Birman Cardiomyopathy Research Update

Birman cats are predisposed to heart muscle disease (cardiomyopathy), which can take a range of forms: hypertrophic (HCM), where the walls of the heart are too thick; restrictive (RCM), where the walls of the heart are too stiff; dilated (DCM) where there is thinning and weakening of the heart muscle and (arrhythmogenic) right ventricular (ARVC), where the right side of the heart may be replaced by fat and scar tissue. It is currently not clear whether HCM, RCM, DCM and ARVC represent different diseases with different causes, or whether these cardiomyopathies are part of the spectrum of one disease with one genetic cause. This is a crucial question that must be answered before a genetic mutation can be identified.

We have been studying Birmans with cardiomyopathy using a combination of cardiac ultrasound (echocardiography), pathology and pedigree analysis, so that we can tease out the features of these heart muscle diseases. Since the start of the study we have screened 21 cats with echocardiography and had 3 cats presented for necropsy examination and pathology. We have also received DNA samples from one cat who was screened elsewhere and died of cardiomyopathy.

Pedigree analysis is underway and we have found families of Birmans with multiple members affected by more than one type of cardiomyopathy, therefore are gaining confidence that we are dealing with one disease. At the end of the July 2015 we have the opportunity to begin our first round of genetic testing, using Next-Generation Sequencing (NGS). In order to do this, we recently made an appeal for Birmans 7 years or older (ideally 10 years or older) with no family history of cardiomyopathy that do not have high blood pressure (hypertension) or an overactive thyroid gland (hyperthyroidism). These older, normal cats will form our ‘control’ group with which we will compare the DNA of cats with cardiomyopathy in the hope of finding the genetic mutation(s) responsible for cardiomyopathy in this breed.

We continue to offer free of charge screening at the Queen Mother Hospital for Animals in Hertfordshire, which includes: 
- Physical examination
- Blood pressure measurement
- Complete heart scan by a board-certified cardiologist
- Blood test for cardiac biomarkers (NT-proBNP and hsTnI), hormones released into the blood if the heart is under stress or being actively damaged.
- Full written report to both owner and vet
You can book your cat in by emailing lwilkie@rvc.ac.uk

We are very grateful to everyone who has donated personally, through Breed Clubs, the Birman Heart Foundation and WINN. Without you this research would not be possible!


Lois 'Mini Llama' Wilkie

 We would like to welcome Jose Novo Matos (DVM, DipECVIM-CA) to our team. Jose will be working with us to understand and further characterise cardiomyopathy in Birmans.

 We will be holding regular screening on Wednesdays and Fridays at the Queen Mother Hospital for Animals, Royal Veterinary College, UK. We offer echocardiography (heart scan) for a small fee of £15 per cat, as part of our research funded by WINN.

If you have a Birman that is 7 years or older, is currently being treated for heart disease or is closely related to cats that have died of cardiomyopathy, we would REALLY like to hear from you!

Please contact us for details or to reserve your place: lwilkie@rvc.ac.uk



VETERINARY ADVICE about breeding until we get the DNA test.

If you have the misfortune to breed a cat that develops HCM don't rush out and neuter all your cats as this would dramatically reduce the gene pool and could be a disaster for the breed.



   1:    Take BOTH cats to be scanned to a highly skilled cardiology clinic.


   2:    Ask for a blood test to be carried out at the same time and make sure the remaining sample is kept for future DNA testing.


   3:   If ONE or BOTH shows any kind of heart anomaly then Neuter THAT cat.


   4:   If BOTH scan clear proceed with caution but NEVER repeat that mating.


   5:   Select a breeding mate that comes from totally different lines.

To help with this you can use World of Birmans Pedigree Database www.worldofbirmans.co.uk



The talk given by Lois Wilkie on Cardiomyopathy

at the joint Southern and Southwestern Birman Cat Club and Birman Cat Club seminar on 25th May 2014 Click this link and go to download


Heart Conditions Affecting the Birman Breed


Talk by Lois Wilkie BSc BVetMed (Hons) MRCVS PhD Student in Veterinary Cardiology

 on 9th November 2013 at the Birman Breed Club 30th Anniversary Championship Show

The Normal Heart

The heart is a muscle that pumps blood around the body. It is made up of four chambers; two on each side of the heart, one at the top and one at the bottom. The two top chambers are called the atria. The two atria (right atrium and left atrium) serve as pre-­‐chambers to collect blood as the heart fills. The two chambers on the bottom are the ventricles (right ventricle and left ventricle), which pump blood out of the heart. The septum is a thick wall of muscle that runs down the middle of the heart, separating the right and left sides.

Deoxygenated blood from the body flows into the right atrium, through the tricuspid valve into the right ventricle. It is then pumped out through the pulmonic valve and via the pulmonary artery to the lungs where oxygen is picked up. Oxygenated blood then flows from the lungs, via the pulmonary vein, into the left atrium. It then continues through the mitral valve into the left ventricle where it is pumped out through the aortic valve and via the aorta to supply blood to the body.

What is Cardiomyopathy?

Cardiomyopathy means primary heart muscle disease, it is not caused by anything else going on within the body. This disease starts in the heart. There are several forms of cardiomyopathy. Cardiomyopathy in cats is similar, if not identical, to cardiomyopathy in humans.

What Causes Cardiomyopathy?

It is thought that cardiomyopathy in cats is a familial, genetically inherited disease caused by a genetic mutation. This is different from a congenital disease. A congenital disease is one the cat is born with, it is present at birth. In cardiomyopathies, the ‘bad’ gene is present from birth, but the disease that we see develops over time and usually does not manifest until cats are adult. There are over 1400 mutations that are known to cause the most common type of cardiomyopathy, HCM, in humans and we think the situation is similar in cats.

Hypertrophic Cardiomyopathy (HCM)

Hypertrophic Cardiomyopathy (HCM) is by far the most common form of cardiomyopathy in humans and cats. In HCM, the walls of the left ventricle thicken (hypertrophy). Along with the thickening of the left ventricular walls, the papillary muscles (small muscles within the heart that anchor some of the heart valves) may be enlarged.

Secondary ‘HCM’

You may have heard people talk about ‘secondary HCM’. It is important to rule out other diseases that can mimic cardiomyopathies. Although these diseases can cause the left ventricle to look thick, they are NOT HCM. HCM is a genetic, primary heart muscle disease. Left ventricular walls may also hypertrophy secondary to (as the result of) other diseases. Rule out:

  • High blood pressure (hypertension):

High blood pressure is common in cats.High blood pressure within the circulation results in the heart having to work harder to pump blood out and around the body. This causes a secondary thickening of the heart muscle in response to demand.

  • Hyperthyroidism (overactive thyroid gland):

This is a common condition in older cats.Excess thyroid hormone causes an increase in metabolic rate, which results in an increase in the work the heart has to do and subsequent enlargement of the heart or heart muscle thickening.

  • Acromegaly (hypersomatotropism):

This is caused by excess growth hormone production and is usually only seen in diabetic cats, especially if their diabetes is difficult to control with insulin,

Is it only Certain Breeds that get HCM?

The following breeds are reportedly predisposed to HCM:

  •  Maine Coon

  •  Ragdoll

  • Norwegian Forest Cat

  • American Shorthair

  • British Shorthair

  •  Sphynx

  •  Persian

  • Bengal

However, the majority of cats with HCM are non-pedigree cats, ‘moggies’. Even wild cats like the cheetah and leopard get HCM.

What is the Prevalence of HCM?

Dr. Rosie Payne at the Royal Veterinary College looked at the prevalence of HCM in cats in rehoming centres (Battersea and Cat’s Protection League) to see how many of them had HCM. She found that 15% of the general feline population in cat shelters had HCM. So, this disease is very common. However, there was a low prevalence of bad disease, most of these cats go on to live a normal lifespan and never show any consequences of their heart disease.

What about Birmans?

Birmans are a very interesting breed. In contrast to most other cats with HCM, which have a low prevalence of bad disease and many of them will go on to live a normal lifespan with their HCM, Birmans seem to get very bad disease and are more likely to suffer the serious consequences.

Why does it Matter?

There can be some very serious consequences, such as arterial thromboembolism (ATE), congestive heart failure and sudden death.

Congestive Heart Failure

When the left ventricle becomes thick or stiffened, it is unable to fill properly. This can lead to a build up of pressure in the left atrium., the pre-chamber that is trying to drain into the left ventricle. This causes enlargement of the left atrium and high pressure, so the blood draining from the lungs into the pulmonary veins and into the left atrium can’t drain very easily. This then causes high pressure within the vessels of the lungs, which can start to leak fluid. This can lead to fluid build-up in the lung tissue (known as pulmonary oedema) or around the lungs (known as pleural effusion).
This can be a life-threatening situation; cats can die if they don’t get treatment quickly enough. Signs that would alert you to the possibility of congestive heart failure are fast breathing or difficulty breathing. Some cats will open-mouth breathe (pant like a dog).

Arterial Thromboembolism (ATE)

This devastating complication of cardiomyopathy occurs when a blood clot (also known as a “thrombus”) forms within the left atrium. As the ventricle is stiff and doesn’t fill with blood very easily, the left atrium becomes enlarged. Blood swirls around in the enlarged left atrium and doesn’t move into the left ventricle properly, so you can start to get a clot forming within the heart. If a small piece of this clot (called an “embolus”) breaks off, moves into the left ventricle and out into the circulation, it can block the blood supply to the major arteries. Rear leg paralysis, a classic example, occurs when a large clot lodges where the major artery to the body (aorta) branches to go to the rear legs. Smaller clots can go many places in the body to cause damage.
This causes sudden paralysis of the legs, which are usually cold because the blood supply has been cut off. This is incredibly painful and cats will usually be crying in pain – it is a really distressing situation! These signs can be so dramatic that they may be mistaken for trauma such as a road traffic accident or disease affecting the spinal cord.

Sudden Death

Sadly there are cats that die suddenly, sometimes with no warning at all. This may be associated with abnormal excitability of the heart muscle cells, leading to fatal heart rhythm disturbances. This is an important consequence of cardiomyopathy that we are currently looking at identifying risk factors for. You may not even know your cat had cardiomyopathy and the first sign of problems may be when they are just found dead. In this most upsetting circumstance, although very difficult to think about, post-mortem examination is very valuable.

Feline Cardiomyopathies

Feline cardiomyopathies include:

  •  Hypertrophic Cardiomyopathy (HCM)

  • Restrictive Cardiomyopathy (RCM)

  • Dilated Cardiomyopathy (DCM)

  • Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)

These consequences can happen with any of the forms of cardiomyopathy we see in cats. We will briefly talk about these other forms of cardiomyopathy, which are much less common than HCM.

Restrictive Cardiomyopathy (RCM)

In restrictive cardiomyopathy (RCM) the wall thickness is normal and the left ventricle can look relatively normal, but in fact it is stiffer than normal so the left ventricle still doesn’t fill very well and generally there will be an enlarged left atrium. This disease can be very difficult to detect in the early stages, as the left ventricle will look normal and the atrium will not be enlarged, therefore it can look like a normal cat!

Dilated Cardiomyopathy (DCM)

DCM is characterised by thinning and weakening of the heart muscle, leading to dilation of the heart chambers because the heart can no longer pump blood effectively. Historically, this disease was associated with a diet deficient in taurine, an essential amino acid. However, since this was discovered in the 1980s, food manufacturers have adjusted taurine levels such that deficiency is no longer seen in cats eating a commercial diet. DCM is now rare in cats and when seen may represent the ‘end-stage’ or ‘burn-out’ phase of another cardiomyopathy such as HCM. This can happen when the blood flow and oxygenation to the heart muscle itself is compromised and heart muscle cells die off.

Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)

ARVC has only recently been recognised in cats and is rare, but there is suggestion that Birmans may be predisposed. In this disease, heart muscle cells of the right ventricle are replaced by fibrous and fatty tissue (‘fibrofatty infiltration’). This causes heart rhythm disturbances and enlargement of the right side of the heart.

What about Birmans?

Initial analysis of family trees indicate that cardiomyopathy in Birmans is likely a genetically inherited disease. The majority of cardiomyopathy in Birmans has been HCM, however RCM is also seen. Birman cats have been reported to develop arrhythmogenic right ventricular cardiomyopathy (ARVC) more frequently than other breeds. This disease is known to be inherited in certain breeds of dog, but there have been no genetic studies in cats.

Early Signs of Cardiomyopathy

It is very difficult to detect early signs of heart disease in cats. In dogs you might notice reduced exercise ability, they are less willing to go on walks, but cats might just spend more time resting or sleeping. Cats are very good at hiding signs of disease! Approximately 15% of apparently healthy cats have HCM. In rare cases, signs include fainting or open mouth breathing (panting) after exercise. In humans, we know that HCM causes angina (chest pain) and we think that this might be what causes cats to suddenly stop and pant after exertion.

Is Coughing a Sign of Heart Disease?

Coughing is rarely seen in cats with heart disease. In cats, coughing is much more likely to be caused by airway disease such as asthma or bronchitis.

My Vet Heard a Murmur Does this mean my Cat has Cardiomyopathy?

Heart murmurs are common in cats. Approximately 15-­‐40% of the healthy feline population have a heart murmur. At the Royal Veterinary College we conducted a study where we listened to the cat’s heart and then went on to scan their heart to determine the link between a heart murmur and heart disease. The results of
this study suggested that in normal healthy cats, a large proportion have heart murmurs. Not all cats with heart murmurs will have cardiomyopathy. On the other hand, not all cats with cardiomyopathy will have a murmur. In Nowegian Forest cats, we have now screened over two hundred and I could count on one
hand those that had a murmur – murmurs are very uncommon with cardiomyopathy in this breed.

Diagnosis: X-Rays

Chest x-rays can show changes in the overall shape and size of the heart. They do not allow precise determination of the type of cardiomyopathy present or the heart function. They are most useful for detecting a build up of fluid (pulmonary oedema or pleural effusion). Repeating x-rays might be useful for monitoring the effectiveness of treatment for congestive heart failure.

Diagnosis: Biomarkers

Can a blood test tell you if your cat has cardiomyopathy? The two biomarkers we look at in a blood sample are NT-proBNP and Troponin I. NT-proBNP concentrations in the bloodstream will increase as the severity of heart disease increases. Troponin I is released by heart muscle cells when they are damaged, so anything that damages heart muscle cells may result in increased concentrations in the blood stream. That means that we can take a blood sample and measure the level of these biomarkers to get some idea of how much stress the heart is under and whether the heart muscle cells are being damaged. It will not give you a definite diagnosis of cardiomyopathy, but a cat with high results would be one that you would want to scan. In Norwegian Forest Cats, we are currently looking at whether these tests are able to detect mild heart disease earlier than we can see changes on a heart scan. This would be particularly important in cats with RCM, where we don’t see changes on a scan until late in the disease course.

Diagnosis: Echocardiography (Heart Scan)

At the moment this is the best test for diagnosing cardiomyopathy. Echocardiography allows definitive diagnosis of the specific cardiomyopathy in most cases, as well as assessment of heart size and function. It may be able to give an indication of prognosis, for example a large left atrium would indicate that blood is starting to back up and the cat is at risk of going in to congestive heart failure. It may be possible to visualize clots or slowing of blood within the heart, which would indicate the cat is at greater risk of a clot (ATE). However, it may not detect mildly affected cats where changes in the heart are minimal. This test should be performed by a specialist cardiologist. Even for very experienced cardiologists, screening cats for cardiomyopathy is very difficult.
Experience is really important for detecting subtle disease and taking very precise measurements. It is a non-invasive and non-painful test. The cat does not need an anaesthetic and very rarely does it require sedation. They simply have to lie on their side for around 10-20 minutes while their heart is scanned with an ultrasound probe.

Screening: Why Scan?

Heart scans will allow you to assess risk for the individual cat. It will also help to identify carriers of the genetic mutation in breeding programs, therefore allowing you to think about removing cardiomyopathy genetic material from future lines.

Diagnosis: Pathology

The other thing that is difficult to discuss, but really important to our understanding of this condition, is to get information on post-mortem (autopsy). Unless we can look at the hearts from cats that have died from this disease, we won’t know some of the really important characteristics. The more cats that we can get a post-mortem examination on, the better our understanding is likely to be of this disease.We would like to look at the heart from cats that:

  •  Die suddenly

  • Have cardiomyopathy and die due to heart failure or a clot

  •  Have cardiomyopathy but die of another cause

  • Screened normal and die of another cause

We look at the whole heart and also do microscopic analysis (histopathology) to identify the arrangement of the heart muscle cells and to look at fibrosis and scarring of areas within the heart.

Treatment in the Early Stage

In cats where cardiomyopathy has been diagnosed, but the disease is mild with no enlargement of the left atrium, there is no clear evidence to suggest any treatment can slow or delay its progression. This is an area of on-­‐going research and more clinical trials are needed.

Treatment: Clot Prevention


If we find a big left atrium with slow, swirling blood flow and poor function we would worry that the cat is at risk of forming a clot. In these circumstances we can give medications to help prevent this including aspirin and clopidogrel.

Treatment: Congestive Heart Failure

Where heart failure develops, various drug treatments may be available to help improve and manage the condition. The most important is diuretic treatment (e.g. Furosemide), which helps to help remove the fluid build-­‐up in the lungs. Cats will often have to be hospitalised and given oxygen while these drugs take effect. If there is fluid around the lungs (pleural effusion), then the most effective treatment is to remove this using a small needle and syringe to drain the chest, a procedure known as thoracocentesis. ACE inhibitors (e.g. Fortekor, Benazecare) help block the activation of a hormone system that is stimulated in cats with heart disease which can add to the fluid retention.


This is a very variable disease. It varies between breeds, but also between individual cats within a breed. Some cats can live a normal lifespan and never show signs related to their heart disease, whereas in others it can progress very quickly and they die of their disease. The best way to assess individual risk is to have a heart scan.


The mutation, or ‘bad’ gene is inherited and present from birth, but the disease that we see develops over time and cats usually don’t show it until they are adult. This is something known as age-dependent penetrance. The progression of cardiomyopathy is very variable, but in most cases the disease will take years to develop if the cat has inherited the ‘bad’ gene. This is why repeat scanning is necessary before we can be sure a cat is not affected, as the disease can develop late in life.
The situation is further complicated by the fact that some cats can carry the mutation but never show signs of the disease themselves. This is known as incomplete penetrance and creates problems because it means that we cannot pick up affected cats by looking at the heart with a scan. Therefore they continue breeding and can pass on the mutation to their kittens, which may show the disease.

Research in Other Breeds

There is a known genetic mutation responsible for HCM in Maine Coons that can be tested for using mouth swabs. Maine Coons often develop disease at around 5 years of age. Some can live a normal lifespan and never show signs related to their heart disease.
The responsible genetic mutation has also been identified in Ragdolls. In contrast to Maine Coons, Ragdolls can develop HCM at around 2 years of age and often develop congestive heart failure. It seems to be a particularly lethal form in this breed. Research at the Royal Veterinary College also found that if they are homozygous (have two copies of the mutated gene instead of just one), they are more likely to develop severe and fatal disease early in life.
The mutation identified in the Ragdoll and Maine Coon is located within the same gene (Myosin Binding Protein C, MYBPC3); however the mutation is different in the two breeds. This may suggest that there may be a different genetic mutation in each cat breed and some breeds may have more than one mutation responsible. There is no point sending DNA from your cat for the Maine Coon or Ragdoll tests, as Birmans do not have the Maine Coon or Ragdoll mutation.
Approximately one third of Ragdolls and Maine Coons tested are positive for the mutation. A cat that tests negative for the genetic mutation means that the cat does not have that particular mutation; however it may still be genetically predisposed to HCM as there are likely hundreds of mutations which can predispose a cat to HCM, as is true in humans.
A lot of work has been done in the Sphynx and they are very close to identifying the responsible mutation in this breed. They have narrowed it down to a very small area of the genome where this mutation is likely to be located and Dr. Kathryn Meurs in the USA has just received further funding from the WINN Feline Foundation to aid this research.
At the Royal Veterinary College we have been involved in screening Norwegian Forest Cats. We were seeing multiple instances of really relatively young cats, often under 2 years of age, that were developing the really serious consequences of cardiomyopathy, such as congestive heart failure, thromboembolism (clot) and sudden death. These cats have shown features of both HCM and RCM on echo and post-mortem. An initial pedigree analysis revealed that an autosomal dominant mode of inheritance was likely in the Norwegian Forest Cat.; as is true in the Maine Coon an Ragdoll. This year we were awarded a research grant by the WINN Feline Foundation to screen cats with echo and biomarkers, perform post-mortem diagnostics and to store DNA for future genetic testing. We are able to do all this free for the owners, thanks to our grant – that’s why raising money for such a grant is so vital to getting research in Birmans started.

Why Would it be Helpful to identify a Mutation?

Once you know which mutation, or which change in a gene you are looking for you don’t need very much DNA and can look for it using mouth swabs; as is possible for Maine Coons and Ragdolls. This is quick and practical and means you can then make more informed decisions about breeding. It will also allow you to monitor particularly closely those cats with a responsible mutation.

Developing a Genetic Test

Identifying a genetic mutation and developing a genetic test takes years. Participation from you is vital; to bring cats to be screened with a heart scan, send DNA samples, and raise money for the cause. It also requires dedicated researchers. When we start thinking about developing a genetic test, we first need to identify the typical features of cardiomyopathy in Birmans. This includes what age they are developing heart disease and the consequences, whether males are more likely affected than females, the measurements on a heart scan and features at post-mortem.
It is not possible to undertake genetic studies until you know which cats are definitely affected and which cats are highly likely to be normal. That is why repeated screening and/or post-mortem analysis is very important. We also perform a pedigree analysis of cats that have been screened to determine the likely mode of inheritance. We start to store DNA of cats that have been screened for future genetic analysis. Blood samples are much better than mouth swabs, as they give us much more DNA to work with. We will need samples from normal cats; that means cats that have a normal heart scan in old age. We will compare these to samples from affected cats.

Screening Protocols

We suggest to start screening with a heart scan at 1 year at older. Screening should be earlier if there is known cardiomyopathy in the line, if history of sudden cardiac death in relative and ideally prior to first mating We do not know the age of onset for cardiomyopathy, so a single normal echocardiogram (heart scan) does not guarantee that the cat will not develop the disease in the future, or that it will not pass the disease on to its offspring. It is recommended for cats to be scanned yearly. We also do not know at what age a normal scan means the cat is truly cardiomyopathy free. In Norwegian Forest Cats, we are considering a normal scan at 7 years or older truly normal. In Sphinx, they are using 8 years old as the cut-off.

Ultimate Goal

The ultimate goal is to reduce the prevalence of cardiomyopathies in Birmans, for the future of the breed.

Dispelling Concerns

Purebred cats like the Birman come from a very small gene pool. We can’t afford to remove all cats that carry this genetic mutation from the gene pool. This would detrimentally change the breed, as if you select for removing one ‘bad’ gene you will inevitable lose some ‘good’ genes in the process. Decisions to remove a cat from the breeding programme should be based on severity of disease, importance of the animal in terms of good features, and whether it is homozygous (two copies of the mutation) or heterozygous (one copy of the mutation). It is important that people are not afraid to share results. We must all work together for the future of this beautiful breed and that cannot happen if people feel they will be outcast from the breeding community if cardiomyopathy is identified within their lines.

A Reminder on Homozygous vs Heterozygous

The cat inherits two copies of a gene, one from each parent. There are three possible genotypes:

  • Homozygous wild-type:

Two copies of the normal gene with no mutation.The cat is negative for this particular genetic predisposition to HCM.

  • Heterozygous mutation:

One copy of the normal gene and one copy of the mutated gene. The cat has the particular genetic predisposition to HCM.

  • Homozygous mutation:

Two copies of the mutated gene. The cat may be more likely to develop moderate to severe HCM earlier in life than a heterozygous cat.

What Does Autosomal Dominant Inheritance Mean?

Only one copy of the mutated gene is necessary for the cat to be affected. Therefore only one of the parents needs to have been affected. The chance that a kitten will inherit the mutated gene is 50%. However, HCM is further complicated by incomplete penetrance. This means that although only one copy is needed, not all kittens that inherit the mutation will go on to develop the disease.


If you have further questions, please do not hesitate to email me:
Lois Wilkie BSc BVetMed (Hons) MRCVS PhD Student in Veterinary Cardiology
Virginia Luis Fuentes MA VetMB PhD CertVR DVC MRCVS DipACVIM DipECVIM

Professor of Veterinary Cardiology



  A Breeders Experience of Cardiomyopathy

I had been breeding for several years and had no idea cardio was lurking in my cattery. Then one day an owner called to say her cat had just been diagnosed with RCM age six years six months. I was sent all his scan results and other tests and there was no doubt. This was the first I knew about heart problems and I really didn't take on board the significance of what I had read. I had no idea that Cardiomyopathy could be inherited and that it could skip generations.  I carried on with my breeding program and sold a few cats for breeding. Everything appeared to be OK for another few years. then a kitten bred by another breeder but with my line behind it died from HCM age 16 weeks. I didn't connect the two, RCM and HCM as possibly being part of the same cardio issue and carried on breeding. Then some "fourteen years" on from the start my becoming a breeder, another cat I sold produced a cat who died from HCM age 2 years. I began to wonder if all these instances were in some way connected and went right back to my first breeding cats. 

I remembered visiting a breeder back in 1995, who she told me she had lost kittens to Cardiac disease each time she mated her cats. The sire of the kittens eventually died of cardio too. I also recalled visiting a stud owner and seeing one of his cats come into the lounge dragging its back legs. It had suffered a blood clot which had paralysed its back legs, it didn't survive. 

At this point I began to realise Cardio can manifest in different forms and that although I had never actually had a cat in my care die from cardio and still have offspring from my original line still doing well at over 14 years of age I could have had a problem with Cardiomyopathy.


Cardiomyopathy can be inherited and does flow down family lines. The problem is that many breeders will never have experienced cardio even though cardio could be lurking in the background. Some breeders will experience just one cat being diagnosed and put that down to a "one off" natural occurrence especially if the cat is a bit older. The fact remains that, old or young, heart problems need to be investigated. To date all we can do is scan the cats but this has shown to be "only a snapshot in time" and cardio can develop later, possibly after the cat has been bred from and the defect passed on.

It is only when a lot of data is collated that the bigger picture emerges.

This diagram shows how cardio can track down different familial lines each merging with other family lines. This diagram contains cats (marked in yellow), who have died of heart disease so it is not a problem within a single cattery and its effect can be global.

 We need a DNA test available to be able to breed away from cardiac disease.

So we are asking breeders, owners and friends to help raise money for research to produce a genetic test breeders can use to breed away from heart disease in our Birmans.