monitoring in
a cat. This advanced ECG recording technique allows
the identification of paroxysmal arrhythmias and
intermittent conduction abnormalities in patients
affected by cardiomyopathy
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ventricular or supraventricular arrhythmias. Further-
more, many patients with cardiomyopathy have con-
duction abnormalities with complete AV block being
the most common finding. The haemodynamic dis-
turbances secondary to arrhythmias contribute to the
complex pathophysiology of feline cardiomyopathy.

Myocardial ischaemia
Regional myocardial ischaemia is commonly rec-
ognised in feline patients with all forms of cardio-
myopathy and is often associated with replacement
fibrosis (Fox 2003a, 2004, Cesta and others 2005).
Ischaemia can be secondary to intramural coronary
arterial disease caused by myocardial hypertrophy,
and is frequently followed by malignant arrhythmias,
as well as systolic and diastolic impairment. The sig-
nificant elevation of cardiac troponin-I (cTn-I) in cats
with HCM might indicate ongoing myocardial dam-
age, possibly secondary to a concurrent myocardial
infarction (Connolly and others 2003).

Systolic anterior motion
Systolic anterior motion (SAM) of the mitral valve is a
form of dynamic LV outflow obstruction that is present
in approximately half of feline HCM cases. It is char-
acterised by an abrupt movement of the anterior leaflet
of the mitral valve towards the IVS, interfering with
the LV outflow in mid-systole. The abnormal position
of the mitral leaflet in systole is also responsible for a
simultaneous mitral regurgitation, resulting in a typi-
cal double jet on colour Doppler echocardiography.
The abnormal movement of the septal leaflet can also
be observed on M-mode imaging of the mitral valve
and on spectral Doppler evaluation of the LV outflow
tract, with an increased aortic peak flow velocity and
an abrupt acceleration in mid-systole, which produces
a characteristic asymmetric waveform (Fig 5).
The dynamic obstruction caused by SAM has many
consequences:
It reduces the stroke volume, hence the cardiac
output;
It causes LV pressure overload, which may stimu-
late further cardiac hypertrophy;
Mitral regurgitation may lead to atrial remodelling
(LA dilation);
The continuous mechanical contact between the
septal mitral leaflet and the proximal IVS induces
fibrotic lesions (contact lesions) that can affect the
normal function of both affected anatomical parts.
The blood flow turbulence originating during SAM
is also responsible for the presence of systolic murmurs
on auscultation in many cats with cardiomyopathy.









iVS
ao


lVot

lVFW
la




a B

Fig 5: Systolic anterior motion of the mitral valve (MV) in a six-year-old male neutered domestic shorthair cat.
(a) Right parasternal long-axis B-mode echocardiography with colour Doppler interrogation of the MV area
and left ventricular outflow tract (LVOT) showing the typical double jet during the dynamic outflow obstruction.
(b) Spectral Doppler interrogation of the LVOT showing increased aortic outflow velocity and the characteristic
asymmetry with a mid-systolic step (arrows). (c) Right parasternal short-axis M-mode echocardiography of the
left ventricle (LV) at the level of the MV showing a mid-systolic movement of the septal mitral leaflet towards the
interventricular septum (IVS) (arrows). (d) Right parasternal long-axis colour M-mode Doppler echocardiography
of the LV at the level of the MV showing a mid-systolic jet during the abnormal movement of the mitral septal
leaflet (arrows). LVFW Left ventricular free wall, LA Left atrium, Ao Aorta









iVS iVS


lVFW

C D


lVFW
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Box 2: Is SAM secondary to HCM or vice versa?

Despite a widespread belief among clinicians, systolic anterior motion (SAM) of the mitral
valve is not necessarily associated with myocardial hypertrophy. Although the degree
of dynamic obstruction is related to the severity of left ventricular hypertrophy (LVH), it
could be speculated that LVH may not solely be a phenotypical manifestation of a
primary hypertrophic cardiomyopathy (HCM) but may also be a consequence of the left
ventricle (LV) pressure overload caused by the outflow obstruction (Schober and Todd
2010). Furthermore, several cases of feline SAM are observed in the absence of LVH, and
this could represent either an early stage of the disease not yet accompanied by LVH, or
a degree of LV pressure overload not sufficient to stimulate hypertrophy. Understanding
the exact pathophysiology of SAM may provide valuable information for treating cats
with obstructive HCM.


The cause of SAM is not fully understood and
several hypotheses have been suggested, with altered
LV geometry associated with intrinsic mitral valve
abnormalities being the most plausible explanation
(Ferasin 2009a, Schober and Todd 2010) (Box 2).


Clinical findings

The clinical presentation of cats affected by cardiomy-
opathy does not differ between the various forms of
the disease, so it is more practical to approach all these
cases simply as patients with myocardial disease.

Heart murmurs
Heart murmurs are very common in cats with cardio-
myopathy (approximately 60 per cent of cases [Ferasin
2009a]) and usually originate from dynamic left ven-
tricular outflow tract obstruction and/or mitral regur-
gitation (Fig 6). The murmurs are systolic, often with
variable intensity, and can easily be heard over both
parasternal regions. They may be present at rest or may
become audible when the heart rate and cardiac contrac-
tility increase (eg, during stress or excitement). Several
cases of cardiomyopathy are diagnosed in asymptomatic
cats following the detection of a heart murmur. Murmurs
originating from SAM can also be present in the absence
of echocardiographically detectable LVH and, for this
reason, may allow early identification of animals that
may develop myocardial changes later in life.

Gallop sounds
Gallop sounds present another common clinical find-
ing in cats with cardiomyopathy. They are caused by
audible diastolic sounds (S3 and/or S4) in the presence


Fig 6: Auscultation of the
thorax allows the identification
of heart murmurs and gallop
sounds, which are frequently
detected in cats with
cardiomyopathy. Although
heart murmurs can sometimes
be detected in apparently
healthy cats, this clinical
finding can also prompt an
early diagnosis of myocardial
disease. Echocardiographic
identification of the source
of the murmur is often
challenging and requires
sophisticated equipment, as
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c
v

i

f

of reduced myocardial compliance (eg, myocardial hypertrophy, infiltration, fibrosis,
tachycardia or a combination of these factors).

Muffled heart sounds
Muffled heart sounds can be heard when a pleural and/or pericardial effusion is
present.

Tachypnoea/dyspnoea
Tachypnoea/dyspnoea is a common clinical sign in cats with cardiomyopathy
complicated by CHF (pul- monary oedema and/or pleural effusion). Laboured breathing
sometimes occurs acutely after a stressful event (eg, a car journey, hospitalisation or
restraint), so cats suspected of having cardiomyopathy should always be examined
gently and cautiously.

Limb paresis/paralysis
Limb paresis/paralysis associated with ATE is often seen in cats with
cardiomyopathy. Although bilateral hindlimb paresis represents the most common
presen- tation (71 per cent of all ATE cases [Smith and others
2003]), unilateral hindlimb or forelimb involvement is also possible. Thromboembolism
can also potentially cause sudden death.

Cardiac arrhythmias
Ventricular or supraventricular cardiac arrhythmias are frequently detected in patients
with cardiomyopa- thy. However, some forms of paroxysmal arrhythmias may not be
detected during physical examination or standard electrocardiographic recording.
Arrhythmias contribute to a reduction in myocardial performance and may cause
syncope and sudden death.

Arterial hypotension
Arterial hypotension (ie, a systolic blood pressure below 120 mmHg) has been
recorded in approximately
15 per cent of cats with cardiomyopathy as a result of reduced cardiac output (Ferasin
and others 2003).

Ascites
Ascites can occur in patients with right-sided CHF and are likely to be associated with
ARVC, DCM or other forms of cardiomyopathy complicated by pulmonary
hypertension.


Diagnosis

Echocardiography
Diagnosis of feline cardiomyopathy is based primarily n echocardiographic examination.
Echocardiographic ecognition of basic patterns is very intuitive but clini- ians should be
aware that incorrect conclusions may esult from inexperience or intra- and
interoperator ariability. For example, LVH can be misdiagnosed if he M-mode cursor is
incorrectly aligned or if a pap- llary muscle or a false tendon is included in the LV
measurements. Therefore, a high frame rate B-mode xamination with good image
quality is often indicated or an accurate diagnosis of LVH. Clinicians should also emember
that changes in preload and afterload can ffect LV measurements. A patients
dehydration sta- us can induce a pseudohypertrophy, and overzealous
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fluid therapy can dilate the cardiac chambers simulating
a dilated form of cardiomyopathy.
The recognition and assessment of SAM is based
primarily on colour flow and spectral Doppler studies,
which require correct positioning, optimal settings
and experienced operator skill and interpretation.
Advanced echocardiographic techniques, such
as TDI and myocardial strain analysis, allow further
quantification of regional myocardial function and
can potentially be useful in the early detection of
myocardial dysfunction in cats.

Radiography
Thoracic radiographs are indispensable for recognising
CHF, which is characterised by cardiomegaly, engorged
a B
pulmonary veins and pulmonary oedema or pleural
effusion with, in some cases, ascites. Pleural effusion
and ascites can easily be detected by percussion and
ultrasonography. The distribution of alveolar infiltrate
can be diffuse or patchy, in contrast to the more consist-
ent caudodorsal localisation of cardiogenic pulmonary
oedema seen in dogs. Cardiomegaly is not always obvi-
ous in feline cardiomyopathy, especially when there is
no significant chamber enlargement (Fig 7).

Genetic tests
Laboratory tests are available for Maine coon and rag-
doll cats to identify individuals with a mutation in the
MYBPC3 gene. The test can be performed on EDTA
blood samples or buccal swabs. However, the mutation
in the two breeds is located in a different gene locus
and therefore the test is not interchangeable. A posi-
tive heterozygous or homozygous result indicates that
an individual may be at risk of developing HCM but it
does not signify a diagnosis of HCM this ultimately
requires echocardiographic examination. Furthermore,
HCM can also occur in animals that are negative on
genetic testing, suggesting that there are likely to be
other mutations that have not yet been identified.

Biomarkers
cTn-I is a sensitive and specific marker of cardiac myo-
cyte injury and an increase in its plasma concentration,
which may occur in all forms of the disease, indicates
ongoing myocardial damage. This assay may provide
useful information on the severity of myocardial
damage and prognosis.
The N-terminal pro B-type natriuretic peptide
(NT-proBNP) assay is a new laboratory test that provides
evidence of ongoing myocardial stress. It is highly sensi-
tive and can detect early myocardial changes associated
with cardiomyopathy. A full cardiac evaluation, includ-
ing echocardiographic examination, should always be
performed to identify the cause of NT-proBNP elevation
and determine the proper clinical management.


Therapy

At present, with the exception of dietary taurine
supplementation in cats with cardiomyopathy second-
ary to taurine deficiency, there are no available treat-
ments that have convincingly demonstrated increased
survival times and/or quality of life in cats with myocardial disease.
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a 2012 | 34 | 204213 a 2012 | 34 | 204213







Fig 7: Thoracic radiography is an invaluable
technique to identify signs consistent with
congestive heart failure (CHF) before instituting
treatment. (a) Dorsoventral view of
a nine-year-old male neutered domestic shorthair
cat presented with acute-onset dyspnoea. The
cardiac silhouette is partially covered by a mild
pleural effusion, the pulmonary vessels are
markedly engorged and the patchy
interstitial/alveolar pattern suggests the presence of
pulmonary oedema. (b) Dorsoventral view of the
same patient 24 hours after the administration of
furosemide. The cardiac silhouette is more
distinguishable and the alveolar pattern less
prominent, indicating a radiographic
near-
resolution of
the
previously
detected
CHF


A
s
y
m
p
t
o
m
a
t
i
c

c
a
t
s
Anecdotal reports
claim that
asymptomatic cats
with HCM that are
treated with
diltiazem or
beta-blockers have
improved physical
activity. However,
randomised
placebo-controlled
studies are lacking
to confirm this and
the clinical use of
these drugs in such
ani- mals has still to
be proven,
especially in cases
that are
accompanied by
SAM, which could
potentially ben- efit
from a reduction of
dynamic outflow
obstruction.
Similarly,
angiotensin-converting enzyme inhibitors and
spironolactone have failed to demonstrate signifi- cant
improvements in cats with subclinical forms of HCM
(Macdonald and others 2004, 2006, Taillefer and Di
Fruscia 2006). Cats with asymptomatic forms of
cardiomyopathy and echocardiographic evidence of
intracavitary thrombi may benefit from antithrom-
botic prophylaxis to reduce the risk of ATE but clinical
evidence has not been demonstrated clearly.

Symptomatic cats
Patients presenting with acute CHF require sedation,
cage rest and oxygen supplementation in addition to
parenteral diuresis (ie, furosemide). Significant pleural
effusion should be treated promptly by thoracocentesis.
Once pulmonary oedema is clinically controlled, furo-
semide can be given orally at the lowest effective dose,
to reduce the risk of prerenal azotaemia and hypoka-
laemia. The risk of hypokalaemia could be reduced
by concomitant administration of potassium sparing
agents, such as spironolactone, although sufficient data
of its clinical efficacy in cats are not available.
Diltiazem is licensed in the UK for the management
of HCM due to its bradycardic, lusitropic and coronary
vasodilating properties. However, its beneficial effects
have not been demonstrated clearly in controlled ran-
domised clinical studies. Moreover, the licensed for-
mulation should be administered three times daily and
many clients struggle to comply with this schedule.
Beta-blockers have also been suggested for the
treatment of feline cardiomyopathy, but the only avail-
able, and still unpublished, controlled study shows
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Companion ani mal pr aC tiCe
that cats receiving atenolol and furosemide survived
for a significantly shorter time than cats treated with
furosemide alone. In the same study, cats receiving
enalapril survived as long as or longer than the place-
bo group, although the difference was not statistically
significant (Fox 2003b).
Pimobendan is not licensed for use in cats, although
small, uncontrolled studies seem to demonstrate an
improvement in appetite and demeanour in patients
with feline cardiomyopathy accompanied by systo-
lic dysfunction. However, the pharmacokinetics of
pimobendan in cats are different from those described
in dogs, with a more rapid absorption and longer
plasma half-life; the correct dosage and frequency of
administration is unknown.
A prudent approach should therefore be taken
when recommending any of these drugs in addition
to furosemide, for the chronic treatment of feline
cardiomyopathy.


Prognosis

The life expectancy of a patient depends on the form of
myocardial damage and its severity, with a shorter sur-
vival time in cats with severe cardiac remodelling and
clinical signs of CHF. A retrospective study conducted
on a population of 127 cats with HCM shows a median
survival of 194 days in symptomatic cats versus 3617 in
the asymptomatic group (Payne and others 2010). In the
same study, left atrial enlargement represents another
negative prognostic variable. Other negative prognostic
indicators include the presence of arrhythmias, gallop
sounds, left atrial smoke (spontaneous echocontrast),
and reduced fractional shortening. Interestingly, the
presence of SAM is associated with a longer survival time
and this is possibly because it produces an audible heart
murmur and allows earlier identification of the disease.
Prospective longitudinal studies in progress at the time
of writing and will hopefully add valuable prognostic
information for cats with HCM in the near future.
Other forms of cardiomyopathy carry a less favour-
able prognosis, with a median survival time of 132
days for RCM and 11 days for DCM (Ferasin and oth-
ers 2003). Such poor prognosis is probably associated
with the fact that a dilated and hypocontractile myo-
cardium could represent the end-stage of another form
of cardiomyopathy (Ferasin and others 2003).


Summary

Feline myocardial disease remains a controversial
topic in veterinary cardiology, despite recent discover-
ies on aetiology and pathophysiology that have helped
the understanding of this important clinical condi-
tion. Although echocardiographic diagnosis remains
extremely challenging, it is often oversimplified by
non-experienced ultrasonographers, especially in cases
that are complicated by dynamic outflow obstruction,
which has important implications for the clinical man-
agement of patients. Hopefully, the completion and
publication of some important longitudinal studies cur-
rently in progress will provide answers to the questions
still arising in this clinical area.
References and further reading
CESTA, M. F., BAT Y, C. J., KEENE , B. W., SMOAK, I. W. & M ALARKEY, D. E. (2005)
Pathology of end-stage remodeling in a family of cats with hypertrophic cardiomyopathy.
Veterinary Pathology 42, 458-467
CON NOLLY, D. J., CA N NATA, J., BOSWOOD, A., ARCHER, J., GROVES, E. A. &
NEIGER, R. (2003) Cardiac troponin I in cats with hypertrophic cardiomyopathy. Journal
of Feline Medicine and Surgery 5, 209-216
CON NOLLY, D. J., GUITIA N, J., BOSWOOD, A. & NEIGER, R. (2005) Serum troponin I
levels in hyperthyroid cats before and after treatment with radioactive iodine. Journal of Feline
Medicine and Surgery 7, 289-300
FER ASIN, L . (2009a) Feline myocardial disease. 1: Classification, pathophysiology and
clinical presentation. Journal of Feline Medicine and Surgery 11, 3-13
FER ASIN, L . (2009b) Feline myocardial disease 2: Diagnosis, prognosis and clinical
management. Journal of Feline Medicine and Surgery 11, 183-194
FER ASIN, L ., STURGESS, C. P., CA N NON, M. J., CA NEY, S. M., GRUFF Y DD-JONES,
T. J. & WOTTON, P. R. (2003) Feline idiopathic cardiomyopathy: a retrospective study
of 106 cats (1994-2001). Journal of Feline Medicine and Surgery 5, 151-159
FOX, P. R. (2003a) Hypertrophic cardiomyopathy. Clinical and pathologic correlates.
Journal of Veterinary Cardiology 5, 39-45
FOX, P. R. (2003b) Prospective, double-blinded, multicenter evaluation of chronic therapies
for feline diastolic heart failure: interim analysis. (Abstract). Journal of Veterinary Internal
Medicine 17, 398
FOX, P. R. (2004) Endomyocardial fibrosis and restrictive cardiomyopathy: pathologic and
clinical features. Journal of Veterinary Cardiology 6, 25-31
FOX, P. R., M ARON, B. J., BASSO, C., LIU, S. K. & THIENE , G. (2000) Spontaneously
occurring arrhythmogenic right ventricular cardiomyopathy in the domestic cat: a new animal
model similar to the human disease. Circulation 102, 1863-1870
HARE , J. (2008) The dilated, restrictive, and infiltrative cardiomyopathies. In Braunwalds
Heart Disease: a Textbook of Cardiovascular Medicine, 8th edn. Eds P. Libby, R. O. Bonow,
D. L . Mann and D. P. Zipes. Elsevier Saunders. pp 1739-1762
HARVEY, A. M., BATTERSBY, I. A., FAENA, M., FEWS, D., DARKE , P. G. & FER ASIN, L .
(2005) Arrhythmogenic right ventricular cardiomyopathy in two cats. Journal of Small Animal
Practice 46, 151-156
KOFFAS, H., DUKES-MCEWA N, J., CORCOR A N, B. M., MOR A N, C. M., FRENCH, A.,
SBOROS, V., SIMPSON, K. & MCDICKEN, W. N. (2006) Pulsed tissue Doppler imaging
in normal cats and cats with hypertrophic cardiomyopathy. Journal of Veterinary Internal
Medicine 20, 65-77
M ACDONALD, J. E., KEN NEDY, N. & STRUTHERS, A. D. (2004) Effects of spironolactone
on endothelial function, vascular angiotensin converting enzyme activity, and other prognostic
markers in patients with mild heart failure already taking optimal treatment. Heart 90,
765-770
M ACDONALD, K. A., KITTLESON, M. D., LARSON, R. F., K ASS, P., KLOSE , T. &
WISNER, E. R. (2006) The effect of ramipril on left ventricular mass, myocardial fibrosis,
diastolic function, and plasma neurohormones in Maine Coon cats with familial hypertrophic
cardiomyopathy without heart failure. Journal of Veterinary Internal Medicine 20, 1093-1105
MEURS, K. M., NORGARD, M. M., EDERER, M. M., HENDRIX, K. P. & KITTLESON,
M. D. (2007) A substitution mutation in the myosin binding protein C gene in ragdoll
hypertrophic cardiomyopathy. Genomics 90, 261-264
MEURS, K. M., SA NCHEZ , X., DAVID, R. M., BOWLES, N. E., TOWBIN, J. A., REISER,
P. J., KITTLESON, J. A., MU NRO, M. J., DRY BURGH, K., M ACDONALD, K. A. &
KITTLESON, M. D. (2005) A cardiac myosin binding protein C mutation in the Maine Coon
cat with familial hypertrophic cardiomyopathy. Human Molecular Genetics 14, 3587-3593
PAYNE, J., LUIS FUENTES, V., BOSWOOD, A., CONNOLLY, D., KOFFAS, H. & BRODBELT,
D. (2010) Population characteristics and survival in 127 referred cats with hypertrophic
cardiomyopathy (1997 to 2005). Journal of Small Animal Practice 51, 540-547
PION, P. D., KITTLESON, M. D., ROGERS, Q. R. & MORRIS, J. G. (1987) Myocardial
failure in cats associated with low plasma taurine: a reversible cardiomyopathy. Science 237,
764-768
RICHARDSON, P., MCKEN NA, W., BRISTOW, M., M AISCH, B., M AUTNER, B., OCON
NELL , J., OLSEN, E., THIENE , G., GOODWIN, J., GYARFAS, I., M ARTIN, I. & NORDET,
P. (1996) Report of the 1995 World Health Organization/International Society and Federation
of Cardiology Task Force on the definition and classification of cardiomyopathies. Circulation
93, 841-842
SCHOBER, K. & TODD, A. (2010) Echocardiographic assessment of left ventricular geometry
and the mitral valve apparatus in cats with hypertrophic cardiomyopathy. Journal of Veterinary
Cardiology 12, 1-16
SMITH, S. A., TOBIAS, A. H., JACOB, K. A., FINE, D. M. & GRUMBLES, P. L. (2003) Arterial
thromboembolism in cats: acute crisis in 127 cases (1992-2001) and long-term management with
low-dose aspirin in 24 cases. Journal of Veterinary Internal Medicine 17, 73-83
TAILLEFER, M. & DI FRUSCIA, R. (2006) Benazepril and subclinical feline hypertrophic
cardiomyopathy: a prospective, blinded, controlled study. Canadian Veterinary Journal 47,
437-445
WAGNER, T., FUENTES, V. L ., PAY NE , J. R., MCDER MOTT, N. & BRODBELT, D. (2010)
Comparison of auscultatory and echocardiographic findings in healthy adult cats. Journal
of Veterinary Cardiology 12, 171-182

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Feline cardiomyopathy

Luca Ferasin

In Practice 2012 34: 204-213
doi: 10.1136/inp.e2271



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