|Idiopathic hypertrophic cardiomyopathy in
the cat |
One of the most common primary feline cardiac diseases is
idiopathic hypertrophic cardiomyopathy (HCM). HCM is characterized
by a massive left ventricular hypertrophy without dilation
and is present without any other cardiac or systemic disease.
The secondary form of HCM is usually associated with disease
processes such as acromegaly, systemic hypertension, or hyperthyroidism.
HCM has been more frequently observed in males than females.
It is most commonly described in middle-aged cats with a range
distribution from 5 months to 17 years. In a study done by
Atkins et al, the median survival rate of cats with HCM was
about two years. Cats without clinical signs survived longer
than those with heart failure or signs of embolism. In the
same study, the survival rates of cats having heart rates
< 200 beats/minute survived longer than those
with heart rates > 200 beats/minute.
Etiology: The etiology of HCM is usually not known.
Multiple etiologies have been proposed including hereditary
predisposition, elevation in circulating catecholamines, abnormal
myocardial calcium metabolism, abnormal compensatory myocardial
hypertrophy due to ischemia and fibrosis, or abnormal primary
collagen resulting in secondary ventricular hypertrophy.
Researchers have found evidence that some cases of HCM are
inherited in the Maine coon cat and the American shorthair
as an autosomal dominant pattern. Kraus et al identified
a litter of five 18-month-old mixed breed cats that all had
Pathophysiology: Clinical signs are generally associated
with myocardial hypertrophy due to decreased left ventricular
diastolic filling and myocardial ischemia. In many cases
there are also systolic abnormalities such as intraventricular
pressure changes leading to asynchrony of the contraction
and relaxation of the heart muscle.
Depending on the type of myocardial alterations found,
there are several complications that can occur. Pulmonary
edema can be present when there is an increase in left atrial
and pulmonary venous pressure. Arrhythmias can also be present
where then is myocardial ischemia. Also, due to localized
endocardial injury, circulatory stasis and altered blood coagulability,
there is a potential risk of developing a thrombus within
the left atrium that could potentially lead to a thromboembolic
Clinical signs: Cats with HCM can be asymptomatic
and often experience sudden and unexpected death. Others
can show symptoms of acute dyspnea after stressful episodes.
On a routine physical exam, HCM can be suspected if there
is a murmur or gallop rhythm. When clinical signs are present,
they are associated with left sided heart failure or arterial
Clinical signs observed with HCM are variable and may include
dyspnea, tachypnea, pulmonary crackles, lethargy, reluctance
to move, syncope, gagging, anorexia, and sometimes abdominal
distention or vomiting. When pericardial or pleural effusion
is present, the heart and lung sounds can be muffled.
Thromboembolism has been recognized in approximately 50%
of cats with HCM. When aortic thromboembolism is present,
the clinical signs will vary according to its location. The
most common sign of thromboembolism is unilateral or bilateral
pelvic limb paresis or paralysis. When the embolization occurs
at the brachial artery, pain and paresis of forelimbs has
been observed. Blockage of the renal artery will produce
acute renal failure. If the thromboembolism occurs at the
cranial mesenteric artery, it is possible to observe clinical
signs of colic. Central nervous system abnormalities can
be seen if the embolus affects the cerebral artery. Respiratory
distress can be observed after embolization of the pulmonary
Diagnosis: It is possible to have a tentative diagnosis
based on the history, physical examination, electrocardiographic
findings, and thoracic radiographs.
Arrhythmias and conduction disturbances have been detected
in 60-70% of cats with HCM. Several types of arrhythmias
have been observed, including premature ventricular contraction,
atrial fibrillation, atrial tachycardia, atrial premature
contraction, paroxysmal ventricular tachycardia, and ventricular
bigeminy. Varying degrees of atrioventricular block, right
and left bundle branch blocks, and Wolff-Parkinson-White syndrome
are some of the conduction disturbances that have been observed.
Prolongation of P waves greater than 0.04 seconds and prolongation
of the QRS complex greater than 0.04 seconds with R wave
amplitude greater than 0.9 mV in lead II are parameters that
have been used as electrocardiographic indications of an enlarged
Depending on the degree of compromise, the thoracic radiographs
may show different degrees of cardiomegaly with pulmonary
edema. On the ventrodorsal view, the classic radiographic
sign of HCM is a “valentine” shaped cardiac silhouette
with biatrial enlargement and normal looking apex. It is
common to observe a banana-shaped cardiac silhouette on the
lateral view. When pericardial effusion is present, it is
possible to observe generalized enlargement and rounding of
the cardiac silhouette on the ventrodorsal view. Radiographic
evidence of cats with pulmonary edema usually has a patchy
and focal distribution along the pulmonary vessels.
Definite diagnosis can be done using echocardiography.
With this method, it is possible to rule out secondary causes
of HCM such as congenital aortic stenosis, chronic systemic
hypertension, chronic anemia and hyperthyroidism. Typical
echocardiographic abnormalities found in HCM are symmetrical
hypertrophy of the left ventricular caudal wall and interventricular
septum, reduced dimensions of the left ventricular chamber,
and ventricular hyperkinesis.
Treatment: Medical therapy of HCM is aimed to control
the clinical signs and has been adapted from that used in
human medicine. To relieve signs of pulmonary edema, diuretics
such as furosemide have been used. If refractory right-sided
heart failure develops, a second diuretic such as hydrochlorothiazide
can be used. For treatment of congestive heart failure, an
angiotensin-converting enzyme inhibitor such as captopril
can be used. Beta adrenergic-blocking agents (propanlol)
or calcium channel blockers (dialtiazem hydrochloride) have
been used for the treatment of the diastolic dysfuntion.
Medical management of thromboembolism has been mostly empirical.
Heparin therapy has been used to prevent additional formation
of thrombi. The use of thrombolytic agents such as streptokinase,
urokinase, and tissue plasminogen activator are expensive
and have not shown to be consistently effective. A potential
complication of their use is uncontrolled bleeding due to
their fibrinolytic effect.
Aspirin has been used to prevent platelet aggregation and
thrombus formation. Follow-up studies have not shown that
aspirin prevents clot formation in all cases. Some cats with
long term aspirin therapy, although presenting thromboembolic
episodes, have shown shorter recovery periods.
Cats with HCM have very little cardiovascular reserve and
are very sensitive to stress. Caution should be observed
when administering rapidly intravenous fluids since there
is the potential to cause rapid decompensation and the initiation
of congestive heart failure.
Pathology: HCM is characterized by hypertrophy of
the left ventricle free wall (> 0.6 cm), papillary
muscles and interventricular septum. The size of the left
ventricular lumen is decreased. The muscle hypertrophy can
be symmetrical or asymmetrical. It is sometimes possible
to find thickening of the mitral valve with enlargement of
the left atria.
In a study performed by Liu, a total of 51 cats with HCM
were studied. In this study, 70% of the cats presented symmetric,
concentric ventricular hypertrophy with normally arranged
cardiac muscle cells in the septum. In the remaining 30%,
the cardiac muscle cells in the septum were disorganized.
This lesions seems to be very specific to primary HCM because
it was rarely found in cats with secondary HCM.
In a previous study (Van Vleet), 10 cats with HCM had gross
lesions including cardiomegaly, diffuse symmetric left myocardial
hypertrophy, small left ventricular cavities, and dilated
left atria. The histopathology lesions found were hypertrophy
and disorganization of cardiac muscle cells, interstitial
fibrosis, and fibromuscular hyperplasia of small intramural
coronary arteries. Other lesions observed include hypertrophy
and disorganizaiton of myocytes of the left ventricular wall
and septum. The endocardium, conduction system, or myocardium
may present focal or diffuse degeneration, interstitial fibrosis,
and chondroid metaplasia. In 50% of cats with HCM, the intramural
coronary artery walls were thickened and had narrow lumens.
-by Luz Borrero-Yu, ECFVG Student
-edited by Dr. Theresa Boulineau, ADDL Graduate student