HCM

 AWARENESS & SUPPORT


This page is dedicated to all of the Canadian Sphynx Hairless Cats that we have loved!  As the Sphynx breed continues its fight with HCM & Genetic Heart Disease we will continue to hope for education and knowledge for all of those hairless kitties and their families fighting the good fight as we have done over the past 10 years working with the breed.  

LEUPOLD 2/03/07-4/17/14
SLEEP WITH THE ANGELS 
MY PRECIOUS BOY...

Photo above taken on 4/16/14, when Leupold received a special gift from our friend Kelly of 
BARE MACHISMO PET JEWELRY

" Unlock a cure "  

is a special line dedicated in helping to fight HCM!

With each piece purchased, we will donate $5.00 to the
NC State University Sphynx HCM Research Fund
.
http://baremachismo.weebly.com/unlock-a-cure.html

This gift is so very special to me as my precious boy passed within 24 hours of our short photo session with him wearing it.  Today 4/17/14, when Leo apparently threw a clot, passing away only moments later he was laid to rest in our Zen Garden wearing this special gift.  I planned this day in my head so many times over the last 4 years since his diagnoses but nothing prepares you for the heart break this disease causes.  Thank You to all of my friends, family and most of all to Leo's breeder who I adore for giving me the opportunity to own my very first Sphynx Pet and opening my eyes & soul to this wonderful breed.  Leo is gone from our home but will never be gone from our hearts.  Leo has made me the breeder I am today and will always be my everything. 

All of the cats here at Nada are scanned at the University of Florida and here are some frequently asked questions from UF. 

Cardiology FAQs

Cardio team in cath lab.

What is involved with a cardiology work up and how much will it cost?

The cardiology work up consists of getting a complete history and a cardiac physical examination along with additional diagnostic tests as indicated, so fees vary from case to case.

  • Exam
  • Echocardiogram
  • ECG (EKG)
  • Radiographs (x-rays)
  • Blood pressure
  • Holter monitor

What does an Echocardiogram show that an X-ray doesn’t?

Although X-rays (radiographs) are an important diagnostic tool, an echocardiogram provides live images from which the cardiologist can measure the size and thickness of the greater vessels, the chambers of the heart and heart valves as well as track the flow of blood through the heart and vessels. A radiograph is a still picture that can be used to determine chamber and vessel enlargement, accumulation of fluid and other cardiac abnormalities. Radiographs allow evaluation of the lungs which an echocardiogram does not.

I already had radiographs and blood work done at my family veterinarian’s office; will you need to repeat them?

In many cases we will not have to repeat the diagnostics done by your family veterinarian, so it is always good to bring these with you to your appointment for evaluation. However, this varies from case to case and we will provide you with an estimate for the diagnostics needed to properly evaluate the condition of your pet.

What kind of procedures does the cardiology department do?

Here at the UFVH we are equipped to perform Echocardiograms, Electrocardiograms (ECG/EKG), Balloon Valvuloplasty, Pacemaker Implantation, Transarterial Patent Ductus Arteriousus Closure, Blood pressure Monitoring, OFA Heart Certification, Holter and Event Monitoring, Pericardiocentisis and Surgical Heartworm Extractions. We also have Bi-monthly Cardiomyopathy screening clinics as well as clinical research trials for new treatments and surgical procedures.

Can I go to my family veterinarian for the follow up exams?

In many cases, your family veterinarian will perform follow up exams, blood work and radiographs with phone consultation from the Cardiology Service. However, there are some cases that will need to have the cardiologist and or the equipment here at the UFVH to perform the follow up care.

How do I know if my pet qualifies for a clinical trial?

Your family veterinarian can help you determine if your pet qualifies for one of our clinical trials by consulting with the Cardiology Service.

My family veterinarian recommended that my pet wear a Holter monitor; why can’t we just do an ECG?

An ECG only records a few minutes of the heart’s rhythm in which case an abnormality could easily be missed. The Holter Monitor records every heart beat over a 24 hour period of time. The recording is then evaluated by the cardiology technicians and the cardiologist. The results are then used to help determine the diagnosis, treatment plan, as well as response to current medical treatment.

How old does my pet need to be to get a heart certification?

Many breeders want to have their puppies screened for congenital cardiac defects before they are sold in which case the cardiologist will sign a “provisional” certification. Otherwise OFA certification is performed when the dog is at least 1 year of age.

Do I need a referral from my veterinarian?

A referral from a family veterinarian is not required; however we would prefer to work with your family veterinarian to provide you and your pet with the most comprehensive veterinary care.

Can you be my family veterinarian?

Because our service is so specialized we are unable to offer your pet the general care that your family veterinarian can. If you need a family veterinarian the UFVH has a general practice that operates within the hospital that can provide your pet with vaccines, flea and heartworm protection and all other general medical needs.

Will my pet be sedated? Do I need to fast him/her?

Although it is not very common, sedation may be necessary for certain procedures. It is recommended that your pet does not eat after midnight, the night before your Cardiology visit. However, if you pet is on any medications, it is important to give the medications at the normal scheduled times. Water is always okay up until the Cardiology appointment.

 

http://smallanimal.vethospital.ufl.edu/clinical-services/cardiology/cardiology-faqs/

 

 

 

Genetics & HCM

 Mark D. Kittleson, DVM, PhD, Diplomate ACVIM (Cardiology)

In human medicine it is becoming more and more clear that HCM is primarily, if not almost entirely, a genetic disease. Fortunately, many mutations that cause the disease have been identified in humans. Unfortunately, the number of mutations is large (over 400) and the mutations are spread across a number of different genes, which makes initial screening to identify the specific mutation in a family difficult and expensive. Most of these genes code for proteins that build sarcomeres, the small units in muscle that are responsible for contraction. Most of the sarcomeric gene mutations (around 80%) that have been identified are in the beta myosin heavy chain (MYH7) and cardiac myosin binding protein C (MYBPC3) genes. When looked at another way, anywhere from 20% to 40% of humans with HCM screened for a mutation have a MYBPC3 mutation. One exception to this is in the Netherlands where three MYBPC3 mutations predominate and so 70% of patients with HCM have a MYBPC3 mutation.

Although HCM is at least as prevalent in cats as it is in humans (where it is 1 in 500 people), to date only two mutations have been identified that cause HCM in cats. Not unexpectedly, both of them are in the cardiac myosin binding protein C gene. The first one (A31P) was discovered in 2005 in Maine Coon cats and the second one (C820T) in Ragdoll cats was discovered in 2007. It is expected that other mutations will be found in other cat breeds. It is also already apparent that at least one more HCM-causing mutation is present in Maine Coon cats since not all Maine Coon cats with HCM in the colony at the University of California, Davis (UCDavis) or in the real world have the A31P mutation.

In order to understand the heritable nature of HCM one must understand the difference between heterozygosity and homozygosity. Following is a simplified explanation. There are primarily two types of proteins in the body – structural proteins and enzymes. In general (although many exceptions exist), mutations in genes that code for enzymes cause autosomal recessive disease and mutations in genes that code for structural proteins cause autosomal dominant disease. Why is that? Mother Nature has many backup systems that she has constructed within the body and for a disease to be produced by an enzyme deficiency usually more than 90% of that enzyme must be absent or nonfunctional before an abnormality is seen. Consequently, both alleles (the gene from each parent) must be mutated to produce disease when a gene that codes for an enzyme is involved. In other words, an individual must be homozygous for a mutation in order for disease to be present. Heterozygous individuals (only one mutated allele from either the mother or the father) still have 50% of the normal enzyme present, which is sufficient to allow normal function. So, in autosomal recessive conditions, heterozygous individuals are called carriers because they never develop disease but have a mutation they can pass on to their offspring.

Mutations in genes that code for structural proteins, on the other hand, only have to be present on one allele (heterozygous) since a 50% reduction in the amount of a structural protein usually causes significant problems with the structure that protein helps build, which causes disease. Cardiac myosin binding protein C is a structural protein. Consequently, mutations in the gene that codes for this protein are said to be inherited in an autosomal dominant fashion. This means that if one parent has one mutated allele (and the other parent has no mutation) the affected parent can pass the mutation on its one allele to an offspring and that offspring can develop HCM. Each offspring would have a 50% chance of inheriting the genetic defect. In a litter, on average, approximately 50% of the offspring would have one mutated allele and one normal allele (heterozygote) while the other 50% should be free of the mutation.

Unlike in humans where inbreeding is frowned upon (except in certain populations), inbreeding in cats is often encouraged or at least tolerated. Consequently, it is extremely rare for two humans who are heterozygous for the same mutation to reproduce and produce offspring. In purebred cats the chance of this happening is much, much greater. As a result, not only are cats that are heterozygous for the mutation seen but cats that are homozygous for the mutation are also seen in both Maine Coon cats and Ragdoll cats. It was originally thought that homozygous individuals would not survive (would die in utero or be stillborn) but it is now well established that cats (and humans) that are homozygous for a mutation do survive. They add another level of complexity to the disease. When a cat that is homozygous for one of the mutations is bred to a cat without a mutation all of the kittens in a litter will be heterozygous for the mutation and so have the potential for developing HCM and, even if they don’t, can still pass the mutation on to descendants. When a cat that is homozygous for a mutation is bred to a cat that is heterozygous, on average, 50% of the kittens will be homozygous and 50% will be heterozygous. Obviously, if two homozygous parents are bred, all of the kittens will be homozygous. These determinations are made by using a simple relationship called a Punnett square. Here are several Punnett squares illustrating the outcome of possible mating combinations.

Hypertrophic cardiomyopathy is a disease that is not present at birth but instead is one that develops over time. The reason for this is unknown. In cats it would appear that the disease develops earlier in cats that are homozygous for a mutation. In humans it is well known that MYBPC3 mutations often produce a form of the disease that develops later in life in individuals that are heterozygous for a mutation. Consequently, patients with a MYBPC3 mutation often are normal until they are in their 50s and beyond. There is evidence that this can occur in Maine Coon cats as well.

There is also evidence in humans that some mutations cause a more malignant form of HCM while others cause a more benign form. MYBPC3 mutations are generally, but not always, on the more benign end of the spectrum.

Not all individuals with an autosomal dominant mutation actually develop demonstrable disease and that is certainly true for MYBPC3 mutations. This is called penetrance. For example, if 100 individuals with a mutation are examined and only 50 have the disease known to be caused by the mutation then the penetrance is said to be 50%. Since it is not 100% in this scenario penetrance is said to be incomplete. In a sense, penetrance is a reflection of our ability to detect or recognize clinical disease, and is often age-related. In humans, penetrance in patients with a MYBPC3 mutation borders on 100% if they are followed out to beyond 50 years of age. In Maine Coon cats it was originally reported that penetrance was 100% in the colony at UCDavis. However, observation in the general population has demonstrated penetrance varying from the initial report. Real world experience suggests that penetrance may be low for cats that are heterozygous for the A31P mutation. Penetrance for homozygous cats is still expected to be very high.

In addition, not all individuals express the disease (HCM) in the same way. Some have very mild disease while others develop more severe disease. This is termed variable expressivity. In humans it has been well established by looking at individual families that mutations that cause HCM have variable expressivity. In other words, in human families it is well known that different family members with the same mutation have varying disease severity, age of onset, or progression of disease – often some will have mild disease while others will have severe disease. This has also been seen in the Maine Coon cat colony at UCDavis. While expressivity is expected to be more uniform in cats homozygous for a mutation and usually is (i.e., all homozygous cats have severe disease) this has not always been the case in the colony at UCDavis. For example, the longest surviving homozygous cat in that colony died at 12 years of age, albeit with severe but somewhat unusual cardiac disease. However, most died at a young (<5 years) age.

Since penetrance is not 100% and because expressivity is variable, it is common to identify Maine Coon and Ragdoll cats with a causal mutation that do not have echocardiographic evidence of HCM. This is more common in young cats but can also be the case in older cats. Also, as already noted, not all Maine Coon cats with HCM have the A31P mutation. These facts inevitably raise questions regarding the validity of the research findings that identified the A31P and C820T mutations as causal in producing HCM. Unfortunately, this may also lead some breeders to rationalize breeding cats that have a mutation. In order to clarify this issue, several factors must be considered to understand how we know that these mutations actually cause HCM.

What is the proof? First, the mutations identified to date are located in regions of the gene that are highly conserved. That means when you look across species that the base pair change (i.e., the mutation) occurs in a position where the base pair is always the same, regardless of species. This means that it’s important that the particular base pair is always the same because if it’s not, bad things (i.e., disease) will happen. Second, when you enter the mutated sequence into a computer program to predict what the mutated protein will look like, that protein looks very abnormal. Third, when examined in two labs now, the amount of cardiac myosin binding protein C protein in cardiac cells is reduced in Maine Coon cats with the A31P mutation, especially those that are homozygous for the mutation.

So there is almost no doubt that the two mutations identified cause HCM in two breeds of cats. What then needs to be done to rid the Maine Coon and Ragdoll breeds of this disease-causing mutation? That is a scientifically, ethically and politically challenging question. It becomes scientifically challenging primarily because the incidence of the mutations is so high. In Maine Coon cats that have been screened for the A31P mutation, although not a random sample, the incidence is over 30%. The scientific argument then becomes, what would happen if all of those cats were removed from the breeding pool? At first blush it looks as if this would be detrimental to the gene pool. By saying that 30% of the cats couldn’t be bred and moving to the remaining 70% it would appear that you would run the risk of compounding other existing mutations in that gene pool and potentially causing more harm to the breed than good. However, this overlooks the fact that the gene pool is already selected by cat breeders. It is estimated that of the kittens produced by cat breeders less than 10% of those cats ever get bred. So cat breeders already remove 90% of the gene pool in their quest to have the best looking, and hopefully healthiest, cats. When that is taken into account one then realizes that 30% of 10% (or 3%) of the cats are really being affected by removing those with a causal mutation. And so the effect on the gene pool becomes much less onerous IF cat breeders are willing to breed cats selected first for good health.

What recommendation has been made to Maine Coon cat and Ragdoll cat breeders? The first recommendation is to have all breeding cats tested for the appropriate mutation. The second recommendation is to never breed a cat that is homozygous for a mutation. The third recommendation is less clear and addresses cats that are heterozygous. Ideally those cats should not be bred also. However, one loophole has been left in place. It states that if a cat has qualities that are deemed by the breeder to be exceptional and of great advantage to the breed, that cat can be bred once. The offspring from that cat then must be tested and the kittens that have the mutation must not be bred. The line is continued with kittens that do not have the mutation. The fourth recommendation is to never sell a kitten that has a mutation. Obviously it is better never to produce a kitten that has a mutation but it certainly is unethical to sell a kitten with a mutation to an unsuspecting (or even knowledgeable) owner. Full disclosure of the DNA status of a kitten or cat should be given to potential owners, prior to offer for placement, with an explanation of the possible complications in the health of a cat with the mutation.

What about purebred breeding cats that belong to breeds where a mutation has not been identified or in which another mutation is believed to be present (e.g., Maine Coon cats)? These cats need to be screened periodically using echocardiography (cardiac ultrasound) for the presence of HCM. However, echocardiographic screening has several shortcomings. First, as noted previously, HCM usually does not show up in young cats and so a cat may be bred before there is echocardiographic evidence of the disease. Second, penetrance is not 100% so some cats with a mutation may never have clinical evidence of HCM although they can pass a mutation on to their offspring and those offspring can develop HCM. Third, cats can express a very mild form of the disease making it difficult to impossible to distinguish them from normal cats (i.e., equivocal diagnosis). Consequently, genetic testing is much preferred over echocardiographic screening when it is available and there is only one mutation in a breed. Unfortunately, this dream has yet to be realized for most breeds. Still, careful attention to the health history of ancestors and closely related cats, plus intelligent and informed use of all the tests available to ascertain the health of a breeding cat can only benefit the breed when individuals who are found to be affected are removed from breeding programs.


Copyright © 1997-2009 Mark D. Kittleson, DVM, PhD, Diplomate ACVIM (Cardiology)

Nada is very serious about fighting the good fight against Genetic HCM.  We believe that HCM scanning of our breeding cats atleast once a year is one of the *TOOLS* to assist in this fight.  If one of our cats appear to have HCM our Cardiologist team insists that tests are completed for Hyperthyroidism, Hypertension, Aortic Stenosis and Acromegaly are completed to ensure the HCM is not secondary to other health issues.  Once we have determined that HCM may be of a genetic nature we send these Cardiology Reports to reputable HCM Databases to allow the public to access this information.  This info is also provided directly to the owners of our babies via our Facebook Cattery page .  Unfortunately we have experienced buying from breeders that claim to scan their breeding cats but have yet to provide any of this information for our records.  We will no longer support  breeding programs by purchasing from catteries that do not provide full disclosure of HCM reports and recommend you do the same.     We insist that all of our cats undergo a necropsy when they cross over the rainbow bridge.  This is a sure way to examine the heart for HCM.  We urge other cat owners to participate proactively in HCM scanning before its too late.  What you must understand is that HCM is typically an adult onset disease with a median age of onset at 5 years old.  So even though we HCM scan our cats for HCM its often not until the cats have been retired from breeding programs that breeders are made aware of a positive result.  Many breeders place their retired cats and never follow up on their heart health.  Nada Sphynx are placed in retired homes under contract to continue to scan their hearts atleast every two years.  Doing this has provided us with three positive results of cats we have owned.  Making our buyer's aware of HCM and including information in our sales contracts has assisted us in monitoring the health of our cat's cardiology health.  Please scan all of your cats regardless of the breed for the love of their lives.    
Congestive Heart Failure in Cats - When HCM is Not HCM
Tony M. Glaus1, PD, Dr.med.vet., DACVIM, DECVIM-CA; Gerhard Wess2, Dr.med.vet., DACVIM, DECVIM-CA
1Zurich, Switzerland; 2Munich, Germany
 
 

Read the German translation: Herzversagen bei der Katze: wann ist HCM keine HCM?

Definitions and Forms of Primary, Genetic HCM

Hypertrophic cardiomyopathy (HCM) is a clinical heterogeneous cardiac disease that is in most cases inherited as an autosomal dominant trait. According to the classification of the American Heart Association (AHA), HCM is a primary genetic heart disease.1 HCM is morphologically characterized as a hypertrophied, no dilated left ventricle (LV) without any underlying systemic or cardiac disease that could cause a hypertrophied LV, such as systemic hypertension or (sub-)aortic stenosis. HCM is a progressive disease that finally leads to congestive heart failure (CHF) or sudden death. Diagnosis is usually based upon two-dimensional (2D) echocardiography.1

The echocardiographic picture is in humans, as in cats very heterogeneous concerning the severity of the hypertrophy and the myocardial hyperechogenicity, as well as concerning the localisation of the hypertrophy. The thickening may be global or regional, and symmetric and asymmetric forms can be distinguished. The symmetric, global from affects the LV homogenous, whereas the asymmetric form involves selectively only the papillary muscles, the LV posterior wall, the interventricular septal wall (IVS), or focal in the IVS, just below the aortic valve.2 In feline HCM, the LV papillary muscles are consistently enlarged.

Systolic anterior motion of the mitral valve (SAM) is common in cats with HCM. Cats with HCM and SAM are commonly said to have the obstructive form of HCM or hypertrophic obstructive cardiomyopathy (HOCM). Secondary obstruction of the LV outflow tract (LVOT) can worsen the LV hypertrophy through additional pressure overload.

HCM SAM; SAM = HCM?

Systolic anterior motion of the mitral valve is the process of the septal (anterior) mitral valve leaflet or the chordal structures inserting on this leaflet being pulled into the LVOT during systole by the enlarged or displaced papillary muscles. Here it is caught in the blood flow and pushed toward and often ultimately against the interventricular septum. The initial pulling of the mitral valve leaflet toward the LVOT in systole can clearly be seen on many echocardiograms from cats with HCM to be due to the grossly enlarged papillary muscles encroaching on the LVOT (the region of the LV between the anterior leaflet of the mitral valve and the interventricular septum) and pulling the mitral apparatus structures into the basilar region of the outflow tract. SAM produces a dynamic subaortic stenosis that increases the velocity of blood flow through the subaortic region and usually produces turbulence. Simultaneously, when the septal leaflet is pulled toward the interventricular septum, a gap in the mitral valve is produced creating mitral regurgitation. These abnormalities are by far the most common causes of the heart murmur heard in cats with HCM.

Occasionally it has been reported that in some cats, the LV hypertrophy regressed with beta-blocker treatment for SAM and that SAM could be found in young, as well in older cats without LV hypertrophy. Therefore, it seems that occasional SAM may be a primary problem causing a secondary LV hypertrophy. A similar, but rare phenomenon has been observed rarely in dogs by D'Agnolo et al. Therefore the question arises concerning the development and the classification of this entity. SAM can be caused experimentally by displacement of the anterior papillary muscle.3 Potentially, the cause of "primary SAM" is different in young, and in older cats. In young cats a congenital abnormality of the anterior papillary muscle resulting in an abnormal attachment of the chordae tendinea, causing abnormal attachment of the mitral valve may be an explanation. However, this entity should be better classified as mitral valve dysplasia. In older cats with a new heart murmur and "primary SAM", myocardial and especially papillary muscle restructuration's secondary to inflammatory, toxic, or ischemic insults may be suspected as the cause of SAM. These entities should be classified as secondary cardiomyopathies.

Myokarditis versus HCM

Myocarditis is known to cause abnormal myocardial function and cardiac dilation in humans for many years. Many cases of dilated cardiomyopathy (DCM) are actually caused by myocarditis. In humans, myocarditis is therefore classified as primary mixed cardiomyopathy.1 Myocarditis in cats is also a recognized entity. Interestingly, echocardiography in cats with myocarditis shows often not DCM, but a hypertrophied LV. In a recent pathological study, cats with cardiomyopathy were examined by histology and by PCR. 55% of the cats with HCM showed signs of active myocarditis on histology, and panleukopenia virus was found in some of these cats.4 The authors have examined several cats that developed pulmonary edema and had the typical picture of HCM on echocardiography, with LV hypertrophy and left atrial dilation, after previous anaesthesia or surgery. Supportive therapy including diuretics, oxygen and antibiotics led to resolution of the pulmonary edema and cats became clinically normal. Repeated echocardiography showed a successive regression of the LV hypertrophy and LA dilation. This presentation and disease course argues against primary HCM, but rather for a reversible defect, such as infectious or toxic myocarditis.

Steroid-Induced "HCM"

A similar picture as in the suspected myocarditis cases, with acute pulmonary edema, has been reported in cats given steroids. Pulmonary edema and LV hypertrophy resolved in these cats, initially diagnosed with HCM due to LV hypertrophy and LA dilation seen on echocardiography.5 However, attempts to cause this form of cardiomyopathy were not successful. The question arises, if the cats need to have a genetic predisposition to react abnormal to steroids, or if the affected cases in fact had myocarditis associated with glucocorticoid application.

Hyperthyroidism-Induced Cardiomyopathy

Thyroid hormones have important metabolic and cardiovascular effects. Hyperthyroidism causes an increased metabolic rate and this result in a demand for an increased cardiac output. In the peripheral blood vessels thyroid hormones cause a decreased resistance. This leads directly to an increased cardiac output. Additionally, thyroid hormones induce multiple genes within the myocardium causing LV hypertrophy. A volume overloaded LV with eccentric hypertrophy should be the resulting changes of these mechanisms. However, concentric hypertrophy secondary to hyperthyroidism has been reported as well.6

Myocardial Hypertrophy Caused by Infiltrations

Infiltrations of the myocardial wall causing LV hypertrophy such as amyloidosis have not been reported in veterinary medicine. Rarely, diffuse neoplastic infiltrations caused by lymphosarcoma have been reported, causing LV hypertrophy that can be found using echocardiography.7

HCM as Cause of Systemic Hypertension (?)

Occasionally, HCM has been reported as differential diagnosis for systemic hypertension. However, as blood pressure is a function of cardiac output and peripheral resistance, there is no rational explanation for such a relationship. LV hypertrophy with or without CHF and elevated blood pressure is therefore more likely a secondary change to the hypertension, and not the cause of hypertension. However, if LV hypertrophy is diagnosed, hypertension should be excluded as cause before the diagnosis of HCM can be made.

If HCM Looks Like DCM--The "Burn Out" Cardiomyopathy

In some case of feline (and human) HCM a regression of the LV hypertrophy can be seen during the disease progression. The myocardial wall becomes thinner and the LV volume overloaded and a progressive systolic dysfunction develops.8 It is difficult to differentiate the echocardiographic picture from a DCM, unless the cats has been examined and diagnosed at previous examinations with HCM. This disease entity is called "burn out" cardiomyopathy. Occasional LV hypertrophy is still present.

Conclusion

When LV hypertrophy is seen on echocardiography, several aspects should be considered, before HCM is diagnosed: Is the hypertrophy only a pseudohypertrophy secondary to dehydratation?9 Is a fixed or dynamic (sub-) aortic stenosis present? Is systemic hypertension present? Did the cat receive steroids? Is there a history of recent anaesthesia, or is there potentially systemic bacterial or viral disease present? Does the cat have hyperthyroidism?

If any of these questions is answered with "yes", treatment should be started according to the underlying entity. Follow-up examinations should be performed carefully and if echocardiographic changes are reversible, the cat has not primary HCM.

To summarize, several myocardial diseases can look like HCM on echocardiography. Clinical and echocardiographic follow-up examinations are necessary to differentiate primary HCM, from secondary LV hypertrophy. Various treatable diseases should be taken into consideration and treated accordingly, before the diagnosis of HCM is made.

References

1.  Maron BJ, Towbin JA, Thiene G, Antzelevitch C, Corrado D, Arnett D, Moss AJ, Seidman CE, Young JB. Contemporary definitions and classification of the cardiomyopathies: An American Heart Association Scientific Statement from the Council on Clinical Cardiology, Heart Failure and Transplantation Committee; Quality of Care and Outcomes Research and Functional Genomics and Translational Biology Interdisciplinary Working Groups; and Council on Epidemiology and Prevention. Circ. 2006, 113: 1807-1816.

2.  Peterson EN, Moise NS, Brown CA, Erb HN, Slater MR. Heterogeneity of hypertrophy in feline hypertrophic heart disease. J. Vet. Intern. Med. 1993, 7: 183-189.

3.  Levine RA, Vlahakes GJ, Lefebvre X, Guerrero JL, Cape EG, Yoganathan AP, Weyman AE. Papillary muscle displacement causes systolic anterior motion of the mitral valve. Experimental validation and insights into the mechanism of subaortic obstruction. Circ. 1995, 91: 1189-1195.

4.  Meurs KM, Fox PR, Magnon AL, Liu S, Towbin JA. Molecular screening by polymerase chain reaction detects panleukopenia virus DNA in formalin-fixed hearts from cats with idiopathic cardiomyopathy and myocarditis. Cardiovasc. Pathol. 2000, 9: 119-126.

5.  Smith SA, Tobias AH, Fine DM, Jacob KA, Ployngam T. Corticosteroid-associated congestive heart failure in 12 cats. Intern. J. Appl. Res. Vet. Med. 2004, 2: 159-170.

6.  Bond BR, Fox PR, Peterson ME, Skavaril RV. Echocardiographic findings in 103 cats with hyperthyroidism. J. Am. Vet. Med. Assoc. 1988, 192: 1546-1549.

7.  Carter TD, Pariaut R, Snook E, Evans DE. Multicentric lymphoma mimicking decompensated hypertrophic cardiomyopathy in a cat. J. Vet. Intern. Med. 2008, 22: 1345-1347.

8.  Cesta MF, Baty CJ, Keene BW, Smoak IW, Malarkey DE. Pathology of end-stage remodeling in a family of cats with hypertrophic cardiomyopathy. Vet. Pathol. 2005, 42:458-467.

9.  Campbell FE, Kittleson MD. The effect of hydration status on the echocardiographic measurements of normal cats. J. Vet. Intern. Med. 2007, 21: 1008-1015.

Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)

Tony M. Glaus, PD, Dr. med. vet., DACVIM, DECVIM-CA
Zürich, Schweiz

Gerhard Wess, Dr. med. vet., DACVIM, DECVIM-CA
München, Germany

Nada Sphynx Cats donate blood after their HCM scans on 12/10/10, at University of Florida for Sphynx HCM Research.  Thank You to the amazing Staff at UF Cardio clinic for helping with the good fight for our Naked Cats!!!!    

The Sphynx below have been affected by HCM and are either fighting to keep their hearts working with the help of medications or have Crossed the Rainbow Bridge and will be waiting patiently for their human companions...... If you or someone you know has been affected by HCM please feel free to send us a picture and a few words and we will add them to our HCM page.  It is extremely important that YOU notify the breeder so they are aware their lines are affected by HCM.  Knowledge is Power and if we are not notified we do not know to make changes. 

Dexter
8/25/03 - 1/23/11

Dexter
August 25, 2003 - January 23, 2011

I had never heard of Hypertrophic Cardiomyopathy (HCM) an acquired heart disease, until I lost my baby boy Dexter on January 23, 2011. He was my beautiful male sphynx only 7 years old. I purchased him from a reputable breeder when he was a kitten. He even flew on an airplane to his new home in Florida. We all have our own stories about our animals, how they sleep with us, wake us up, eat with us and even sometimes go to the bathroom with us. Dexter of course did all of those things and more.  He was the healthiest acting and looking cat from the outside, but I didn�t know what was happening on the inside with his heart.  He couldn't tell me that his heart hurt him. It wasn't until that night when we were snuggled up watching TV, that he started howling, jumped off my chest to the floor and couldn't move his back leg. He kept wailing in pain, panting, his tongue sticking out of his mouth, fidgeting in my arms as I tried to console him. We took him to the emergency vet, and after an examination, she told me that he had a blood clot in his leg, more than likely a symptom caused by HCM. His prognosis wasn't very good and the Dr. explained to me the different options, neither of them what I wanted to hear. My baby was in so much pain, I just wanted to take the pain away for him. I had to make one of the hardest decisions in my life. I ended his suffering, but that will always be with me. He will always be with me in my heart. My healthy heart.

We recently decided to purchase not one, but two new sphynx kittens. They are brothers and are adorable, of course.  The breeder that we are getting them from has helped me become aware of HCM and she herself is a HCM Champion. She tests all of her cats on a regular basis and is a self-motivated spokesperson on making more cat owners aware of HCM.

Besides feeding our cats the best food, playing with them all the time, loving them as much as we can, we need to do one more thing, GET THEM TESTED FOR HCM on a regular basis.

T. Mullin
St. Petersburg, Florida

 Kahne

5/15/08-11/30/10

owner: Suzanne Ely

 

Harry B Ely

Bambino

Fighting the Good Fight

owner: Suzanne Ely

Harold

deceased

owner: Brooke Arnold

Written bY our dear friend  Brooke :

My boy Harold (pictured above & below) —who I lost to HCM— was adopted and I didn’t know his background at all. It wasn’t until after he passed that I was able to trace him back to his breeder, and just recently found his pedigree online.

My other four Sphynx are also rescues, so again here I am with no back-ground on them, and no idea if they came from a reputable breeder who scanned. As such, I have no choice but to scan them, if for no other reason than to be able to sleep at night! I also feel that I have to make every effort possible to encourage other owners to scan as well.

Sphynx owners must have their cats scanned and make an attempt to educate other potential owners to ask the breeder if they are scanning their breeding cats yearly. It amazes me how many people are unaware! But, in fact, I was one of them not too long ago myself.

I’m sure people get tired of me sounding like a broken record, preaching about HCM, but I don’t care! I can’t help but wonder... if I can educate just one person and help them not have to deal with the heartache I felt... then maybe losing Harold had some sort of purpose. Harold was the love of my life, my alarm clock, my little snuggle monster, my best friend. He was the Sphynx by which all my future Sphynx will be judged. My heart is still broken into a million pieces, and I would give the world just to hug him one more time. — Brooke Arnold

Prospective Echocardiographic and Tissue Doppler Imaging Screening of a Large Sphynx Cat Population: Reference Ranges, Heart Disease Prevalence and Genetic Aspects

21st ECVIM-CA Congress, 2011

A. Petit1; R.T. Tissier2; M. Abitbol3; V. Gouni1; E. Trehiou-Sechi1; C. Misbach1; C. Carlos Sampedrano1; D. Balouka1; J.L.P. Pouchelon4; V. Chetboul4
1Unité de Cardiologie d'Alfort CHUVA, Maisons-Alfort; 2UMR INSERM U955, Unité de Pharmacie-Toxicologie, Maisons-Alfort; 3UMR955 INRA-ENVA Génétique Moléculaire et Cellulaire, Maisons-Alfort; 4Unité de Cardiologie d'Alfort CHUVA, UMR INSERM U955, Maisons-Alfort, France

22088491

The Sphynx is a hairless feline breed that has become increasingly common in Europe over the past 10 years. A Sphynx club was created in 2003 in France. However, few data are available in this breed for echo-Doppler variables or for the prevalence of heart diseases such as hypertrophic cardiomyopathy (HCM), which is the most common feline heart disease and remains a major cause of morbidity and mortality.

The aims of this prospective observational study were therefore 1) to investigate heart morphology and function using echocardiography and tissue Doppler imaging (TDI), and 2) to determine heart disease prevalence and potential genetic features in a population of Sphynx cats presented for cardiovascular screening between 2004 and 2011 at the Cardiology Unit of Alfort.

A total of 140 echocardiographic examinations, including 34 follow-ups, were performed by trained observers on 106 Sphynx.

Conventional echocardiographic findings included 65% (91/140) normal examinations, 17% (24/140) congenital heart diseases of which 50% (12/24) exhibited mitral dysplasia (MD) and 18% (25/140) HCM (17 different cats and 8 follow-ups). Conventional echo-Doppler reference ranges were established from 53 healthy Sphynx (21 males and 32 females) older than 12 months (mean ± SD age, 2.0±1.3 years [1 to 8 years]; body weight, 3.8 ± 1.1 kg [2.0 to 7.1 kg]). In this healthy population, a significant body weight effect (p < 0.0001) was observed for several echocardiographic variables, including diastolic left ventricular (LV) free wall (4.2 ± 0.6 mm [3.0 to 5.3 mm]), interventricular septum (4.4 ± 0.4 mm [3.6 to 5.3 mm]), and LV diameter (15.2 ± 1.6 mm [12.0 to 18.4 mm]). No body weight effect was observed for any TDI variables. Most cats with HCM (8 males and 9 females, aged 4.3 ± 2.1 years [1 to 6 years]) were more than 4 years old (9/17, 53%), showed a left systolic apical heart murmur (15/17, 88%) and a asymmetric concentric hypertrophy with predominant interventricular septal thickening (8/17, 47%). Pedigree analysis of a large family (14 HCM, 13 MD, and 10 healthy cats) suggested an autosomal dominant mode of inheritance for HCM. Five MD cats from 3 generations were first-degree relatives.

In conclusion, body weight should be taken into account when interpreting values of diastolic myocardial wall thicknesses, particularly equivocal values within the upper reference ranges. Additionally, HCM and MD are two relatively common heart diseases in Sphynx cats. More pedigree data are required to analyse the segregation of MD in this family and to confirm our results for HCM at the breed level.

  

Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)

A. Petit
Unité de Cardiologie d’Alfort CHUVA
Maisons-Alfort, France

This is our sweet boy Kerrick above with Dr. Maisenbacher III

preparing for his HCM scan on 4/30/10. Kerrick was diagnised with HCM at the age of 4 in his retired pet home and passed away at the age of 7.  

Nelson

Lost his fight with HCM but donated his heart to HCM research thanks to his loving mom Broooke Arnold in 2012

HCM+: Nelson P. Wrinkle Butt.....sporting his K9 Closet collar below

and yet more words from my dear friend Brooke.....dealing with her second battle with feline HCM,,,,,

 

Nelson likely didn’t have the easiest start in life. He was a stud cat for a backyard breeder. At  3 1/2 years old, he and his breeding partner, Mandy, were dumped at the SPCA when the breeder decided they were no a longer useful part of his baby-making program. Mandy’s tiny body showed tell-tale signs of having raised far too many kittens in her lifetime and Nelson was suffering from IBD and horrible diarrhea. The SPCA contacted a local Sphynx breeder for help with placing Nelson and Mandy, and through that breeder, I was thrilled to adopt them! From the moment the carrier door opened it was love at first sight! There was no hesitation – Nelson charged out of the carrier with the power of a steam engine and nearly broke my nose with one of his (now-infamous) skull-cracking headbutts! For an hour, I just lay on the floor while he climbed all over me, burrowing in my hair, purring louder than anything I’d ever heard before, climbing all over my back, and I was laughing hysterically the entire time. This cat was simply amazing! I couldn’t believe he was mine!

Nine months prior, I had lost my first beloved Sphynx to HCM. I knew in the back of my mind that taking in a rescue was a risk, but I still hoped after losing Harold it couldn’t possibly happen to me again. A few days after adopting Nelson, we went to the vet for his checkup. My heart sank when the vet heard a grade 2/3 heart murmur. I immediately scheduled his appointment for an echocardiogram. The result was Equivocal – meaning, not HCM, but not normal. I was relieved, but worried. Not quite sure what this meant. We were instructed to recheck in 6 months. Shortly after, Nelson started having breathing problems and fainting episodes called Syncope. A trip to the emergency room prompted me to schedule another echocardiogram.


Sadly, 4 months after the first echo in March 2010, Nelson was diagnosed with Moderate HCM. I am at peace knowing that his disease was caught at its earliest stages. By catching it so early, and starting his treatment right away, I’m able to give him the best chance at the longest life. I’ve been able to make diet and lifestyle changes to promote his heart health. His vet has said the goal is to give him one more good year. I’m determined to give him a lot more than that!

We had a setback last month, when he had an aortic thromboembolism – meaning, he threw a blood clot. Most often when this happens, it will affect both legs, called a “saddle thrombus”, and the cat will be in screaming pain and paralyzed in both legs. In Nelson’s case, though, it only affected one leg, and he didn’t have any pain from it. It was heartbreaking to watch him dragging one leg around the house, and the vet told me if he didn’t regain the use of his leg after 5 days, I should consider putting him down. On day 4, guess who miraculously got up and started walking around on all fours as if nothing had been wrong!? He was rolling around on his back and purring like a ham that day, while I was sobbing tears of joy!!

Now I’ve been looking into other forms of therapy for Nelson. Instead of sitting back and waiting for this disease to take him, I want to be proactive, instead of reactive. Oxygen is used in human medicine for a number of things, and it’s used in animal medicine to pull cats out of congestive heart failure – but it’s never been cost effective or realistic for at-home therapy as a preventative treatment option for cats. However, the more I research it, the more it seems to make sense. My own mother was in heart failure at one point, and at-home oxygen therapy was a life-saver for her. So, I’ve started giving Nelson oxygen treatments at home, using an oxygen concentrator, and a make-shift oxygen chamber made from a duct taped cat carrier, until I can save up for a real ICU cage. It’s only been a few days, but since I started him on his oxygen therapy, Nelson has been sleeping better than ever and he’s been running around the house with more energy than I’ve seen in months! This is not the behavior of a cat who, according to my vet’s estimation, only has 8 months left to live! Nelson and I are determined to prove him wrong!

Despite everything I have tried and will try with Nelson’s care, I made a promise to him the day he was diagnosed with HCM, and I fully intend to keep it. I read it often so I’ll never forget. This is my promise to him:
My sweet boy, I promise to do everything within my power to give you the absolute best chance at a long, healthy, comfortable life. I promise to make sure you never suffer. I promise to cherish every moment I have with you. I promise to love you as unconditionally as you love me. I promise to not be selfish if the time comes to take your pain away. I promise to keep telling your story in hopes that someone will benefit from the lessons you've taught me

 

Nelson is pictured below on the day he was diagnosed with HCM.  With that thought in mind please consider your cat may look big and healthy and strong on the outside while his heart is fighting to keep their blood pumping on the inside........Has your cat been scanned???

This Angel belongs to our dear friend Heidi of k9closet. 

 

http://k9closet.com/Gigicollectioncollars.html

 

Gigi Collection

For cats and dogs!

I lost my sweet Lady Godiva aka Gigi on June 29, 2010.
This has been the hardest thing imaginable.  Gigi had HCM (hypertropic cardiomyopathy) which led her into CHF (congestive heart failure) several times.   I will explain more at a later time, now it is just too hard for me to go into detail about that horrific night.
  Harry and I (my Sphynx in the photo to your left) have decided we want to raise money for HCM research.    Harry has HCM as well.  Both of my Sphynx are rescues, both from different countries, yes- HCM is a huge problem.
My first proceeds from these collars will go to Brooke and Nelson, please read their story below.  Once we have raised enough for Nelsons oxygen tank, we will donate 100% of the proceeds to the Winn Foundation.
Thank you to all of you for your cards, emails, calls, flowers and food.  We wouldn't be able to do it without you!  Thank you for your support.
Love always,
Heidi, Blake, Harry and Gigi Schamberger

PLEASE CLICK ON GIGI'S PHOTO **BELOW**TO SEE MORE OF HER PRECIOUS MOMENTS!!!!

PICTURED BELOW IS HARRY.  HE WAS DIAGNOSED WITH HCM MANY MOONS AGO AND IS A WONDERFUL MEMBER OF THE K9CLOSET HOME.  

"We are saddened to report that Harry went to spend eternity with Gigi yesterday 9/12/10.        Rest in Peace sweet boy, you will be missed more than words can say....     

Our very first Sphynx Alter LEUPOLD was diagnosed HCM+ on 8/27/10. Leo passed away on 4/17/14, when he threw a clot and passed away at home with my mother present and his kitty siblings with him.

 

http://www.scf-fr.net/sphynxmanager/genealogie.php?id=3242&gen=4