| HYPERTROPHIC CARDIOMYOPATHY or HCM |
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| What is HCM? And why we test for it! |
Etiology
The cause of primary or idiopathic hypertrophic cardiomyopathy (HCM) in cats is unknown,
although a genetic basis or predisposition is likely in some cases. The disease appears to
be highly prevalent in certain bloodlines of several breeds. Most cases of HCM in people
are familial, and several specific abnormalities of genes for myocardial proteins have been
identified in different kindreds. In addition to mutations of genes that encode for
myocardial contractile or regulatory proteins, postulated causes of the disease include an
increased myocardial sensitivity to or excessive production of catecholamines; an
abnormal hypertrophic response to myocardial ischemic, fibrosis, or trophic factors; a
primary collagen abnormality; or abnormalities of the myocardial calcium handling process.
Some cats with HCM have high serum growth hormone concentrations.
Secondary Hypertrophic Myocardial Diseases
Myocardial hypertrophy develops as a compensatory response to certain identifiable
stresses or disease; marked left ventricular wall and septal thickening and clinical heart
failure can occur in some cats. Such cases are not considered idiopathic HCM. Secondary
causes should be ruled out if left ventricular hypertrophy is identified.
Testing for hyperthyroidism is indicated in cats with myocardial hypertrophy that are 6 years
of age or older. Hyperthyroidism alters cardiovascular function by its direct effects on the
myocardium and through the interaction of heightened sympathetic nervous system
activity and excess thyroid hormone on the heart and peripheral circulation. Cardiac
effects of thyroid hormone include myocardial hypertrophy and enhanced heart rate and
contractility. The metabolic acceleration accompanying hyperthyroidism creates a
hyperdynamic circulatory state characterized by increased cardiac output, oxygen demand,
blood volume, and heart rate.
The cause of primary or idiopathic hypertrophic cardiomyopathy (HCM) in cats is unknown,
although a genetic basis or predisposition is likely in some cases. The disease appears to
be highly prevalent in certain bloodlines of several breeds. Most cases of HCM in people
are familial, and several specific abnormalities of genes for myocardial proteins have been
identified in different kindreds. In addition to mutations of genes that encode for
myocardial contractile or regulatory proteins, postulated causes of the disease include an
increased myocardial sensitivity to or excessive production of catecholamines; an
abnormal hypertrophic response to myocardial ischemic, fibrosis, or trophic factors; a
primary collagen abnormality; or abnormalities of the myocardial calcium handling process.
Some cats with HCM have high serum growth hormone concentrations.
Secondary Hypertrophic Myocardial Diseases
Myocardial hypertrophy develops as a compensatory response to certain identifiable
stresses or disease; marked left ventricular wall and septal thickening and clinical heart
failure can occur in some cats. Such cases are not considered idiopathic HCM. Secondary
causes should be ruled out if left ventricular hypertrophy is identified.
Testing for hyperthyroidism is indicated in cats with myocardial hypertrophy that are 6 years
of age or older. Hyperthyroidism alters cardiovascular function by its direct effects on the
myocardium and through the interaction of heightened sympathetic nervous system
activity and excess thyroid hormone on the heart and peripheral circulation. Cardiac
effects of thyroid hormone include myocardial hypertrophy and enhanced heart rate and
contractility. The metabolic acceleration accompanying hyperthyroidism creates a
hyperdynamic circulatory state characterized by increased cardiac output, oxygen demand,
blood volume, and heart rate.
Left ventricular concentric hypertrophy is the expected response to increased ventricular systolic pressure
(afterload). Systemic arterial hypertension increases afterload because of high arterial pressure and resistance.
Increased resistance to ventricular outflow also occurs in the presence of a fixed (e.g., congenital subaortic
stenosis) or dynamic left ventricular outflow tract obstruction. The latter occurs in some cats with idiopathic HCM
and is described later.
Cardiac hypertrophy also develops in cats with hypersomatotropism (acromegaly) as a result of growth hormone's
trophic effects on the heart; congestive heart failure ensues in some of these cats. Increased myocardial
thickness occasionally results from infiltrative myocardial disease, most notably from lymphoma.
Psychophysiology (Diastolic Dysfunction)
The myocardial thickening that occurs in HCM leads to increased ventricular stiffness and the development of
relaxation abnormalities. Left ventricular filling is impaired and higher diastolic pressures are required when the
ventricle is stiff and less distensible. Furthermore, the myocardial relaxation process may be prolonged and
incomplete, especially if the myocardium becomes ischemic. Fibrosis and disorganized myocardial cell structure
can also contribute to the development of abnormal ventricular stiffness.
Because progressively higher filling pressures are required as the left ventricle becomes more stiff, left atrial and
ventricular enddiastolic pressures rise. The atrium enlarges, sometimes markedly, but the left ventricular volume
remains normal or decreased. A reduced ventricular volume results in a lower stroke volume and may contribute
to the activation of the renin-angiotensin system and sympathetic nervous system. Geometric changes of the left
ventricle and papillary muscles or abnormal (anterior) systolic motion of the mitral valve may prevent normal valve
closure. The resulting mitral regurgitation exacer bates the increased left atrial volume and pressure and may lead
to pulmonary congestion and edema. Higher heart rates further interfere with left ventricular filling, exacerbate
myocardial ischemic, and promote venous congestion by shortening the diastolic filling period. Contractility, or
systolic function, is usually normal in affected cats.
What is hypertrophic cardiomyopathy?
Hypertrophic cardiomyopathy (HCM) is the most common heart
disease of cats, whether they are random bred or pedigreed. It is a
heart muscle disease in which the papillary muscles (the muscles
in the left ventricle that anchor the mitral valve) and the walls of
the left ventricle become abnormally thickened. HCM is often a
progressive disease, and a proportion of affected cats develop
heart failure if the muscle hypertrophy and subsequent scarring
of the heart muscle significantly affects heart function. Cats with the disease may die suddenly and may develop a
blood clot in the chamber above the left ventricle (i.e., the left atrium) that often then gets carried into the
systemic arterial system, most commonly lodging in the terminal aorta, stopping blood flow to the rear legs.
For more information on HCM, see: members.aol.com/jchinitz/hcm/index.htm
What causes HCM in cats?
This is currently unknown in most cats although familial (hereditary) HCM has been observed in several breeds,
such as the Maine Coon and American Shorthair. Anecdotal information suggests there is familial HCM in many
other breeds. Heart muscle hypertrophy in cats can be caused by other diseases, such as systemic hypertension
(high blood pressure) and hyperthyroidism. HCM is a primary disease of the heart muscle. Hypertension and
hyperthyroidism cause secondary thickening of the left ventricle and so are not causes of HCM (although it is
possible that they may exacerbate the disease if they become present in a cat with mild to moderate HCM). HCM is
diagnosed when these other causes are ruled out.
Is HCM genetic?
In Maine Coons and American Shorthairs, HCM has been confirmed as an autosomal dominant inherited trait, as it
is in humans where over 200 gene mutations in 10 genes have been found to cause the disease. The disease has
variable expression; meaning some cats are severely affected, others are only mildly to moderately affected, and
some cats may not have evidence of the disease yet produce affected offspring. Recently, a mutation in the
cardiac myosin binding protein C (cMyBP-C) gene causing HCM in the Maine Coon cat has been identified.
doubtedly, other mutations responsible for HCM in cats remain to be discovered. However, since few veterinary
cardiologists and geneticists have the expertise to study genes, it may be some time before the responsible gene
or genes for each affected breed will be found. The mutation identified as a cause of HCM in Maine Coon cats may
not be the same mutation or even on the same gene in other breeds. The genetics of HCM in each breed will
require investigation of each individual breed.While a specific feline gene mutation has not yet been identified,
research is underway in the Maine Coon cat. However, since few veterinary cardiologists and geneticists have the
expertise to study genes, it is unlikely that the responsible gene or genes for each affected breed will be found at
any time in the near future. If a gene is identified as a cause of HCM in Maine Coon cats, it may not be the same
gene responsible for HCM in other breeds. HCM will require investigation in each breed individually.
Can HCM have a nutritional cause?
There is no evidence in cats, humans or other species of animals that HCM can have a nutritional cause. Some
researches show raw food diet may have some connection with HCM. More research is needed.
How is HCM diagnosed?
HCM is diagnosed using ultrasound of the heart – an echocardiogram. Echocardiography is a good way to detect
moderate to severely affected cats. However, it may not always detect mildly affected cats where changes in the
heart can be minimal. Ideally, an echocardiogram to test cats for HCM should be performed by a board-certified
cardiologist or radiologist. In addition to an echocardiogram, other tests may also be useful in assessing cats with
HCM. For example, a chest x-ray is necessary to detect heart failure in cats with severe HCM.
An electrocardiogram is useful in cats that have abnormal heart rhythms. Blood pressure measurement and blood
testing for hyperthyroidism are indicated to rule out other diseases that mimic HCM, especially mild to moderate
HCM. A genetic test is now available for the known cMyBP-C mutation causing HCM in Maine Coon cats.
The test is available from the Veterinary Cardiac Genetics Lab of Dr. Kathryn Meurs at the College of Veterinary
Medicine, Washington State University (http://www.vetmed.wsu.edu/deptsvcgl/). The test can identify which cats
have the mutation. If a cat is identified as having the mutation, the test can also determine whether the cat carries
one copy of the gene (a heterozygote) or two copies of the gene (a homozygote).
Should my cats be tested for HCM and how often should they be tested?
In clinical practice, the most common patients tested for HCM with echocardiography are cats with suggestive
clinical signs of heart disease, such as a heart murmur. Testing cats used in a pedigreed breeding program is a
more difficult endeavor. Echocardiography is not a perfect tool for diagnosis of HCM – some affected individuals
will escape detection and access to good quality ultrasound services may be difficult and expensive for some
breeders.
At the very least, breeding cats should be ausculted (examined by a vet with a stethoscope) for heart murmurs or
arrhythmias once yearly. Any cat with an abnormality should have an echocardiogram. A significant percentage of
cats with HCM will not have a heart murmur, however. Since HCM can occur at any age, a single normal
echocardiogram does not guarantee a cat is free of disease. Breeding cats should probably have an
echocardiogram yearly during their breeding years.
Examining retired cats periodically is also advantageous as this may allow the identification of affected cats that
have offspring in a breeding program. A Maine Coon cat that tests negative for the cMyBP-C mutation is not
guaranteed to be free of HCM, for it is not known if other mutations causing HCM are present in this breed. Ideally,
cats that test negative for the cMyBP-C mutation should still undergo echocardiogram screening. Cats that test
positive for the disease should not be bred. They will most likely develop the disease at some time during their life
although it may be too mild to detect even on an echocardiogram.
At what age should a cat be tested for HCM?
HCM can affect cats at any age. It has been seen in kittens only a few months of age and in cats over the age of 10.
In Maine Coons, most affected male cats have evidence of disease by 2 years of age, and most affected females
have evidence of disease by 3 years of age although instances have been documented where the disease has not
shown up until much later. Ragdolls with severe disease seem to develop it earlier in life, often at under 1 year of
age. Guidelines for other breeds have not yet been developed. It is therefore hard to recommend a specific age to
start testing. It may make sense to screen most breeding cats with an echocardiogram for the first time around the
age of 2 years. Maine Coons may be tested for the cMyBP-C mutation as kittens.
What do I do if my cat is diagnosed with HCM?
The cat should be removed from the breeding program and all offspring should be watched closely for the
development of HCM. Statistically, 50% of the cat’s offspring would be expected to have the genetic mutation that
causes HCM if one parent was a heterozygote. However, the most prudent approach may be not to use any of the
offspring in a breeding program. The offspring of Maine Coon cats with the cMyBP-C mutation should be
individually tested to determine their status. The parents of an affected cat should also be examined with
echocardiography (and tested for the cMyBP-C if a Maine Coon), as one of them likely carries a gene mutation for
HCM. In some cases, identification of the affected parent may be difficult, especially if the disease is mild. In these
cases, the most prudent approach may be to remove both parents from the breeding program. It is possible for a
cat to develop a spontaneous mutation that causes HCM during embryonic development but this is an unlikely
cause in a breed known to have the problem. All breeders that are using cats related to an affected cat should be
notified that a cat has been diagnosed with HCM. Similarly, pet owners should be notified that a relative has been
diagnosed with the disease. Echocardiographic examination (and genetic testing if a Maine Coon) of cats related
to the affected cat should be performed.
Will we ever eliminate HCM from my breed?
The tools we currently have to diagnose HCM (i.e., echocardiography and necropsy) are not perfect and will not
allow us to totally eliminate this disease. However, echocardiographic screening will be able to reduce the
incidence of HCM within a breed if enough breeders are involved. The identification of the cMyBP-C mutation in
the Maine Coon and the development of a genetic test provide breeders with a new tool to reduce the prevalence
of or theoretically eliminate the mutation within this breed by not breeding affected cats.
Breeders should use all the information they can gather about HCM in family lines, including pedigree analysis
based on accurate identification of affected cats. Any cat that dies suddenly or dies from HCM should have a
necropsy (i.e., post mortem examination). Most cats with HCM will have a heart that weighs more than 20 grams
and most cats with severe HCM will have a heart that weighs more than 30 grams.
Myocardial fiber disarray, the hallmark microscopic heart muscle abnormality seen in humans with familial HCM is
seen in all Maine Coon cats with HCM. Unfortunately, most veterinary pathologists are not trained to recognize this
lesion. In the long term, we will need a genetic test for HCM in each breed. A genetic test allows us to identify
affected cats before they were bred and do so accurately.
Since the disease is inherited as an autosomal dominant trait, once a mutation is identified, if all breeders
cooperated by testing their breeding cats for the mutation the disease could be eliminated from the breed within
several generations. However, the money and resources necessary to identify the gene or genes and to develop a
genetic test for each breed are scarce in veterinary medicine. Breeders and cat fanciers can help by supporting
research through organizations such as the Ricky Fund established by the Winn Feline Foundation.
Can two normal parents produce a kitten with HCM?
Since HCM is known to be an autosomal dominant trait in the breeds where the inheritance is known, each
affected cat must have one affected parent. However, there are possible situations in which an affected cat may
come from two apparently normal parents. The first possibility is that one of the parents has been misdiagnosed.
This can happen due to inexperience of the ultrasonographer or poor quality equipment. It can also happen if a cat’
s status is decided on the basis of only one or two ultrasounds early in life. Since HCM can develop at any age, a
cat that is normal on ultrasound one year could still have HCM and show signs later in life. Since the trait has
variable expression, not every affected cat will have echocardiographic evidence of HCM. It is therefore possible
for a cat to test negative for HCM on ultrasound, and yet still carry a genetic mutation and pass it to offspring.
Finally, it is possible for spontaneous mutations to occur in cats from normal parents. These cats may then pass on
their mutation to offspring. We do not know how often spontaneous mutations causing HCM occur in cats.
Statistically, spontaneous mutations are more likely to occur in random bred cats than in pedigreed cats.
What does "HCM free cattery" mean?
There is no universally agreed upon definition of an HCM free cattery. The terminology is currently unclear, as
different breeders mean different things when they use this term. Ideally, each breed should develop a specific
definition and guidelines for use of this designation for catteries.
(afterload). Systemic arterial hypertension increases afterload because of high arterial pressure and resistance.
Increased resistance to ventricular outflow also occurs in the presence of a fixed (e.g., congenital subaortic
stenosis) or dynamic left ventricular outflow tract obstruction. The latter occurs in some cats with idiopathic HCM
and is described later.
Cardiac hypertrophy also develops in cats with hypersomatotropism (acromegaly) as a result of growth hormone's
trophic effects on the heart; congestive heart failure ensues in some of these cats. Increased myocardial
thickness occasionally results from infiltrative myocardial disease, most notably from lymphoma.
Psychophysiology (Diastolic Dysfunction)
The myocardial thickening that occurs in HCM leads to increased ventricular stiffness and the development of
relaxation abnormalities. Left ventricular filling is impaired and higher diastolic pressures are required when the
ventricle is stiff and less distensible. Furthermore, the myocardial relaxation process may be prolonged and
incomplete, especially if the myocardium becomes ischemic. Fibrosis and disorganized myocardial cell structure
can also contribute to the development of abnormal ventricular stiffness.
Because progressively higher filling pressures are required as the left ventricle becomes more stiff, left atrial and
ventricular enddiastolic pressures rise. The atrium enlarges, sometimes markedly, but the left ventricular volume
remains normal or decreased. A reduced ventricular volume results in a lower stroke volume and may contribute
to the activation of the renin-angiotensin system and sympathetic nervous system. Geometric changes of the left
ventricle and papillary muscles or abnormal (anterior) systolic motion of the mitral valve may prevent normal valve
closure. The resulting mitral regurgitation exacer bates the increased left atrial volume and pressure and may lead
to pulmonary congestion and edema. Higher heart rates further interfere with left ventricular filling, exacerbate
myocardial ischemic, and promote venous congestion by shortening the diastolic filling period. Contractility, or
systolic function, is usually normal in affected cats.
What is hypertrophic cardiomyopathy?
Hypertrophic cardiomyopathy (HCM) is the most common heart
disease of cats, whether they are random bred or pedigreed. It is a
heart muscle disease in which the papillary muscles (the muscles
in the left ventricle that anchor the mitral valve) and the walls of
the left ventricle become abnormally thickened. HCM is often a
progressive disease, and a proportion of affected cats develop
heart failure if the muscle hypertrophy and subsequent scarring
of the heart muscle significantly affects heart function. Cats with the disease may die suddenly and may develop a
blood clot in the chamber above the left ventricle (i.e., the left atrium) that often then gets carried into the
systemic arterial system, most commonly lodging in the terminal aorta, stopping blood flow to the rear legs.
For more information on HCM, see: members.aol.com/jchinitz/hcm/index.htm
What causes HCM in cats?
This is currently unknown in most cats although familial (hereditary) HCM has been observed in several breeds,
such as the Maine Coon and American Shorthair. Anecdotal information suggests there is familial HCM in many
other breeds. Heart muscle hypertrophy in cats can be caused by other diseases, such as systemic hypertension
(high blood pressure) and hyperthyroidism. HCM is a primary disease of the heart muscle. Hypertension and
hyperthyroidism cause secondary thickening of the left ventricle and so are not causes of HCM (although it is
possible that they may exacerbate the disease if they become present in a cat with mild to moderate HCM). HCM is
diagnosed when these other causes are ruled out.
Is HCM genetic?
In Maine Coons and American Shorthairs, HCM has been confirmed as an autosomal dominant inherited trait, as it
is in humans where over 200 gene mutations in 10 genes have been found to cause the disease. The disease has
variable expression; meaning some cats are severely affected, others are only mildly to moderately affected, and
some cats may not have evidence of the disease yet produce affected offspring. Recently, a mutation in the
cardiac myosin binding protein C (cMyBP-C) gene causing HCM in the Maine Coon cat has been identified.
doubtedly, other mutations responsible for HCM in cats remain to be discovered. However, since few veterinary
cardiologists and geneticists have the expertise to study genes, it may be some time before the responsible gene
or genes for each affected breed will be found. The mutation identified as a cause of HCM in Maine Coon cats may
not be the same mutation or even on the same gene in other breeds. The genetics of HCM in each breed will
require investigation of each individual breed.While a specific feline gene mutation has not yet been identified,
research is underway in the Maine Coon cat. However, since few veterinary cardiologists and geneticists have the
expertise to study genes, it is unlikely that the responsible gene or genes for each affected breed will be found at
any time in the near future. If a gene is identified as a cause of HCM in Maine Coon cats, it may not be the same
gene responsible for HCM in other breeds. HCM will require investigation in each breed individually.
Can HCM have a nutritional cause?
There is no evidence in cats, humans or other species of animals that HCM can have a nutritional cause. Some
researches show raw food diet may have some connection with HCM. More research is needed.
How is HCM diagnosed?
HCM is diagnosed using ultrasound of the heart – an echocardiogram. Echocardiography is a good way to detect
moderate to severely affected cats. However, it may not always detect mildly affected cats where changes in the
heart can be minimal. Ideally, an echocardiogram to test cats for HCM should be performed by a board-certified
cardiologist or radiologist. In addition to an echocardiogram, other tests may also be useful in assessing cats with
HCM. For example, a chest x-ray is necessary to detect heart failure in cats with severe HCM.
An electrocardiogram is useful in cats that have abnormal heart rhythms. Blood pressure measurement and blood
testing for hyperthyroidism are indicated to rule out other diseases that mimic HCM, especially mild to moderate
HCM. A genetic test is now available for the known cMyBP-C mutation causing HCM in Maine Coon cats.
The test is available from the Veterinary Cardiac Genetics Lab of Dr. Kathryn Meurs at the College of Veterinary
Medicine, Washington State University (http://www.vetmed.wsu.edu/deptsvcgl/). The test can identify which cats
have the mutation. If a cat is identified as having the mutation, the test can also determine whether the cat carries
one copy of the gene (a heterozygote) or two copies of the gene (a homozygote).
Should my cats be tested for HCM and how often should they be tested?
In clinical practice, the most common patients tested for HCM with echocardiography are cats with suggestive
clinical signs of heart disease, such as a heart murmur. Testing cats used in a pedigreed breeding program is a
more difficult endeavor. Echocardiography is not a perfect tool for diagnosis of HCM – some affected individuals
will escape detection and access to good quality ultrasound services may be difficult and expensive for some
breeders.
At the very least, breeding cats should be ausculted (examined by a vet with a stethoscope) for heart murmurs or
arrhythmias once yearly. Any cat with an abnormality should have an echocardiogram. A significant percentage of
cats with HCM will not have a heart murmur, however. Since HCM can occur at any age, a single normal
echocardiogram does not guarantee a cat is free of disease. Breeding cats should probably have an
echocardiogram yearly during their breeding years.
Examining retired cats periodically is also advantageous as this may allow the identification of affected cats that
have offspring in a breeding program. A Maine Coon cat that tests negative for the cMyBP-C mutation is not
guaranteed to be free of HCM, for it is not known if other mutations causing HCM are present in this breed. Ideally,
cats that test negative for the cMyBP-C mutation should still undergo echocardiogram screening. Cats that test
positive for the disease should not be bred. They will most likely develop the disease at some time during their life
although it may be too mild to detect even on an echocardiogram.
At what age should a cat be tested for HCM?
HCM can affect cats at any age. It has been seen in kittens only a few months of age and in cats over the age of 10.
In Maine Coons, most affected male cats have evidence of disease by 2 years of age, and most affected females
have evidence of disease by 3 years of age although instances have been documented where the disease has not
shown up until much later. Ragdolls with severe disease seem to develop it earlier in life, often at under 1 year of
age. Guidelines for other breeds have not yet been developed. It is therefore hard to recommend a specific age to
start testing. It may make sense to screen most breeding cats with an echocardiogram for the first time around the
age of 2 years. Maine Coons may be tested for the cMyBP-C mutation as kittens.
What do I do if my cat is diagnosed with HCM?
The cat should be removed from the breeding program and all offspring should be watched closely for the
development of HCM. Statistically, 50% of the cat’s offspring would be expected to have the genetic mutation that
causes HCM if one parent was a heterozygote. However, the most prudent approach may be not to use any of the
offspring in a breeding program. The offspring of Maine Coon cats with the cMyBP-C mutation should be
individually tested to determine their status. The parents of an affected cat should also be examined with
echocardiography (and tested for the cMyBP-C if a Maine Coon), as one of them likely carries a gene mutation for
HCM. In some cases, identification of the affected parent may be difficult, especially if the disease is mild. In these
cases, the most prudent approach may be to remove both parents from the breeding program. It is possible for a
cat to develop a spontaneous mutation that causes HCM during embryonic development but this is an unlikely
cause in a breed known to have the problem. All breeders that are using cats related to an affected cat should be
notified that a cat has been diagnosed with HCM. Similarly, pet owners should be notified that a relative has been
diagnosed with the disease. Echocardiographic examination (and genetic testing if a Maine Coon) of cats related
to the affected cat should be performed.
Will we ever eliminate HCM from my breed?
The tools we currently have to diagnose HCM (i.e., echocardiography and necropsy) are not perfect and will not
allow us to totally eliminate this disease. However, echocardiographic screening will be able to reduce the
incidence of HCM within a breed if enough breeders are involved. The identification of the cMyBP-C mutation in
the Maine Coon and the development of a genetic test provide breeders with a new tool to reduce the prevalence
of or theoretically eliminate the mutation within this breed by not breeding affected cats.
Breeders should use all the information they can gather about HCM in family lines, including pedigree analysis
based on accurate identification of affected cats. Any cat that dies suddenly or dies from HCM should have a
necropsy (i.e., post mortem examination). Most cats with HCM will have a heart that weighs more than 20 grams
and most cats with severe HCM will have a heart that weighs more than 30 grams.
Myocardial fiber disarray, the hallmark microscopic heart muscle abnormality seen in humans with familial HCM is
seen in all Maine Coon cats with HCM. Unfortunately, most veterinary pathologists are not trained to recognize this
lesion. In the long term, we will need a genetic test for HCM in each breed. A genetic test allows us to identify
affected cats before they were bred and do so accurately.
Since the disease is inherited as an autosomal dominant trait, once a mutation is identified, if all breeders
cooperated by testing their breeding cats for the mutation the disease could be eliminated from the breed within
several generations. However, the money and resources necessary to identify the gene or genes and to develop a
genetic test for each breed are scarce in veterinary medicine. Breeders and cat fanciers can help by supporting
research through organizations such as the Ricky Fund established by the Winn Feline Foundation.
Can two normal parents produce a kitten with HCM?
Since HCM is known to be an autosomal dominant trait in the breeds where the inheritance is known, each
affected cat must have one affected parent. However, there are possible situations in which an affected cat may
come from two apparently normal parents. The first possibility is that one of the parents has been misdiagnosed.
This can happen due to inexperience of the ultrasonographer or poor quality equipment. It can also happen if a cat’
s status is decided on the basis of only one or two ultrasounds early in life. Since HCM can develop at any age, a
cat that is normal on ultrasound one year could still have HCM and show signs later in life. Since the trait has
variable expression, not every affected cat will have echocardiographic evidence of HCM. It is therefore possible
for a cat to test negative for HCM on ultrasound, and yet still carry a genetic mutation and pass it to offspring.
Finally, it is possible for spontaneous mutations to occur in cats from normal parents. These cats may then pass on
their mutation to offspring. We do not know how often spontaneous mutations causing HCM occur in cats.
Statistically, spontaneous mutations are more likely to occur in random bred cats than in pedigreed cats.
What does "HCM free cattery" mean?
There is no universally agreed upon definition of an HCM free cattery. The terminology is currently unclear, as
different breeders mean different things when they use this term. Ideally, each breed should develop a specific
definition and guidelines for use of this designation for catteries.
| We at Sandalwood Bengals take every precaution to test and screen ALL of our breeding cats YEARLY in our program. This is one of many tools, we use as responsible breeders, as an aid to continually improve our breeding program.. |
| Here is some useful information on HCM AND why it is SO important to have your breeding cats tested! This is from the Winn Foundation where you can find lots of useful information on cat health! http://www.winnfelinehealth.org/Pages/Health.html |
Systemic hypertension can result and further stimulate myocardial hypertrophy. Clinical
cardiovascular signs often include a systolic murmur, hyperdynamic precordial and arterial
impulses, tachycardia and arrhythmias, and evidence of left ventricular enlargement or
hypertrophy, seen on electrocardiograms (ECGs), thoracic radiographs, or echo cardiograms.
Signs of congestive heart failure develop in an estimated 15% of hyperthyroid cats; most
have normal to high fractional shortening, but a few have poor contractile function.
cardiovascular signs often include a systolic murmur, hyperdynamic precordial and arterial
impulses, tachycardia and arrhythmias, and evidence of left ventricular enlargement or
hypertrophy, seen on electrocardiograms (ECGs), thoracic radiographs, or echo cardiograms.
Signs of congestive heart failure develop in an estimated 15% of hyperthyroid cats; most
have normal to high fractional shortening, but a few have poor contractile function.
Specific therapy, in addition to the antithyroid treatment, may be necessary to manage the cardiac complications of
hyperthyroidism. ß-Blockers can temporarily control many of the adverse cardiac effects of excess thyroid hormone,
especially tachyarrhythmias. Diltiazem is another alternative therapy. Treatment for congestive failure is the same as
that described later for HCM. The rare hypodynamic (dilated) cardiac failure is treated in the same way as dilated
cardiomyopathy. (ß-Blocker or other cardiac therapy is not a substitute for antithyroid treatment, however.
hyperthyroidism. ß-Blockers can temporarily control many of the adverse cardiac effects of excess thyroid hormone,
especially tachyarrhythmias. Diltiazem is another alternative therapy. Treatment for congestive failure is the same as
that described later for HCM. The rare hypodynamic (dilated) cardiac failure is treated in the same way as dilated
cardiomyopathy. (ß-Blocker or other cardiac therapy is not a substitute for antithyroid treatment, however.
| Breeding cats should have an echocardiogram *YEARLY* during their breeding years. |
