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Introduction
Getting to the heart of the matter can be tricky –
especially when the heart is what’s the matter. Just ask
Laura Clutz.
Laura was the proud owner of Rooney, Riley, and Michael,
three young robust male cats. Michael and Riley,
brothers from the same litter, were two years old.
Rooney, the baby of the bunch, was four months younger.
In July, all three cats were examined as part of their
annual check-up.
Rooney passed his physical examination with flying
colors. Michael and Riley, however, had more than their
kinship in common. They both had periodontal disease
that required professional dental scaling. More
disconcerting, though, was the discovery that both had
identical sounding heart murmurs.
Morning television news programs and pharmaceutical
company advertising has made Americans keenly aware that
heart disease is the number one cause of death in people
in the United States. Most cat owners, however, probably
don’t realize that cardiovascular diseases are also
quite common in cats. In fact, disorders of the
myocardium (heart muscle) are the major cause of heart
failure in cats.
Michael and Riley’s heart murmurs were sending a message
that something might be amiss in the heart department.
Before these boys could be anesthetized for their dental
cleaning, it would be necessary to prove that their
hearts were healthy. Sadly, after a battery of tests
that included cardiac ultrasound, the cause of Michael
and Riley’s murmurs were revealed: both boys were
suffering from a troublesome cardiac condition called
hypertrophic cardiomyopathy (HCM).
Hypertrophic Cardiomyopathy
“Hypertrophic cardiomyopathy is the most commonly seen
cardiovascular disease in cats”, says Dr. Jim Ross,
board-certified cardiologist at Tufts School of
Veterinary Medicine. “We see cats with the disease every
day--either as follow-up cases, or new cases that are
referred because the primary veterinarian heard a heart
murmur or suspected heart failure.”
To understand the pathology of HCM, a brief lesson in
heart anatomy is in order. The heart has four chambers
that pump blood. The two chambers on the left side (the
left atrium and left ventricle) are separated from the
chambers on the right (the right atrium and right
ventricle) by a dividing wall, called the septum. The
atria are found near the top of the heart; the
ventricles reside below the atria. The normal thickness
of the walls of the feline heart have been measured and
documented and are well-known to veterinary
cardiologists. In cats suffering from HCM, the walls of
the heart become progressively thicker and thicker. The
thickening of the heart mainly affects the left
ventricle, the chamber that pumps blood out through the
aorta to the rest of the body. Very often, the lower
part of the septum – the part that separates the left
ventricle from the right ventricle – is also affected.
When the left ventricle becomes thickened, the chamber
becomes smaller and the muscle becomes very stiff,
making it difficult to fill with blood. It also becomes
difficult for the blood to be pumped out of the
ventricle and through the aorta. Sometimes, a portion of
the valve that separates the left atrium from the left
ventricle gets sucked into the aorta’s outflow tract as
the thickened ventricle tries to pump blood out of the
aorta. This makes it even more difficult for blood to
flow out of the aorta, and it also causes the valve to
malfunction. As a result, the left atrium become
stretched out and dilated. This can lead to increased
pressure in the atrium. This increased pressure may be
transmitted to the lungs, resulting in fluid retention
in the lungs and eventual congestive heart failure. This
phenomenon, in which one of the leaflets of the mitral
valve is drawn into the aortic outflow tract, is called
systolic anterior motion (SAM), and it occurs in about
2/3 of cats diagnosed with HCM.
Although there are specific conditions that can cause
the heart muscle to become thicker (such as
hyperthyroidism and high blood pressure), HCM is
considered to be a primary disease because an
identifiable disease process cannot be found. Excessive
amounts of serum grown hormone and magnesium deficiency
have been investigated as possible causes, but a
cause-and-effect relationship could not be proven. For
now, the cause remains unknown.
Clinical Signs
Cats of either sex can be affected, although males are
typically affected more than females. Although the
disease has been reported in cats ranging in age from 3
months to 17 years, most cases occur in middle age,
usually between the ages of 4 and 8.
The clinical signs of HCM can vary greatly from cat to
cat. Some cats present with very non-specific signs,
such as lethargy, inappetence, weight loss, hiding, and
reluctance to socialize with the owner and with other
cats. Coughing occurs occasionally, but it fairly
uncommon, especially when compared to dogs with heart
disease. In most cases a cat has no clinical symptoms,
however, some abnormality is detected when the
stethoscope is placed on the cat’s chest. “Most of our
referral (non-emergency) cases that come to our
cardiology service are referred because a murmur and/or
a gallop rhythm is detected during the cat’s annual
physical exam”, confirms Dr. Ross. Such was the case
with Michael and Riley. “I had no idea anything was
wrong with either of my cats” recalls Laura Clutz. “They
were both acting perfectly normal”.
Michael and Riley’s case is typical. In fact, 55% of
cats with HCM present with no symptoms at all.
Unfortunately, a fair number cats are discovered to have
HCM when they present to the veterinarian already in
congestive heart failure. An even more upsetting (and
dire) scenario is the discovery that a cat has HCM when
it presents as an emergency with sudden painful hind
limb paralysis. This devastating complication of HCM
occurs when a blood clot (also known as a “thrombus”)
forms within the left atrium, and a small piece of this
clot (called an “embolus”) breaks off from the main clot
and travels down the aorta, lodging at the end of the
aorta, rapidly cutting off the blood supply to the legs.
This condition is known as arterial thromboembolism
(ATE). In the next issue of Catnip, subscribers can read
about this devastating complication of HCM, and the
possible new treatments on the horizon.
Despite a lot of research, the cause of
the HCM remains unknown, although there is substantial evidence that the
disease is inherited in at least 2 breeds: the Maine Coon and the
American Shorthair. In fact, researchers have recently identified the
gene mutation responsible for causing HCM in Maine Coons. It is the
first time that a spontaneous genetic mutation has been reported to
cause any type of heart disease in a cat or a dog. This discovery paves
the way for the development of a screening test that will identify Maine
coon cats carrying this genetic mutation, so they can be identified
before they are bred. Until such a test becomes available, however, if
HCM is identified in any cat it is advisable not to breed the affected
cat, and to carefully screen closely related family members. The
majority of cases, however, are domestic shorthaired cats without any
family history of disease.
Making the diagnosis
X-rays, an electrocardiogram (EKG) and echocardiography
(cardiac ultrasound) are the common diagnostic tests
performed on animals with suspected heart disorders. For
cats with HCM, x-rays tend to be of limited usefulness.
X-rays tend to be normal in the early stages of the
disease. As the disease progresses, however, the left
ventricle and left atrium may appear enlarged on an
x-ray. Classically, a valentine-shaped heart silhouette
is seen. If the cat goes into heart failure, pulmonary
edema (fluid in the lungs) and/or pleural effusion
(fluid in the chest cavity) may be visible on the
x-rays.
An EKG can provide the veterinarian with useful
information, as disturbances in the electrical
conduction system of the heart occur in about 30% of
cats with HCM. Although EKG abnormalities are common,
changes are often non-specific, and can even be normal
in cats with HCM.
Ultimately, a definitive diagnosis of HCM is achieved by
means of echocardiography (cardiac ultrasound).
Ultrasound allows for evaluation and measurement of
numerous parameters, including the size of the chambers,
the thickness of the heart muscle, the function of the
valves, how well the heart is contracting, how
efficiently the blood is flowing through the heart, and
whether or not there is a blood clot in the left atrium.
Echocardiography revealed that Michael and Riley both
had thickening of their heart muscle. Riley’s left
ventricle was a bit thicker than Michael’s, but the rest
of his chambers were normal or only mildly dilated.
Michael’s left ventricle wall and septum were a little
less thickened than Riley’s, however, the thickening was
seriously affecting the ability of the ventricle to push
blood out of the aorta. Michael also had SAM - a portion
of his mitral valve was also being drawn into the aortic
outflow tract – further taxing the ventricle’s ability
to pump.
Treatment
Therapy is mostly palliative, as there is no way to
reduce the thickness of the heart muscle. The goals of
managing cats with HCM are to improve the ability of the
ventricle to fill, prevent or delay the onset of
congestive heart failure, and prevent such complications
as arterial thromboembolism.
Several drugs are available to the veterinary
practitioner. Medications are prescribed to slow down
the heart, so that there is adequate time for the stiff
ventricles to fill, and to relax the heart muscle, again
to facilitate filling of the stiffened chambers. Which
drug or drugs are prescribed depends on the ultrasound
findings, whether or not the cat has concurrent
congestive heart failure, and the personal preference
and experience of the veterinarian or veterinary
cardiologist. Dr. Ross weighs in with his treatment
philosophy: “If the cat has no symptoms, and relatively
mild left atrial enlargement, we begin treatment with
either a beta-blocker such as atenolol, or a calcium
channel blocker such as diltiazem. Both can slow the
heart rate, improve ventricular relaxation, reduce
myocardial oxygen consumption, and reduce abnormal
rhythms. Some cats respond better to beta blockers,
others to calcium channel blockers – it’s impossible to
predict how an individual cat will respond. We start
with one drug, and follow-up to see how they are doing
after several weeks of therapy, and make adjustments as
necessary.”
For cats with HCM that are already in congestive heart
failure, Dr. Ross says that more aggressive therapy is
necessary. “If cats present in heart failure, oxygen
therapy, cage rest, and nitroglycerine ointment may be
necessary to get the cat stabilized.”, he says. 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. Another category of drugs,
called angiotensin converting enzyme (ACE) inhibitors
has been shown, in some studies, to be useful in
managing HCM. Some veterinarians use ACE inhibitors only
when the cat has developed congestive heart failure.
Others believe the drug to be beneficial in cats with
HCM regardless as to whether or not they have CHF. To
reduce the chance of a thrombus forming within the
heart, many cats are given medications that reduce the
blood’s ability to clot, such as aspirin or heparin.
Prognosis
The prognosis for HCM varies. Hypertrophic
cardiomyopathy can progress rapidly in some cats, while
in others, the condition remains relatively static for
years. Many cats will have slowly progressive disease
that ultimately leads to congestive heart failure. A
significant number of cats with HCM will be fine for a
while, only to develop rear limb paralysis due to ATE.
Although the end of the aorta, where it branches off to
supply the rear legs is the most common site for an
embolus to lodge, other arteries can be affected,
including those that supply the kidneys or the front
legs. When the heart muscle becomes thickened, the
coronary arteries have trouble supplying enough blood to
the heart muscle. The areas of inadequate blood supply
may serve as a site where abnormal rhythms are
generated. These abnormal heart rhythms can lead to
fainting, or in some instances, sudden death.
Cats who have no clinical signs and whose only evidence
of disease is limited to physical exam findings such as
a heart murmur or a gallop rhythm have a better survival
rate than cats that present to veterinarians already in
congestive heart failure or with rear limb paralysis due
to a blood clot. Two large studies have looked at
survival times for cats diagnosed with HCM. Both studies
reach the same conclusion: cats that develop a blood
clot do the worst; those that survive their initial 24
hours have a median survival time of 2 to 6 months. Cats
with congestive heart failure fare somewhat better,
surviving for 3 to 18 months. Those with no symptoms
survive for 3 to 5 years after the diagnosis.
Sadly, Michael’s HCM progressed rapidly. The increased
force needed to pump blood out of Michael’s partially
obstructed aorta put too much of a strain on his left
ventricle. Three months after Michael’s initial
diagnosis, despite medical therapy, Michael’s heart
began to fail, and he died of congestive heart failure.
His brother Riley continues to do well on medication.
“Each cat with HCM is unique in its disposition,
environment, ability to administer and tolerate
medication, and concurrent medical problems in other
body systems. You need to work with your veterinarian to
provide the best hospitalization and home care that fits
your situation”, says Dr. Ross.
Sidebar: possible outcomes of HCM
• No symptoms - Cat remains asymptomatic for years, does
well on medication
• Heart failure - Cat’s condition gradually progresses,
cat develops congestive heart failure
• Arterial thromboembolism (ATE) – A thrombus (blood
clot) forms within the heart, and an embolus (a piece of
the clot) breaks off, lodges in a branch of the aorta,
causes sudden hind limb paralysis
• Fatal arrhythmia – a disturbance in the electrical
conduction system of the heart develops, leading to an
abnormal rhythm and sudden death
Updated 2/9/06
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