Well today was an HCM Clinic here in AZ. We had 2 of our girls at. Kender's Faithful SErvant and Kender's Reluctant Voyager , both girls will turn 5 yrs old soon and both have produced wonderful CFA Grand Champion offspring. And both today were found Normal/Clear for HCM (Hypertrophic Cardiomyopathy). Both Bella and B'Lana are sweet loving kitties who produce superior quality Siberians. Both are genetically PKD1 free. While HCM is very prevalent in some breeds , up to 30% based on studies by population , it is NOT a huge problem in the Siberian cat. we are still a hardy and genetically diverse breed. However this does not mean we should be negligent in scanning our breeding cats.
Some very technical information can be found here -= http://www.winnfelinehealth.org/Health/HCM.html
and here it is laid out a bit more lay terms -http://www.cat-world.com.au/feline-hypertrophic-cardiomyopathy
Taken from the site www.veterinarypartner.com website -=
Hypertrophic Cardiomyopathy
Authored by: Dr. Robert Prošek
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 and Ragdoll 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 over 200
different genetic mutations in more than a dozen genes 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, but sudden death is relatively uncommon in cats (compared to humans with HCM).
A small number of 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.
Figure 1. 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. 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. Echocardiography is required to confirm both the presence and severity of SAM and of HCM.
An echocardiogram (ultrasound of the heart) with color flow and spectral 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.
Two breeds (Maine Coon and Ragdoll) have been identified with mutations in the same gene (Myosin-binding protein C) as a cause of HCM. A genetic test has been developed to test these breeds for the mutation, and is offered through North Carolina State University. The test does not work in other breeds.
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:
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 to 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 to 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.
..............................................................................................................................................
Date Published: 2/23/2007 7:24:00 PM
Date Reviewed/Revised: 09/07/2011
We will continue to test our breeding cats as they mature typically at 2 and then again around 5. And while this is no guarantee that every cat we ever produce will be HCM free, it is the best medical evidence we can provide and will continue to do so. We have been in this breed 20 years now. Longer than any other US breeder. Our concern is, has been and always will be, what we perceive as best for our great breed.
Some very technical information can be found here -= http://www.winnfelinehealth.org/Health/HCM.html
and here it is laid out a bit more lay terms -http://www.cat-world.com.au/feline-hypertrophic-cardiomyopathy
Taken from the site www.veterinarypartner.com website -=
| VP Client Information Sheets By VIN Community Contributors |
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Authored by: Dr. Robert Prošek
|
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, but sudden death is relatively uncommon in cats (compared to humans with HCM).
A small number of 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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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. Echocardiography is required to confirm both the presence and severity of SAM and of HCM.
An echocardiogram (ultrasound of the heart) with color flow and spectral 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.
Two breeds (Maine Coon and Ragdoll) have been identified with mutations in the same gene (Myosin-binding protein C) as a cause of HCM. A genetic test has been developed to test these breeds for the mutation, and is offered through North Carolina State University. The test does not work in other breeds.
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.
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 to 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 to 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.
..............................................................................................................................................
Date Published: 2/23/2007 7:24:00 PM
Date Reviewed/Revised: 09/07/2011
We will continue to test our breeding cats as they mature typically at 2 and then again around 5. And while this is no guarantee that every cat we ever produce will be HCM free, it is the best medical evidence we can provide and will continue to do so. We have been in this breed 20 years now. Longer than any other US breeder. Our concern is, has been and always will be, what we perceive as best for our great breed.
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