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Canine Cardiomyopathy
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What is Cardiomyopathy?
Dilated Cardiomyopathy
DCM in Dogs
Hypertrophic Cardiomyopathy
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What
is cardiomyopathy?
http://www.upei.ca/cidd
related terms: dilated cardiomypathy, Doberman cardiomyopathy, boxer
cardiomyopathy
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Cardiomyopathy refers to
disease of the heart muscle (the myocardium) without malformation of the
heart or its valves. There is a breed predisposition to dilated cardiomyopathy
in giant breeds, as well as in Doberman pinschers and boxers. Cardiomyopathy
can also develop as a result of some toxins or infections.
There are 3 types of cardiomyopathy:
dilated cardiomyopathy. This is by far the most common type
in the dog. There is dilation of the chambers of the ventricles of the heart
with some increase (hypertrophy) in the heart muscle mass, and a loss of
the normal contracting abilities of the ventricles.
hypertrophic cardiomyopathy. In this form of cardiomyopathy,
there is a tremendous increase in the mass of the heart muscle in the
ventricles, with a resultant decrease in chamber size. Relatively few
cases of hypertrophic cardiomyopathy in dogs have been reported, and no
significant breed predisposition has been identified. Most of the dogs
affected have been male.
restrictive. This type has not been reported in dogs.
The heart works harder to compensate for the loss of contractility,
eventually leading to congestive heart failure. The abnormalities in the
heart muscle cells give rise to irregular heart rhythms which may cause
sudden death.
How is cardiomyopathy inherited?
The pattern of inheritance is not known.
What breeds are affected by cardiomyopathy?
Dilated cardiomyopathy is seen more often in Doberman pinschers than
in all other breeds combined. It also occurs in giant breed dogs including
the Great Dane, St. Bernard, Irish wolfhound, and Scottish deerhound.
A distinctive form of cardiomyopathy occurs in the boxer, with extensive
changes in the heart muscle and serious rhythm abnormalities, but without
the dramatic dilation of the ventricles seen in other breeds.
Dilated cardiomyopathy is also seen in English cocker spaniels. In
all breeds affected, it is more common in males.
For many breeds and many disorders, the studies to determine the mode
of inheritance or the frequency in the breed have not been carried out,
or are inconclusive. We have only listed breeds for which there is a strong
consensus among among those investigating in this field and among veterinary
practitioners, that the condition is significant in this breed.
What does cardiomyopathy mean to your dog & you?
Giant breeds with dilated cardiomyopathy typically show signs associated
with abnormalities of heart rhythm (particularly atrial fibrillation) and
generalized heart failure. These signs may include weakness, loss of appetite,
weight loss, depression, episodes of collapse, respiratory difficulties,
a soft cough (especially at rest), and an enlarged abdomen. There is severe
enlargement of all 4 chambers of the heart. Dogs are affected in middle-age
on average, although they may be affected as early as a few months of
age. Abnormalities may be seen on an electrocardiogram before there are
any clinical signs.
In addition to signs of heart failure as outlined above, a distinctive
feature of this disorder in Doberman pinschers and boxers is that the abnormal
heart rhythms that are seen originate most commonly in the ventricles,
and are quite serious. As well, Dobermans often have left atrial rather than
generalized enlargement of the heart and boxers may show no heart enlargement.
In Doberman pinschers there is a relatively long period of 2 to 4
years without clinical signs of illness ( the "occult" phase), during
which changes occur in the heart muscle and rhythm disturbances progressively
worsen. Sudden death occurs in about 25% of these dogs. Others will go
on to develop congestive heart failure. Weight loss is often sudden and
dramatic in these dogs. Death usually occurs fairly soon after clinical
signs develop, often within 6 months.
In boxers, there are 3 distinct stages of cardiomyopathy:
Stage I. An irregular heart rhythm is discovered incidentally
during a routine examination, or examination for other purposes. The dog
has no clinical signs of illness.
Stage II. These dogs are examined because of intermittent episodes
of collapse or weakness. On examination, an abnormal heart rhythm (generally
originating in the ventricles) is found.
Stage III. These dogs show signs of heart failure which may
include weakness, depression, exercise intolerance, a soft cough (particularly
at rest or at night), a loss of appetite, weight loss which may be dramatic,
and fainting or collapse.
The episodes of fainting, collapse, or weakness are generally due
to abnormal rhythms in the heart, because of the damaged heart muscle.
For this reason, regular monitoring by electrocardiogram is the best way
of assessing the progression of cardiomyopathy in these dogs. Dogs in either
of the first stages may develop heart failure at any time.
For all dogs with dilated cardiomyopathy, the arrhythmias that can
cause fainting or collapse can also cause sudden death. Up to 50% of affected
dogs die suddenly, often without having shown any other signs of the disorder.
Once dogs with cardiomyopathy develop congestive heart failure, the
prognosis is poor.
How is cardiomyopathy diagnosed?
X-rays generally show an enlarged heart, predominantly on the
left side. Boxers may show no abnormalities on radiographs.
In both Dobermans and boxers with cardiomyopathy, there may be no
abnormalities on radiographs, on physical exam, or on the resting electrogardiogram.
If cardiomyopathy is suspected and all routine diagnostic tests are normal,
a 24 hour ambulatory electrocardiogram ( a Holter monitor) is recommended.
The unobtrusive monitor is worn by the dog during its normal activities,
and records irregular heart rhythms.
FOR THE VETERINARIAN:
RADIOGRAPHS:see generalized cardiomegaly with left atrial and
ventricular enlargement predominating. In Dobermans, only left atrial
enlargement may be evident. In boxers, thoracic radiographs may be normal,
or there may be mild to moderate cardiomegaly.
ELECTROCARDIOGRAM: atrial fibrillation is seen in 75 to 80
per cent of giant-breed dogs with dilated cardiomyopathy. There may be
subtle changes such as high amplitude or widened QRS complexes (left ventricular
enlargement), or widened P waves (left atrial enlargement). In Dobermans
and boxers, one sees ventricular premature contractions of variable
frequency, singly or in runs, and, later, paroxysms of ventricular tachycardia.
ECHOCARDIOGRAM: reduced contractility, ventricular dilation
(may not be seen in boxers).
PHYSICAL EXAM: occasional to frequent premature beats, pulse
deficits, paroxysmal tachyarrhythmias or a totally irregular ventricular
rhythm, variability in femoral pulse strength.
How is cardiomyopathy treated?
Decisions about treatment are based on several factors: whether the
dog is showing clinical signs such as weakness or collapse, what arrhythmias
are seen on the electrocardiogram, and whether congestive heart failure
is present. If your dog has an abnormal heart rhythm without any evidence
of congestive heart failure, your veterinarian may prescribe anti-arrhythmic
drugs, depending on the severity of the arrhythmia.
Episodes of collapse indicate a serious arrhythmia and must be treated
as an emergency.
Treatment for dogs with signs of congestive heart failure involves
rest, diet restrictions, and drugs to stabilize and support the failing
heart as well as to control the arrhythmias. If low doses of anti-arrhythmic
drugs are effective, then the heart can often be stabilized. Serious ventricular
arrhythmias that can only be controlled by high doses of anti-arrhythmic
drugs have a poorer prognosis.
New treatments are being used in Dobermans and boxers with cardiomyopathy
in an attempt to delay the onset of congestive heart failure or sudden
death.
Breeding advice
Affected individuals and their parents should not be used for
breeding. Siblings should only be used after careful screening.
How can cardiomyopathy be controlled?
There are ways to approach the control of this disease. Although signs
of heart failure are often not evident until middle age, abnormalities
on the electrocardiogram are often apparent earlier. In affected breeds
with a family history of cardiomyopathy and in ALL Doberman pinschers, breeding
animals should be evaluated yearly for evidence of cardiac arryhthmias,
using an ambulatory (Holter) monitor if possible. Dogs in which occult dilated
cardiomyopathy has been identified (ie. no clinical signs) should not be
used for breeding.
FOR MORE INFORMATION
ABOUT THIS DISORDER, PLEASE SEE YOUR VETERINARIAN.
Resources
Calvert, C.A. 1995. Diagnosis and management of ventricular
tachyarrhythmias in Doberman pinschers with cardiomyopathy. In
R.W. Kirk and J.D. Bonagura (eds.), Current Veterinary Therapy XII Small
Animal Practice, p. 799-806. W.B. Saunders Co., Toronto.
Jacobs, G. 1998. Comprehensive update on Doberman cardiomyopathy.
ACVIM-Proceedings of the 16th Annual Veterinary Medical Forum: 107-109.
Meurs, K.M., Brown, W.A. 1998. Update on boxer cardiomyopathy.
ACVIM-Proceedings of the 16th Annual Veterinary Medical Forum: 119-120.
Copyright © 1998 Canine Inherited Disorders
Database. All rights reserved.Revised: October 30, 2001.
This database is funded jointly
by the Animal Welfare Unit at the Atlantic Veterinary College, University
of Prince Edward Island, and the Canadian Veterinary Medical Association.
Copyright © 1998 Canine Inherited
Disorders Database. All rights reserved.Revised: December 15, 2000.
reprinted
with kind permission from:-
Alice
Crook, DVM,Coordinator, Sir James Dunn Animal Welfare Centre, Atlantic
Veterinary College,University of Prince Edward Island, 550 University
Ave.Charlottetown, PEI C1A 4P3
http://www.upei.ca/cidd
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Dilated Cardiomyopathy
Dilated cardiomyopathy
(DCM) is one of the most common acquired heart diseases in dogs.
DCM is a disease of the heart muscle (“cardio” – heart; “myo’ – muscle;
“pathy” – disease) in which the muscle (myocardium) of the lower pumping
chambers (ventricles) loses its ability contract normally. DCM
most commonly affects the left side of the heart (the side that receives
blood from the heart and pumps it to the body) – specifically, the left
ventricle. Since the myocardium cannot pump blood out of the left
heart effectively, blood begins to “back up” within the left side of
the heart and within the pulmonary veins that feed into the left heart.
This leads to an enlargement of the heart in an attempt to compensate for
the ineffective pumping.
As blood “backs up,” left-sided congestive heart failure (CHF)
or pulmonary edema (fluid within the lungs) develops. This is
not a feature exclusive to DCM, but is a common feature of many types
of left-heart disease.
Although less common, DCM affecting the right ventricle can also
occur. Blood “backs up” on the right side (which receives blood
from the body and pumps it to the lungs) resulting in right-sided CHF,
where fluid accumulates in the abdomen (ascites) and chest (pleural
effusion).
In some dogs, DCM affects BOTH the right and the left side.
What Breeds Get DCM?
There are several breeds that are genetically predisposed to
DCM. These include Doberman Pinschers, Great Danes, Boxers, Newfoundlands,
Portuguese Water Dogs, Dalmatians and Cocker Spaniels. No genetic
tests exist to identify affected individuals at this time, but researchers
are trying to identify the genes associated with DCM.
DCM is not just limited to specific breeds. Large and giant
breeds are most commonly affected, but it also occurs in smaller breed
dogs and cats as well.
The causes of DCM in these breeds vary, as explained below.
What Causes DCM?
Because of the strong breed association, DCM almost certainly
is inherited. However, specific genetic defects have not yet been
identified and no genetic tests exist. When they are developed,
these tests will likely be breed-specific.
In some dogs, DCM is due to a nutritional deficiency. Taurine
is an amino acid required for the development and function of the myocardium.
Consequently, pets may develop DCM on taurine deficient diets, such
as vegetarian diets, and may benefit from appropriate supplementation.
Some breeds, such as Cocker Spaniels and Newfoundlands may have a predisposition
to Taurine-deficiency, possibly through defects in metabolizing taurine.
Not all cases that are supplemented with taurine will improve.
If your pet is diagnosed with DCM, testing for a taurine deficiency
may be warranted. Breeds such as Doberman Pinschers and Great
Danes do not have taurine-deficient cardiomyopathy. Some cats may
develop taurine deficient DCM, although this has become rare with taurine
supplementation of virtually all quality cat foods.
L-carnitine is another amino acid that has been implicated in
the development of DCM in people. It is required for the myocardial
cells to produce energy and thus contract. There is some evidence
that a deficiency in this molecule will contribute to myocardial dysfunction
in Boxers (one small study only). However, the role of carnitine
in most DCM cases seems limited but has not been fully explored in dogs.
Occasionally, toxins can cause DCM. The most common “toxin”
is doxorubicin – an anti-cancer drug used to treat various cancers in
dogs. In some cases, dogs receiving doxorubicin (Adriamycin) will
develop DCM.
Infectious causes of DCM are rare. Puppies infected with
parvovirus at 2 to 4 weeks of age, can develop DCM. These days,
vaccination of the dam confers protection to puppies against parvovirus
during this susceptible period, so this cause of DCM is rarely seen.
Chagas’ disease (Trypanosomiasis) can cause DCM in areas where it is
found (Texas, Mexico).
What Are the Signs of DCM?
Signs of DCM vary depending on the breed of dog and stage of
the disease. Loss of appetite, pale gums, increased heart rate,
coughing, difficulty breathing, periods of weakness, and fainting are
signs commonly seen. Since blood is “backed up” into the lungs,
respiratory signs (CHF) are due to pulmonary edema. Blood returning
to the right side of the heart from the body may also back up leading
to fluid accumulation in the abdomen (ascites) or in the chest cavity
(pleural effusion). Weakness or collapse may be caused by abnormal
heart rhythms (arrhythmias) and occasionally, decreased blood flow to
the body (depressed cardiac output).
In some breeds, sudden death or fainting can occur well before
any signs of CHF.
How Is DCM Diagnosed?
The diagnosis of DCM can be complicated. There are two
different types of diagnosis: (A) during a screening exam of an apparently
normal dog (e.g. as part of a breeding program), and (B) during examination
of a dog with clinical signs of heart disease.
Screening Exams for DCM
Many conscientious breeders and owners screen their pets for
heart disease to minimize the risk of transmitting the disease to offspring.
Screening for DCM in dogs can be expensive and complex. The screening
test of choice depends on the breed of the dog and the stage of the
disease.
The first step is a good physical examination. In most
cases, the physical examination is completely normal. Occasionally,
the veterinarian may detect an arrhythmia (abnormal heart rhythm).
In Doberman Pinschers and Boxers, a 24-hour ECG recording using an ambulatory
monitor (Holter monitor) is often the best way to screen dogs for early
signs of DCM – abnormal rhythms occur before any detectable changes in myocardial
contractility. An echocardiogram (an ultrasound scan of the heart)
can also help identify dogs with DCM before they develop clinical signs,
but many dogs with mild disease have equivocal findings. This examination
is best performed by a certified veterinary cardiologist.
Diagnosis in Dogs with Clinical Signs
A thorough physical examination by your veterinarian, coupled
with your pet’s clinical signs and specific breed, may help make the presumptive
diagnosis of DCM. Tests that help support the diagnosis are an
ECG (electrocardiogram) and x-rays (radiographs) of the chest. The
ECG may show an arrhythmia and/or an elevated heart rate. The chest
radiographs may show an enlarged heart and/or fluid in the lung tissue
or chest cavity. Some dogs may have normal chest radiographs, but
have arrhythmias on their ECG. These pets may be in the early stages
of DCM (see above).
In dogs with clinical signs of heart failure, an echocardiogram
is necessary to confirm the diagnosis of DCM. With an echocardiogram
a cardiologist can visualize the interior of the heart and assess its
function. A decrease in heart pumping function (contractility) means
that the patient has DCM. Your veterinarian may also perform blood
tests to look for any underlying nutritional or infectious conditions
if the specific case warrants such investigation.
How Is DCM Treated?
Treatment is based on clinical presentation of each individual
patient. Drugs commonly used are diuretics, ACE inhibitors, and
digoxin. Newer drugs, such as pimobendan, are also generally recommended
for treatment of DCM, but still require government approval for their
use. In nutritional DCM, specific supplements will be prescribed.
Patients with right-sided heart failure will also have fluid physically
removed from the abdomen and/or chest cavity by the veterinarian to make
the patient more comfortable.
Novel therapies such as stem-cell therapies are currently being
investigated in animal models of disease, but are not available to the
general public.
In humans, heart transplants are usually performed for patients
with DCM, however, this option does not exist for veterinary patients,
as it would require the killing of another animal to obtain a suitable
heart (human donors are largely motor vehicle accident victims).
No veterinarians are performing heart transplants.
Other surgical procedures have been evaluated, but currently
none are being offered for patient care.
What Is the Prognosis of a Pet Diagnosed With DCM?
Unfortunately, in many cases, DCM is a progressive, irreversible,
and ultimately terminal disease. Survival depends on the stage
of diagnosis, the breed of the patient, the specific type of DCM that patient
has, and patient/owner treatment compliance. In taurine-deficient
DCM, correction of the deficiency in cats results in complete cure.
In dogs, correction of the deficiency may result in prolonged survival;
however some cases relapse after several years.
DCM is a slowly progressive disease. If it is diagnosed
in the early stages, the patient may live several years before developing
clinical signs. In some breeds, such as Doberman Pinschers, sudden
death accounts for 30% of the deaths from DCM, well before these dogs
ever develop CHF.
In other breeds with DCM, such as Doberman Pinschers and Great
Danes, that are showing clinical signs of CHF, medical therapy can help
prolong survival. Historical average survival for Doberman Pinschers
with clinical DCM was 2 to 3 months. However, with pimobendan, recent
studies have extended survival for this breed to 1 year. Less is
known about outcomes of other breeds with DCM. Once the diagnosis of DCM
is made, ask your veterinarian to discuss your pet’s prognosis on an individual
basis.
Can I Do Anything to Prevent DCM or Slow Its Progression?
Currently, no therapies have been shown to alter the course of
DCM, unless it has a nutritional basis (i.e., taurine deficiency).
Since the majority of cases are thought to be genetic, breeding from
lines unaffected by the disease helps reduce the chance of inheriting
DCM. Genetic tests, when they become available, will be of value
in determining breeding strategies. Drug therapies in early stages
of the disease do not appear to affect outcome, but there has been little
research into this.
What about Other Supplements?
Multivitamin supplements, nutritional supplements, Co-enzyme
Q10, and non-western herbal supplements have all been used for DCM,
but none have been examined critically to determine if they hurt or
help patients. Use of these supplements is best discussed with
your veterinarian.
Copyright
2007 - 2007 by the Veterinary Information Network, Inc. All rights reserved.
This work was originally published by Veterinary
Information Network, Inc. (VIN)
and is republished with VIN's permission.
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Dilated Cardiomyopathy (DCM) in Dogs
Affected Animals
The dogs most frequently diagnosed with DCM are large and giant
purebred dogs, including Scottish deerhounds, Doberman pinschers, boxers,
Saint Bernards, Afghan hounds, Newfoundlands, and old English sheepdogs.
Recently, both English and American cocker spaniels have been diagnosed
more frequently with DCM than other small breed dogs. Most dogs with DCM
are older, as the prevalence of DCM increases with age. Male dogs are affected
more commonly than female dogs for most breeds.
Overview
The term cardiomyopathy literally means "sick heart muscle".
Dilated cardiomyopathy, or DCM, occurs when the heart muscle is thin,
weak, and does not contract properly. DCM most commonly affects large
or giant purebred dogs, but it also can be seen in smaller breeds such
as cocker spaniels, and in mixed breed dogs. The condition can lead to
congestive heart failure, in which fluid accumulates in the lungs, the
chest or abdominal cavities, or under the skin. Because of reduced blood
flow to the rest of the body, DCM also can result in weakness, fainting,
and exercise intolerance. Abnormal heart rhythms, or arrhythmias, frequently
accompany DCM, and can complicate the treatment of dogs with this disease.
In rare cases, supplementation with substances such as l-carnitine
or taurine may dramatically reduce signs in individual patients, but for
most dogs, the main goals of treatment are to lessen signs due to congestive
heart failure and to attempt to improve the heart's ability to pump blood.
The long-term outlook for dogs with DCM is usually quite poor, and most
dogs with DCM eventually die from the disease. Despite the poor long-term
outlook, however, many dogs with DCM can benefit from medical treatment
that helps control symptoms.
Clinical Signs
Signs may be consistent with right heart failure, left heart failure,
or both. Right heart failure signs can include abdominal distention due
to ascites, jugular venous engorgement or pulsation, hepatomegaly, pleural
effusion, edema, pericardial effusion, and weight gain due to fluid retention.
Left heart failure signs can include cough due to pulmonary edema, shortness
of breath, tachypnea, and dyspnea. Some signs can be seen with right or
left sided heart failure, including fatigue and weakness, exertional dyspnea,
gallop rhythm, pallor, increased capillary refill time, cyanosis, cool
extremities, and weight loss.
Symptoms
Dogs with dilated cardiomyopathy can show symptoms due to right-sided
congestive heart failure including abdominal enlargement; distention of
the veins in the neck or other parts of the body; and fluid accumulation
in the abdomen or chest, in the sac around the heart or underneath the skin,
especially in the legs and on the underside of the body. This fluid retention
can lead to weight gain. Other dogs will show evidence of lung problems
due to left-sided congestive heart failure, including shortness of breath,
rapid, shallow breathing, difficulty resting comfortably at night, and
coughing.
It is also common for dogs with DCM to show signs of both right and
left heart failure. These signs can include weakness and exercise intolerance,
and difficulty breathing with increased activity. Weight loss is common
in dogs with DCM that do not retain fluid. Some animals exhibit signs
due to reduced blood flow to tissues, including pale mucous membranes,
bluish color to the mucous membranes, and cold feet and legs. Fainting
may occur if abnormal heart rhythms are present, or if the heart's output
is severely reduced.
Description
Heart failure occurs when the blood returning to the heart from the
rest of the body cannot be pumped out fast enough to meet the demands of
body tissues. Heart muscle disease is one of the potential causes of heart
failure. Dilated cardiomyopathy is a condition characterized by a variety
of changes in the heart muscle that result in pump failure. As the name
implies, the heart chambers are usually dilated or enlarged, and the heart
muscle itself is usually thin and weak, contracting with much less vigor
than normal. The term cardiomyopathy literally means "sick heart muscle."
The primary abnormality occurring with DCM is impaired function of
the ventricles due to decreased strength of the heart muscle. The left
ventricle pumps blood from the lungs to the rest of the body, and the
right ventricle pumps blood from the rest of the body to the lungs. When
the heart muscle fails, pressures can increase and ultimately lead to
left- or right-sided heart congestive heart failure. Reduced output from
the heart may result in signs such as weakness, exercise intolerance, fainting,
and shock. Heart valve insufficiencies, abnormal heart rhythms or arrhythmias,
and the results of the body's compensatory responses to reduced heart
muscle performance can compound the problems seen with DCM. Ventricular
arrhythmias can often lead to sudden death, especially in boxers and Doberman
pinschers. The development of an atrial arrhythmia called atrial fibrillation
can have important short-term and long-term consequences for dogs with
DCM. This arrhythmia can be seen in all breeds of dogs.
Medications are used to treat the consequences of heart muscle failure,
to attempt to improve the heart muscle's ability to contract, and to normalize
or improve rhythm disturbances. Drugs used to accomplish these goals
include diuretics, digoxin, and angiotensin converting enzyme inhibitors.
Supplementation with substances such as taurine or l-carnitine may be
helpful for some dogs with DCM.
Diagnosis
The diagnosis often is first suspected when symptoms compatible with
DCM are present in a large or giant purebred dog or cocker spaniel. Physical
examination abnormalities frequently include the presence of an extra
heart sound called a gallop rhythm, or a soft heart murmur. Arrhythmias
can be detected while listening to the heart with a stethoscope and while
feeling for the pulse or heartbeat. Abnormal lung sounds are heard in dogs
with left-sided heart failure, while distention or pulsation in the jugular
veins, liver enlargement, or abdominal fluid accumulation may be present
in dogs with right-sided heart failure. In addition, laboratory results may
indicate mild changes in serum protein concentrations, sodium and potassium
levels, liver enzymes, and mild increases in serum urea nitrogen and creatinine
levels, or kidney values.
Although they will not always reveal major changes, chest x-rays
should always be evaluated in patients suspected of having heart disease.
Heart enlargement and blood vessel changes consistent with heart failure
may be seen, and fluid accumulation in or around the lungs can be identified
if heart failure has developed.
The most definitive diagnostic test for DCM is the echocardiogram,
an ultrasound evaluation of the heart. Heart chamber dilation and enlargement,
reduced heart muscle wall thickness, and decreased heart muscle wall movement
are the hallmarks of DCM. In addition, mild heart valve abnormalities may
be seen. Doppler echocardiography may be used to assess the severity of
valvular abnormalities based on changes in blood flow through the heart.
The electrocardiogram may identify abnormal rhythms or changes in
the normal tracings. The most common rhythm disturbance occurring with
DCM is atrial fibrillation, a condition characterized by a tremendous increase
in the rate of contraction of the atria, the uppermost chambers of the heart,
coinciding with an increased rate of contraction of the ventricles, the
lower and larger chambers of the heart. Other rhythm disturbances, including
premature ventricular beats, may be detected.
Prognosis
Currently, DCM is almost always fatal. Most dogs die within six to
24 months after being diagnosed. Severely ill dogs often do not survive
the first two days in the hospital. Doberman pinschers may have a worse
prognosis compared to other breeds. However, the response to treatment
will vary for any individual dog. Treatment should always be attempted
before rendering a prognosis. As with almost any disease, dogs diagnosed
with DCM before serious complications have developed may be able to live
longer with treatment.
Transmission or Cause
There appears to be a strong association between breed and DCM. Infectious
diseases, including Lyme disease, bartonellosis, and trypanosomiasis,
have been reported in association with DCM and are usually accompanied
by other symptoms.
Treatment
DCM generally is not curable, and spontaneous recovery is unlikely.
The primary goals of treatment are to lessen clinical signs of heart failure
and to prolong survival. Treatment of an individual dog is dictated by the
severity of its signs at the time of diagnosis, and the presence or absence
of changes such as congestive heart failure and arrhythmias. The primary
drug to reduce fluid accumulation secondary to congestive heart failure
is furosemide, marketed as Lasix. It can be used to treat acute, life-threatening
fluid accumulation or to control and prevent congestive abnormalities in
chronic settings.
Digoxin is used for several reasons in the treatment of DCM. It may
help increase the heart's ability to contract and slow down the ventricular
response rate in dogs with atrial fibrillation. Digoxin also blunts some
of the neurological and hormonal responses to heart failure that lead
to worsening of the condition. Drugs such as dobutamine, amrinone, and
milrinone may be used to increase the heart muscle's ability to contract,
but they are indicated primarily for short-term emergency situations.
Recently, the use of drugs called angiotensin converting enzyme,
or ACE, inhibitors has been shown to benefit dogs with DCM by reducing
the signs due to heart failure and improving exercise tolerance. ACE-inhibitors
have many effects, including blood vessel dilation, which reduces the resistance
the heart has to pump against. The drug also remodels the diseased heart
muscle. Other types of blood vessel dilators can be used in the short-term
or long-term treatment of DCM to reduce the load that the heart has to
pump against to get blood to flow.
Other drugs control heart rhythm disturbances. Digoxin is commonly
used in dogs with atrial fibrillation. Other anti-arrhythmic drugs, including
procainamide, marketed as Procan, and mexiletine, marketed as Mexitil, are
used for dogs with ventricular arrhythmias due to DCM.
L-carnitine is a compound that plays an important role in fatty acid
metabolism and in neutralizing potential toxins in cells. Carnitine deficiency
in the heart muscle has been shown to be potentially reversible in at
least one family of boxers with DCM. Although the diagnosis of heart muscle
carnitine deficiency is difficult, and the appropriateness of supplementation
with l-carnitine for all dogs with DCM is unknown, such supplementation
is not known to be harmful. L-carnitine supplementation can be considered
for all dogs with DCM.
Another substance that may play a role in the treatment of DCM, particularly
in cocker spaniels, is taurine. Taurine deficiency was found to be the
most important factor associated with DCM in cats in the 1980's, and correction
of cat food formulations to eliminate taurine deficiency resulted in
the almost complete elimination of DCM as a major heart muscle disease
in cats. However, the exact role of taurine in the treatment of DCM in
dogs remains undetermined. Other substances, such as coenzyme Q-10, may
also play a role in the treatment of this disease.
Prevention
Affected dogs should not be bred. Early screening of dogs of breeds
that have a high incidence of DCM may help identify important changes prior
to the onset of signs. This can help prevent the breeding of dogs that
could pass DCM on to their offspring.
Reprinted with kind permission
from Roger Ross DVM,
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Hypertrophic Cardiomyopathy
Authored by: Dr. Robert Prošek
What Is Hypertrophic
Cardiomyopathy?
Hypertrophic cardiomyopathy
(HCM) is the most common acquired heart diseases in cats but very rare
in dogs. HCM is a primary heart muscle disease where the muscular
walls of the ventricles become abnormally thickened (hypertrophied.)
The name hypertrophic cardiomyopathy literally means “thick heart muscle
disease” (Figure 1 below). This thickening has several consequences
(see below). HCM is diagnosed once other secondary causes of left
ventricular wall thickening (hypertrophy), such as hyperthyroidism, systemic
hypertension, aortic stenosis and others have been ruled out.
Like the similar disease
in humans, HCM is often familial in cats, thought to be inherited in an
autosomal dominant manner. A specific mutation has been identified
in Maine Coon cats and a genetic test exists to identify affected cats.
While many purebred cats (such as American shorthairs, oriental breeds and
Persians) are predisposed to the disease, the domestic short hair (regular
house cat) is the type most commonly diagnosed with HCM. Cats are usually
middle aged to older; however, the disease can be diagnosed at any age,
often less than 5 years in purebred cats. In humans, HCM is also
familial and several different genetic mutations have been identified as
being able to cause the disease. To date, no viral or nutritional
causes of HCM have been identified in humans or cats.
What Are the Consequences
of the Thickened Left Ventricle?
Unlike thickening of the
walls in response to a physical stress (e.g. weight lifting, or running
marathons) where the thickening occurs to deal with the extra workload
placed on the heart, the thickening with HCM is not normal. The degree
to which the muscle walls thicken ultimately determines the clinical severity
of the disease – some cats (and people) have mild disease, others have severe
disease.
As HCM develops and progresses,
the structure and function of the heart is altered in several ways.
The hallmark problem with HCM lies in the inability of the left ventricle
to relax appropriately. The thickened left ventricular walls become
less flexible which prevents the left ventricle from relaxing or stretching
sufficiently to fill with blood from the left atrium. This abnormal
relaxation and inability to stretch may ultimately result in a build-up
of blood “upstream” of the left ventricle – namely the left atrium and the
pulmonary circulation. As the blood backs up, fluid is forced from
the pulmonary capillaries into the lungs and chest cavity causing pulmonary
edema and pleural effusion, respectively (commonly called “congestive heart
failure,” or CHF).
In some cats, the thickening
leads to arrhythmias and can result in sudden death (akin to what is seen
in young basketball players that suddenly die on the court). It is
difficult to predict which cats are likely to do
Other cats can suffer from
feline aortic thromboembolism (FATE) – a blood clot in the aorta that causes
blockage of blood flow to the back legs (most commonly), leading to sudden
paralysis, severe pain, and often, death.
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On the left is a graphic representation
of a normal left ventricle and on the right is an enlarged (concentric hypertrophy)
left ventricle as noted in hypertrophic cardiomyopathy.
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How is HCM Diagnosed?
The clinical signs of HCM
are variable. To some degree, the clinical signs depend on the severity
– mild disease doesn’t cause obvious problems, but severe disease often
does. Additionally, cats are masters at masking problems until they
become severe, so cats with severe HCM may appear completely normal or have
only subtle signs that go unnoticed (i.e., mildly increased respiratory
rate) or they may be very nonspecific to heart disease (i.e., decreased
appetite). On the other hand, an owner may notice signs such as respiratory
distress secondary to congestive heart failure or leg paralysis secondary
to a thromboembolic (blood clot) event. In addition, your veterinarian
can clue in on signs when he or she listens to your cat’s chest during their
physical exam. An increased heart rate, heart murmur, and/or gallop
rhythm (extra heart sound) may be appreciated as the disease advances.
A common feature of HCM
is termed systolic anterior motion (SAM) of the mitral valve. This
abnormal motion of the mitral valve partially obstructs the outflow of
blood from the left ventricle into the aorta, resulting in a heart murmur
which can be heard by your veterinarian with a stethoscope during your pet’s
physical examination. However, it is important to note that not all
murmurs in cats are due to SAM. Additional diagnostic tests are required
to confirm both the presence of SAM and of HCM.
An echocardiogram (ultrasound
of the heart) with color flow Doppler imaging offers the best means to
diagnose HCM. Echocardiography allows a veterinarian to observe the
physical structure and dynamic function of the heart. Fortunately,
the test is non-invasive and poses essentially no risk to the cat.
Electrocardiograms and radiographs provide additional useful information
and are often used to assist a veterinarian in diagnosing HCM, but cannot
be used alone to diagnose the disease. Since very subtle structural
and functional changes can occur within the heart in the early stages of
HCM, it is strongly recommended that a veterinary cardiologist be consulted
for diagnosis as well as subsequent management of the disease.
As previously mentioned,
additional tests might be needed to rule out underlying diseases such as
systemic hypertension or hyperthyroidism which may cause similar hypertrophy
of the left ventricle as HCM. If no other causes are found, the diagnosis
of HCM is made.
In Maine Coon cats, a blood
test is now available to determine if the pet has the genetic mutation
associated with this condition. The test does not work for other cats
with HCM. You can request this test from your veterinarian.
How is HCM Treated?
Currently, there is no
cure for HCM. The changes occurring to the heart muscle are irreversible.
However, if your pet’s left ventricular hypertrophy is secondary to some
other underlying heart disease, such as hyperthyroidism, treatment of the
primary disease may result in some or complete resolution of the heart condition.
As previously mentioned,
hypertrophy of the heart muscle affects the ability of the left ventricle
to relax properly, and therefore, function appropriately. While veterinarians
may prescribe one or more medications to try to improve the heart’s relaxing
ability, it is important to recognize that no drugs have been shown to
be effective in achieving this. Thus, attempts to reduce the risk
of heart failure and to help the heart function efficiently are largely
theoretical and may ultimately be of no value.
Some treatment options
that may be prescribed include:
Drugs that are thought
to alter relaxation of heart muscle, or slow down the heart rate to allow
a longer time for the heart to fill, or both. No proof exists that
either of these approaches actually benefits cats with HCM. It is
quite acceptable to not treat cats with HCM prior to the onset of CHF –
when information becomes available showing a benefit of any treatment, guidelines
may change.
Drugs to treat congestive
heart failure (diuretics and ACE inhibitors). These medications are
not specific for HCM, but are used in cats with heart failure secondary
to any heart condition. With severe fluid build up in the chest cavity,
the veterinarian may physically remove the fluid with a catheter to help the
cat breathe.
Drugs that are thought
to reduce the risk of clot formation, or clot recurrence. A medication
that reduces the ability of the blood to clot may be prescribed if the
patient is felt to be at risk for blood clot formation or currently has
a blood clot in one of its arteries or heart chambers. The use of
certain drugs for this purpose must be closely monitored to insure the patient
is not placed at risk for hemorrhage. Treatment does not guarantee
that a blood clot will not form, nor is it designed to break down previously
formed clots. There are no studies showing that any of these medications
actually do what they’re claimed to do. Currently a study is underway
examining the effect of one type of anti-clotting drug on survival of cats
that have had a thromboembolic episode.
As an owner of a cat with
HCM, you should be very sensitive to changes in your pet's condition and
should not hesitate to seek veterinary advice. Your veterinarian
may show you how to monitor your cat's respiratory rate as an increased
rate may be a sign that congestive heart failure is developing or worsening.
Cats with congestive heart failure do not cough like dogs or people, but
often exhibit open mouth breathing and panting. A cat that is having
difficulty breathing from heart failure or has loss of function of hindlimbs
or front limbs, requires veterinary care as quickly as possible.
In the acute setting, these problems may need specific treatments (oxygen
therapy, injectable medications, anticoagulation medications, or pain medications)
that can only be offered by a veterinarian.
What Is the Prognosis?
The prognosis of
a cat with HCM is highly variable. Some cats may develop only mild
hypertrophy and suffer little compromise of heart function, while others
progress to more severe disease. HCM may worsen quickly over a period
of months, or it may progress slowly over several years. Its severity
may not change for many years and then suddenly worsen. Some cats with
HCM die very suddenly even though they had no clinical signs of heart disease.
A cat with mild to moderate
disease may enjoy an essentially normal life for a number of years.
However, the prognosis is much more guarded once the cat has more severe
disease. The risk of developing congestive heart failure is proportional
to disease severity, which is often classified by measuring wall thicknesses
and left atrial size. Although congestive heart failure can be treated
medically, severe heart failure may become difficult to manage over time
as the disease progresses. The prognosis for a cat with heart failure,
unfortunately, is guarded to poor. On average, survival for cats with
HCM and heart failure is 12-18 months after diagnosis.
Thromboembolism is a severe
uncommon complicating condition in HCM. It can cause acute pain and
various clinical signs such as loss of function of the hindlimbs (most
commonly, although other organs or limbs can be affected). Although
treatment to break down or remove the clot is available, the high treatment
costs of the procedure, death during administration of the drugs and high
recurrence rate of thromboembolism dissuades most from attempting this type
of therapy. With supportive care, about 40-50% of patients with thromboembolic
disease will break down clots on their own and regain limb function over
time. However, despite the best medical efforts to prevent their reoccurrence,
a cat that has survived a thromboembolic event has a significant risk of
developing another over the following weeks to months.
How Can I Participate
in Clinical Trials of HCM?
Currently, there is a clinical
trial examining the efficacy of anti-clotting medications in the prevention
of recurrence of aortic thromboembolism (FATE). If your pet has suffered
such an episode, your veterinarian can help you enroll your pet in this
trial by visiting the study website at http://www.vin.com/fatcat/.
Copyright
1991 - 2007, Veterinary Information Network, Inc.
This work was originally published by Veterinary Information
Network, Inc. (VIN)
and is republished with VIN's permission.
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The above information is simply informational.
It's intent is not to replace the advice of a veterinarian nor to assist
you in making a diagnosis of your pet. Please consult with your own veterinarian
for confirmation of any diagnosis. Your pets life may depend on it.