British cats heart surgery enlarged atrium. Hypertrophic cardiomyopathy in cats: signs and symptoms

Cardiovascular disease is rare in cats. Alas, sometimes this does happen. Moreover, if we talk about such diseases in cats, then this is most likely cardiomyopathy. Other diseases are even rarer. That is why, if this fluffy pet lives in your home, it is very important to know the main symptoms of cardiomyopathy in cats, as well as the causes of the disease and methods of treatment.

What is cardiomyopathy and what it can be

To begin with, cardiomyopathy is a disease that affects the hearts in cats. An organ that pumps blood throughout the body cannot contract normally. Consequently, the amount of oxygen supplied to the organs is significantly reduced, which leads to the most various diseases, including myocardial damage, and in some cases, death of the cat.

Doctors distinguish several varieties of cardiomyopathy. Let's list them:

• Hypertrophic occurs due to an increase in the thickness of the walls of the heart. Because of this, the "pump" holds less blood - as a result, the vital organs do not receive enough oxygen. Hypertrophic cardiomyopathy in a cat is more common than other types of the disease.
• Dilated- at the same time, the volume of the heart increases markedly, while the thickness of its walls remains the same. Over time, the organ can no longer contract normally, which causes oxygen starvation liver, brain and whole body.
• Restrictive causes fibrosis of the heart. At the same time, the muscle becomes harder, it can no longer fully contract, which leads to a sharp reduction in life span - usually cats with this diagnosis rarely live longer than two years.

As you can see, the disease can come to unfortunate cats in a variety of ways. But what can cause the development of cardiomyopathy? Let's deal with this in more detail.

Why does the disease appear?

Unfortunately, even the best veterinarians in the world cannot unambiguously answer this question. But many believe that this disease is a consequence of other abnormalities. Indeed, most often in cardiomyopathy, changes in the heart occur for various reasons.

For example, this may be the reason for too active work thyroid gland. It also often occurs due to high blood pressure. Pathology can be congenital. For example, the so-called "Bull's heart" is often found. The kitten is already born with an enlarged heart. In young individuals, excellent health can partially compensate for the deviation from the norm. Alas, over the years, the cat feels worse and worse - cardiomyopathy takes its toll and such individuals live for a relatively short time.

Finally, the cause may be a malignant formation. Usually such a disease does not end in anything good - treatment most often does not alleviate the suffering of the animal.

How to identify cardiomyopathy in cats?

In order not to miss the time and timely contact veterinarians who can diagnose cardiomyopathy in cats and prescribe the appropriate treatment, you need to know the symptoms characteristic of the disease.

Unfortunately, usually signs of cardiomyopathy appear only after the heart muscle has passed irreversible changes. Because of this, it is usually not possible to get rid of the disease, returning the joy of life to the cat and its owner. But in any case, you should take the help of professionals, if you notice your pet the following symptoms disease:

1. Shortness of breath, appearing with minor exertion and even at rest.
2. Incessant vomiting.
3. Suffocation attacks.
4. General weakness that does not stop for weeks.
5. Drop in body temperature below 37 degrees Celsius.
6. Loss of consciousness with thready pulse and shallow breathing.

What can a veterinarian do

As mentioned above, even the best doctors usually cannot really effective treatment cardiomyopathy. The only thing they can do is to subject the cat to procedures that will allow them to gather more information about the disease and give the owner recommendations that will make life easier for the animal, giving a few extra months or even years of life.

You need to do an x-ray chest. This usually allows you to identify the pathology of the development of the heart chambers.

Electrocardiography is also often used. It makes it possible to determine tachycardia and arrhythmia - very often it is at this stage that the diagnosis of CGMP is made.

Ultrasound of the heart is not always used, but it is thanks to this method that you can collect the most information about the form of deviation. For example, you can determine how thick the myocardial wall is, whether there are blood clots in the arteries, and also set the amount of blood flow.

Cats that are predisposed to cardiomyopathy should be examined as closely as possible. This includes not only individuals, but also entire breeds, among which heart disease is common.

Can something be done?

Many cat owners, having heard such a diagnosis, perceive it as a sentence. Unfortunately, in some cases they really have every reason to do so. However, not always. The main thing is to know what to do if the cat has cardiomyopathy.

As practice shows, if a cat receives appropriate treatment, it may well live for quite a long time.

First of all, a good doctor will prescribe medication for a sick animal.:

• Diuretics. They are an auxiliary drug that allows you to avoid congestion, and therefore pleural effusions and pulmonary edema.
• ACE inhibitors will be needed to reduce high blood pressure and alleviate heart failure.
• The calcium channel blocker will decrease the heart rate, helping to relax the overdeveloped wall of the myocardium. In some cases, the heart even partially recovers.
• Beta-blockers can prevent arrhythmia and related complications.

Proper nutrition

It is very important. On the one hand, getting a properly formulated diet, cats are less likely to suffer from cardiomyopathy. On the other hand, when a dangerous disease is detected proper nutrition helps to alleviate the disease.

Let's start with prevention

The cat's diet should contain a sufficient amount of taurine. This supports the body under significant stress. It is no coincidence that all athletes adhere to a special high-taurine diet during intensive training. It is found in beef, rabbit meat, cod, squid, and turkey.

At the same time, food should not be too fatty - deposits on the heart can kill even a healthy cat without any cardiomyopathy in a short time.

If the sad diagnosis has already been made, then it can be recommended to prescribe a salt-free diet to the cat. Due to this, it decreases blood pressure and, consequently, stress on the heart. Of course, you should not forget about taurine in this case.

As you can see, cardiomyopathy is a very insidious and dangerous disease. However proper care and observation by a veterinarian in most cases allows you to minimize the risk of disease. Yes, it's quite troublesome. But the health of the cat and the joy that he will give you are completely priceless.

The heart of four-legged pets suffers from various diseases in the same way as a human one. Among the known ailments of cardio-vascular system animals - HCM (hypertrophic cardiomyopathy). In cats, this pathology is dangerous with severe, sometimes incompatible with life complications. The article is devoted to a detailed review of the disease and methods of its treatment.

HCM in cats: symptoms, treatment

Pathologies are found both congenital and acquired. All existing diseases classified by localization and cause of occurrence:

Among these problems, cardiomyopathy is the most common in cats.

Cardiomyopathy: etiology and pathogenesis

Feline hypertrophic cardiomyopathy (HCM) is a pathology accompanied by thickening of the walls of the ventricle. With the development of the disease, the volume of the heart chambers is significantly reduced, subsequently provoking heart failure. Timely treatment helps prevent death, but with an advanced form of the disease, the prognosis is unfavorable. The disease mainly manifests itself at the beginning of the pet's life - at the age of 6 months.

HCM is considered a relatively new disease. Studies of this pathology actively took place at the beginning of the last decade in the United States.

Scientists concluded that breeds such as the Ragdoll, Norwegian Forest, Persian, and Maine Coons are most susceptible to the disease. The transmission of the disease at the genetic level has been confirmed. Most often, the disease occurs in males.

Among such massively bred breeds as the Siberian and Russian Blue, no hereditary predisposition has been identified. Representatives of these species suffer from secondary forms of pathology.

What happens to the heart in HCM?

The clinical picture of a typical cardiomyopathy is characterized by the following manifestations:

1. Reducing the size of the left ventricle, which is fraught with a decrease in the amount of incoming blood. In addition, the mobility of the walls is reduced. This leads to the release of blood into the vessels of the lungs.
2. Expands as the disease progresses left atrium. The resulting blood clots contribute to impaired hemostasis, leading to paralysis hind limbs.
3. Further, the mitral valve is involved in the pathological process. As a result of a change in its location, an obstruction arises in the exit of blood into the aorta. This blockage in the blood flow is accompanied by a systolic murmur.
4. Compaction of the myocardium causes stagnation of blood in the atria and malfunctions of the atrioventricular valve. As a result, obstruction of the aorta and circulatory deficit are noted.

Types of HCMP

Hypertrophic cardiomyopathy in furry pets is divided into 2 varieties: primary and secondary. The origin of the first species, which occurs in obstructive and non-obstructive forms, is currently under investigation. The second (acquired) develops under the influence of another disease.

Table 1 Types of HCM in cats

The primary variety of the disease, which is characterized by a genetic origin, manifests itself up to 5 years. The secondary form occurs mainly in older cats after 7 years.

Possible Complications

Progression hypertrophic cardiomyopathy affects all parts of the heart and the circulatory system as a whole. This is due to the congestion of the vessels of the lungs with blood. Due to slow blood circulation in the heart chambers, blood clots form in the cat.

Symptoms of the disease

The main manifestations of hypertrophic cardiomyopathy are poor tolerance physical activity and shortness of breath. If the disease is asymptomatic, there is a high probability of death due to thromboembolism, which develops as a result of pulmonary edema.

The main symptoms of HCM are:

1. The physical state. An exhausted animal loses interest in active games and sleeps a lot.
2. Breath. Severe, accompanied by wheezing and gurgling. At heavy load Your pet is having difficulty breathing. This is caused by the slowing down of blood flow in the veins. The cat breathes with its belly, sticking out its tongue.
3. Dyspnea. Attacks of suffocation often lead to fainting as a result of a lack of oxygen.
4. The nature of the pulse. Filiform.
5. Mucous condition. Due to oxygen starvation, the shells acquire a blue tint.
6. Cough. Reflex, caused by excessive pressure of the enlarged heart on the trachea. To cope with an attack, the cat sticks out its neck, spreading its front limbs for greater ventilation of the lungs.
7. Hydrothorax and ascites. The release of exudate contributes to the formation of swelling in the peritoneum and chest.
8. Paralysis of the hind limbs. If a blood clot blocks the lumen in the vessels, the animal's paws in the pelvic region fail.
9. Body mass . Bad weight gain.
10. Murmurs in the heart and tachycardia.

Reasons for the development of the disease

The main cause of the disease is considered to be a gene mutation. Pathology is inherited among some breeds of cats. American experts concluded that the gene responsible for myosin, a binding protein, is to blame. Maine coons and ragdolls are subject to a similar gene mutation. It has been proven that more than 10 genes are involved in the development of the disease.

Except breed predisposition, the development of cardiomyopathy is influenced by a number of reasons.

The complexity of detection is caused by the hidden nature of the pathology. It is possible to identify malfunctions in the work of the organ while listening to heart murmurs. In the presence of HCM, they resemble a gallop.

Echocardiogram is considered the most informative way to diagnose HCM

Main methods:

1. Collection of anamnesis. The owner must describe in detail the condition of the pet. Any deviation in behavior can signal the development of the disease.
2. Echocardiography is the most accurate diagnostic method. It makes it possible to scrupulously study the structure of the heart muscle. Each cat at risk for breed should be examined at least once a year. Before surgery involving the use of anesthesia, it is also necessary to check for the presence of HCM.
3. Electrocardiography. This survey is not informative enough. It can be used to detect tachycardia, ventricular arrhythmias, and widening of the QRS interval. However, as independent method not used to diagnose pathology.
4. X-ray diagnostics. The shape and size of the heart muscle, as well as the presence of fluid in the pleural cavity.
5. Auscultation. Listening allows you to identify extraneous noise and evaluate the heart rate.
6. Pressure measurement. With HCM, blood pressure will be elevated.
7. visual assessment. Blueing of the mucous membranes indicates a malfunction of the heart muscle.

If the animal has a severe form of hypertrophic cardiomyopathy, hardware examinations are not performed. Any manipulation will negatively affect emotional state pet and exacerbates the manifestation of unpleasant symptoms.

Treatment of the disease

The developed schemes for the treatment of pathology do not make it possible to completely overcome the disease. The main focus is on symptomatic therapy. In severe cases, in addition to drug exposure, special equipment is used.

Hospital treatment

The length of stay in the clinic is 3 days. Any hardware intervention is carried out as carefully as possible in relation to the animal. Basic procedures:

1. To stabilize the condition, the animal is placed in an oxygen box, which is a chamber with a constant supply of oxygen.
2. After feeling better, if necessary, the fluid accumulated in the pleura is removed (thoracocentesis). This helps to facilitate the respiratory process.

While in the clinic, owners are allowed to visit their pets. Such visits speed up the healing process.

Medical treatment

Therapy is based on stabilization heart rate, preventing the formation of blood clots and stopping pulmonary edema.

Used drugs:

1. Beta blockers. Verapamil and Carvedilol. Reduce the workload on the heart.
2. Thrombolytics. Alteplaza. Dissolve thrombi.
3. Antiplatelet agents. "Heparin" and "Aspirin". Prevent the formation of blood clots.
4. Diuretics. "Temisal", "Eufillin" and "Furosemide". Reduce congestion and eliminate puffiness.
5. Taurine-containing preparations. They thin the blood and improve the condition of the vessels. Vitamins for cats from manufacturers CEVA, Doctor ZOO, GimP.

Beta-blocker "Verapamil" has a positive effect on cardiac tone

For older pets suffering from secondary hypertrophic cardiomyopathy, the root cause is eliminated. Animals must be registered with a veterinarian and undergo regular examinations.

Diet food

In addition to the use of drugs, the cat is transferred to special diet which helps to stabilize blood pressure. It is based on the rejection of salt. This substance promotes fluid retention.

It is important to enrich the power scheme with the following elements:

• taurine;
• fatty acid;
• L-carnitine.

With a lack of vitamins, they give nutritional supplements sold in veterinary pharmacies.

If before the advent of HCM, the diet consisted of dry food, it is necessary to transfer the animal to food designed for pets with pathologies of the cardiovascular system.

During treatment, you should not overfeed the animal, since obesity contributes to the formation of additional stress on the heart.

Disease prognosis

The scenario of the development of the disease is determined by the following factors:

• timely detection of the disease;
• severity of symptoms;
• edema and thromboembolism.

If the pathology is found in early stage, subject to the rules of nutrition and well-chosen therapy, the prognosis is favorable. Life expectancy is not reduced. If left untreated, the pet dies. Death occurs due to thrombosis or heart failure.

It is important to remember that any stress can worsen the physical condition of the pet. Therefore, it is necessary to protect the animal from emotional overstrain.

Prevention of HCM

Leading preventive direction - early diagnosis. The pet should be regularly brought for examination using echocardiography. You should also enrich the diet of the animal with proteins and taurine.

Cats suffering from cardiomyopathy do not take part in breeding offspring.

Hypertrophic cardiomyopathy is a common pathology among cats. Maine Coons and Ragdolls are more susceptible to diseases than others. Therefore, the owners of representatives of these breeds should be extremely attentive to physical condition pet.

Video - Hypertrophic cardiomyopathy. disease in cats

Cardiomyopathy is a group of non-inflammatory heart diseases that result from various changes in the structure of the myocardium (heart muscle). As a result of these changes, the work of the heart is disrupted: it does not cope with its main task - to properly pump blood, moving it through the vessels, and quickly wears out.

We will try to figure out how cats with cardiomyopathy live, why a hypertrophied heart muscle is dangerous, and how you can help your pet.

Types of cardiomyopathy

Cardiomyopathies in cats are better understood than in other animals. There are the following types of disease:

• hypertrophic cardiomyopathy, when myocardial cells thicken and stop working well and smoothly;
• dilatational, when the walls of the left ventricle, on the contrary, overstretch, become thinner and cannot fully contract;
• restrictive - the walls of the ventricles remain of normal thickness, but cannot completely relax, which is why they fill with blood worse.

The most common type of pathology is feline hypertrophic cardiomyopathy. Echocardiography of apparently healthy animals shows corresponding changes in the heart muscle in 15–34%, so today we will dwell on this problem in detail.

Symptoms of Hypertrophic Cardiomyopathy in Cats

The main danger of the disease lies precisely in the fact that the symptoms of hypertrophic cardiomyopathy in cats may not be observed at all. The owners are unaware of the illness of their pet for years until sudden deterioration condition or even unexpected death of the animal as a result of heart failure.

Most often, the following picture unfolds: as a result of sudden stress, physical activity, as well as after a dropper or anesthesia with surgical intervention, before the "healthy" cat begins to feel bad. She develops increasing dyspnea (breathing with open mouth and protruding tongue, like a dog), while fluid accumulates in the chest cavity, which prevents the animal from breathing normally.

The general condition worsens, short-term loss of consciousness may appear or even refuse hind legs due to thrombus development. Obviously, such signs require an immediate response from the owners and examination by a cardiologist.

What to do when threatening signs appear?

The sooner the cat is seen by a cardiologist, the better. Normal veterinarian general practice, unable to perform echocardiography and other studies, is likely to help an animal in critical condition (provided that the disease has not gone too far), but will not prescribe adequate treatment.

A veterinary cardiologist will examine the cat, including assessing the condition of the fundus, listening, doing an x-ray of the chest cavity and echocardiography, and taking blood for analysis. If the diagnosis is confirmed, then treatment for feline hypertrophic cardiomyopathy will be prescribed depending on the severity of the disease and the changes that have already occurred in the work of the heart and blood flow.

The owner can also independently fix the change in the state of his pet, for this you do not need to have special knowledge and skills. All that is required is to count the number respiratory movements at rest.

Look at the cat when she sleeps. Record the time and count how many times per minute her sides rose to inhale. It is best to count the frequency of respiratory movements at least a couple of times a day. The results should be recorded and shown to the attending physician - this will help him assess the patient's condition in dynamics.

Treatment of hypertrophic cardiomyopathy

Asymptomatic cats that are doing well are usually only scheduled for follow-up with a doctor, with follow-up visits every six months. Animals with certain signs of heart failure are prescribed complex therapy:

• With the accumulation of fluid in the pleural cavity, near the lungs, which occurs due to stagnation of blood, it is necessary to give diuretics - first in high doses, then in supportive ones. In severe cases, a puncture is necessary to drain the fluid and allow the animal to breathe normally.
• For daily intake, drugs are prescribed that affect the contraction of the heart.
• Blood-thinning drugs are essential to prevent thrombosis, as blood clots often form when the heart is disturbed. If thromboembolism has already occurred, then intensive therapy is carried out using various drugs.

Life expectancy of cats with cardiomyopathy

Of course, the owner of a cat with such a serious diagnosis is primarily interested in the prognosis. Do not be angry with the doctor if he cannot give an exact answer to the question of how long your pet will live. The life expectancy of a cat with cardiomyopathy depends on many factors. And if animals without symptoms can live for years, then after the onset of signs, their life span varies from a couple of months to 2-3 years.

Hypertrophic cardiomyopathy in cats - genetic disease, especially common in cat breeds such as Maine Coon, Ragdoll, American Shorthair, British, Scottish Fold and some others. Unfortunately, mestizos can also get sick. Therefore, you should responsibly approach the purchase of a thoroughbred kitten and purchase an animal from trusted breeders.

Do not neglect research: genetic tests are now available that can identify a dangerous mutation responsible for the development of the disease. It also makes sense to undergo a medical examination with mandatory research hearts in breeds prone to the disease.

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The most common heart disease in cats is what is known as hypertrophic cardiomyopathy (HCM). This is a pathology of the heart, accompanied by a pronounced thickening of the heart muscle (myocardium) and leading to the development of heart failure, up to death.

A distinctive feature of this disease is the insidious development of symptoms and the difficulty in treating late stages.

Reasons for the development of the disease

The reasons for the development of this disease are still not well understood, but a number of studies have identified genetically inherited abnormalities that can lead to the development of HCM. It has been proven that representatives of the following breeds are especially predisposed to this pathology: Maine Coon, Ragdoll, Sphynx, British and American Shorthair, Scottish Fold, Norwegian Forest cats and possibly some others.

The mechanisms of inheritance of this disease have not yet been fully studied, but it has been proven that, for example, in the Maine Coon breed, HCM is inherited in an autosomal dominant manner. At the same time, special tests (blood tests) are even common abroad for the presence of corresponding deviations in the genotype in cats of this breed. In the UK, for example, one in three Maine Coons are positive for HCM.

Hypertrophic cardiomyopathy is the most common heart disease in cats, leading to a risk of sudden death in affected animals due to defects that lead to thickening of the left ventricular muscle. Maine Coon cats have been found to have a mutation in the genes that code for proteins responsible for contraction of the heart muscle, associated with an increased risk of developing HCM. A reduction in a protein called myomesin - one of the proteins required for normal heart muscle contraction - has been documented in Maine Coons with HCM.

Hypertrophic cardiomyopathy is a disease in which the heart muscle becomes uncharacteristically dense (in the case of dystrophic cardiomyopathy, the muscle becomes thinner) and makes it difficult for the heart to work effectively, which ultimately leads to cardiac arrest and / or embolism (formation blood clots, blood clots). This mutation can cause the development of the disease and the sudden death of the animal at the age of 4 years or more. young age in individuals who carry two copies of this mutation (homozygotes). In cats with one copy of the mutation in the genome average duration life longer, but they can still develop HCM.

Currently, a test has been developed to determine the presence of this mutation in the cat genome. The test results should be interpreted as follows:

Symptoms of cardiomyopathy

• Shortness of breath - occurs mainly after vigorous pastime or stressful situation, the cat begins to breathe with its mouth slightly open.
• High fatigue - the animal is less active than before, plays little, sleeps a lot, external weakness appears.
• Cyanosis is a bluish discoloration of the skin on the lips and near the nose, as well as the lining of the gums and inside the ears.
• Pulmonary edema (shortness of breath even at rest)
• Enlargement of the heart (according to ultrasound).
• Accumulation of fluid in the chest cavity.
• Thromboembolism is the formation of blood clots and blockage of blood vessels.

Behind the combination recent symptoms usually followed by death. Some symptoms can only be diagnosed by examination by a veterinary cardiologist.

Hidden killer

Although HCM is hereditary disease, it does not manifest itself at the birth of a kitten. Instead, this disease develops over time. The development and severity of HCM can vary even among animals that are born in the same litter. These changes are due to the unique features of autosomal dominant inheritance known as "fluctuation" and "incomplete penetrance". Often the fluctuations are due to gender differences.

The mechanism of development of this pathology is that as the heart muscle thickens, the volume of the left ventricle decreases, as a result of which the volume of blood pumped through it decreases. Stagnation develops, leading first to an increase in the left atrium, pulmonary veins, and then, in later stages, to the development of pulmonary edema and / or hydrothorax (accumulation of free fluid in the pleural cavity). Moreover, the insidiousness of this disease lies in the fact that the first symptom may be pulmonary edema and / or death. In some cases, symptoms such as shortness of breath (breathing with an open mouth) and poor exercise tolerance may appear in the early stages.

One of the most frequent complications HCM, sometimes manifesting against the background of the absolute visible well-being of a cat, is thromboembolism. Expansion of the left atrium and blood stasis leads to an increased risk of blood clots, which in turn lead to blockage of vital vessels and sometimes death, especially in the case of late treatment veterinary care. Most often, blockage occurs at the level of the femoral arteries, in which case the first symptom will be sudden paralysis pelvic limbs and pronounced pain syndrome- the cat screams and does not get up on its hind legs. In such cases, the count goes to hours, if not minutes. The sooner the patient arrives at a specialized clinic, the greater the chance of restoring blood flow and minimizing the risk of complications.

Early diagnosis of cardiomyopathy

Given all of the above, timely diagnosis is extremely important. The sooner the doctor starts treatment, the longer the patient can live and the less the risk of developing adverse complications.

by the most exact method diagnosis of HCM is ECHO-cardiography - ultrasound procedure heart by a cardiologist. However, in some cases, additional chest X-ray and electrocardiography are also important.

During ultrasound examination the doctor conducts a series of measurements and calculations, while obtaining clear objective data, on the basis of which a conclusion is made whether the patient has a pathology or not, whether there is a risk of its development in the future.

Moreover, considering increased risks, representatives of the breeds described above, it is especially important to undergo such an examination. Evidence of the particular importance of this problem is, for example, the fact that in Western European countries it is legally prohibited to use for breeding or for sale cats of risk group breeds that do not undergo regular examinations by a cardiologist for the presence of HCM-screening tests. According to the results of such tests (ECHO-KG), the cat is issued a certificate confirming the absence of signs dangerous pathology. The results of such tests are recognized by foreign colleagues. As a rule, such examinations in breeding cats are carried out annually, starting from the second year of life.

In addition, if you are the owner of a cat of one of the risk group breeds or have sometimes noticed in your pet (no matter what breed) the symptoms described above and are going to do general anesthesia(for example, regarding castration or sterilization), it is highly advisable to undergo an examination by a cardiologist before anesthesia for the absence of HCM in your pet. Unfortunately, cases of serious complications (up to pulmonary edema and death) are not uncommon. postoperative period(first 2 weeks after anesthesia) in patients with hidden form GKMP.

Treatment of hypertrophic cardiomyopathy

If the doctor still detects HCM in a patient, do not despair. There are modern efficient schemes treatment of this disease, especially effective in identifying the disease at an early stage. The drug of choice for such patients is, first of all, drugs of the beta-blocker group, and, if necessary, drugs for the prevention of thromboembolism, diuretics, calcium channel blockers, ACE inhibitors, etc. are prescribed. However, it is important to remember that the treatment should be prescribed by the attending doctor according to the examination, worth self-medicating and getting involved " folk remedies". The intake of drugs should be permanent, the patient must be shown for scheduled follow-up examinations and not interrupt the prescribed treatment regimen.

Hypertrophic cardiomyopathy and breeding

It is extremely important to understand that if a cat is diagnosed with HCM, it must be immediately removed from breeding plans and the entire line checked to avoid further spread of the pathology.

The isolation of HCM from the Maine Coon genetic base is of utmost importance for the subsequent development of the breed.

Photo from the magazine Clinician's Brief

Article from Textbook of Veterinary Internal Medicine Fourth Edition, 2009

Translation from English. Vasiliev AV

Etiology

The cause of primary or idiopathic hypertrophic cardiomyopathy (HCM) in cats is unknown, but hereditary pathology probably exists in many cases. The disease appears to be widespread in several breeds such as the Maine Coon, Persian, Ragdoll, and American Shorthair. There are also reports of HCM in littermates and other close relatives of domestic shorthair cats. Some breeds have been found to have an autosomal dominant pattern of inheritance. It is known that there are many different gene mutations in familial HCM in humans. Although some common human gene mutations do not yet appear to be found in cats with HCM, others may be found in the future. Some investigators (Meurs 2005) have also found a mutation in myocyte myosin-binding protein C in this breed. Another mutation has been found in ragdolls; testing for these mutations is currently available (www.vetmed.wsu.edu/deptsVCGL/felineTests.aspx).

In addition to mutations in genes that code for proteins responsible for myocardial contractility and regulatory proteins, possible reasons diseases include increased sensitivity of the myocardium to excess production of catecholamines; pathological hypertrophic response to myocardial ischemia, fibrosis or trophic factors; primary pathology of collagen; disturbances of the myocardial, relating to calcium, processes. Myocardial hypertrophy with foci of mineralization occurs in cats with hypertrophic feline muscular dystrophy, which is an X-linked recessive dystrophic deficiency similar to human Duchenne muscular dystrophy; however, congestive heart failure is uncommon in these cats. Some cats with HCM have high serum concentrations of growth hormone. It is unclear whether viral myocarditis plays a role in the pathogenesis of feline cardiomyopathy. In one study, myocardial samples from cats with HCM were evaluated by polymerase chain reaction(PCR) and showed the presence of panleukopenia virus DNA in approximately one third of cats with myocarditis and did not show its presence in healthy control cats (Meurs, 2000).

Pathophysiology

Thickening of the left ventricular wall and/or interventricular septum is characteristic, but the extent and distribution of hypertrophy in cats with HCM is variable. Many cats have symmetrical hypertrophy, but some have asymmetric ventricular septal thickening and a few have hypertrophy limited to the left ventricular free wall or papillary muscles. The lumen of the left ventricle usually looks small. Focal or diffuse areas of fibrosis occur in the endocardium, conduction system, or myocardium; narrowing of the small coronary arteries may also be present. Areas of myocardial infarction and malpositioning of myocardial fibers may be present.

Myocardial hypertrophy and its accompanying changes increase the stiffness of the ventricular wall. In addition, early active myocardial relaxation may be delayed and incomplete, especially in the presence of myocardial ischemia. This further reduces ventricular compliance and contributes to diastolic dysfunction. Ventricular stiffness impairs left ventricular filling and increases diastolic pressure. The volume of the left ventricle remains normal or decreases. Decreased ventricular volume causes a decrease in stroke volume, which may contribute to neurohormonal activation. A higher heart rate further affects left ventricular filling, contributing to myocardial ischemia, pulmonary venous congestion, and edema, shortening the duration of diastolic filling. Contractility or systolic function is usually normal in affected cats. However, some cats gradually develop systolic ventricular failure and ventricular dilatation.

The progressive increase in left ventricular filling pressure leads to an increase in pressure in the left atrium and pulmonary veins. The result may be progressive left atrial enlargement and pulmonary congestion and edema. The degree of left atrial enlargement varies from mild to severe. Thrombi are sometimes found in the left ventricular lumen or attached to the ventricular wall, although they are more commonly found in the left atrium. Arterial thromboembolism is a major complication of HCM, as is the case with other forms of cardiomyopathies in cats. Some affected cats develop mitral regurgitation. Changes in left ventricular geometry, papillary muscle structure, or systolic motion mitral valve(Systolic anterior leaflet movement (SAM) can prevent the valve from closing normally. Valvular insufficiency contributes to an increase in left atrial size and pressure.

Systolic dynamic left ventricular outflow tract obstruction occurs in some cats. This phenomenon is also called hypertrophic obstructive cardiomyopathy or functional subaortic stenosis. Excessive asymmetric hypertrophy of the base of the interventricular septum may be evident on echocardiogram and at autopsy. Systolic outflow tract obstruction increases left ventricular pressure, adversely affects the ventricular wall, increases myocardial oxygen demand, and contributes to myocardial ischemia.

Mitral regurgitation increases the tendency for the anterior leaflet of the mitral valve to move toward the interventricular septum during ventricular systole (SAM). Increased turbulence in the left ventricular outflow tract often causes systolic murmurs of varying intensity in these cats.

Various factors likely contribute to the development of myocardial ischemia in cats with HCM. These include narrowing of the intramural coronary arteries, increased left ventricular filling pressure, decreased perfusion pressure in coronary arteries and insufficient density of myocardial capillaries depending on the degree of hypertrophy. Tachycardia promotes ischemia by increasing myocardial oxygen demand while decreasing diastolic coronary perfusion time. Ischemia impairs early active ventricular relaxation, which later increases ventricular filling pressure and eventually leads to myocardial fibrosis. Ischemia can cause arrhythmia and possibly chest pain.

Atrial fibrillation and other tachyarrhythmias further impair diastolic filling and increase venous congestion; especially detrimental are the loss of normal atrial contractions and the increased heart rate associated with atrial fibrillation. Ventricular tachycardia or other arrhythmias may lead to syncope or sudden death. Pulmonary venous congestion and edema are caused by increased pressure in the left atrium. Increased pulmonary venous and capillary pressure causes pulmonary vasoconstriction; increased pulmonary arterial pressure and symptoms of secondary right-sided congestive heart failure may occur. Over time, some cats with HCM develop refractory biventricular insufficiency with massive pleural effusion. The effusion is usually a modified transudate, although it may be (or become) chylous.

Clinical manifestations

HCM is most common in middle-aged male cats, but clinical signs can occur at any age. Cats with mild disease may be asymptomatic for several years. Symptomatic cats most commonly present with varying degrees of respiratory symptoms or symptoms of acute thromboembolism. Respiratory symptoms include tachypnea; dyspnea associated with activity; dyspnoea and very rarely cough (which can be confused with vomiting). The onset of the disease may be acute in sedentary cats, even if pathological changes develop gradually. Sometimes lethargy and anorexia are the only manifestation of the disease. Some cats experience syncope or sudden death without other symptoms. stresses such as anesthesia, surgical operations, fluid injection, systemic disease(eg hyperthermia or anemia) or transportation may contribute to the manifestation of heart failure in compensated cats. Asymptomatic disease is detected in some cats by detecting heart murmurs or gallops on routine auscultation.

Systolic murmurs due to mitral regurgitation or left ventricular outflow tract obstruction are common. Some cats do not have audible murmurs, even those with severe ventricular hypertrophy. A diastolic gallop sound (usually S4) may be audible, especially if heart failure is obvious or imminent. Cardiac arrhythmias are relatively common. The femoral pulse is usually strong, except in cases of distal aortic thromboembolism. The heartbeat is often amplified. Increased breath sounds, pulmonary rales, and sometimes cyanosis accompany severe pulmonary edema. Crackles in the lungs are not always audible with pulmonary edema in cats. Pleural effusion usually attenuates ventral lung sounds. Physical examination may be normal in subclinical cases.

Diagnosis

Radiography

Radiographic features of HCM include left atrial enlargement and varying degrees of left ventricular enlargement. The classic dorsoventral and ventrodorsal view of the heart in the form of a valentine is not always present, although the position of the left ventricular apex is usually preserved. The silhouette of the heart appears normal in most cats with mild HCM. Extended and tortuous pulmonary veins may be seen in cats with chronically elevated pulmonary venous and left atrial pressures. Left-sided congestive heart failure causes patchy infiltrates expressed to varying degrees with interstitial or alveolar pulmonary edema. Radiographically, the distribution of pulmonary edema is variable; there is usually a diffuse or localized distribution within the lung fields, in contrast to the characteristic hilar distribution of cardiogenic pulmonary edema in dogs. Pleural effusion is common in cats with advanced or biventricular congestive heart failure.

Electrocardiography

Most cats with HCM (up to 70%) have electrocardiographic abnormalities. These include abnormal left atrial and left ventricular enlargement, ventricular and/or (less often) supraventricular tachyarrhythmias, and signs of left bundle branch block. Occasionally, atrioventricular conduction delay, complete atrioventricular block, or sinus bradycardia occur.

echocardiography

Echocardiography is the best method for diagnosing and differentiating HCM from other diseases. The extent of hypertrophy and its distribution within the free wall of the left ventricle, interventricular septum and papillary muscles is detected in M-mode and B-mode echo studies. Doppler sonography can demonstrate left ventricular systolic and diastolic abnormalities.

Widespread myocardial thickening is commonly encountered, and hypertrophy is often seen asymmetrically in the left ventricular free wall, ventricular septum, and papillary muscles. Focal areas of hypertrophy also occur. Using the B-Mode helps ensure that the scanning direction is correct. Standard M-Mode measurements should be taken, but areas of thickening outside of these standard positions should also be measured. Diagnosis at an early stage of the disease may be suspect in cats with mild or only focal thickening. False positive thickening (pseudohypertrophy) may occur with dehydration and occasionally with tachycardia. False diastolic thickness measurements also occur when the ultrasound beam does not cross the wall/septum perpendicularly and when measurements are not made at the end of diastole, which can occur without a simultaneous ECG, or when using B-mode is insufficient for a good measurement. A free wall thickness of the left ventricle or interventricular septum (correctly measured) greater than 5.5 mm is considered abnormal. Cats with severe HCM have a diastolic septal or left ventricular free wall thickness of 8 mm or more, although the degree of hypertrophy does not necessarily correlate with the severity of clinical symptoms. Doppler measures of diastolic function, such as isovolumic relaxation time, mitral inlet, and pulmonary vein velocity, as well as tissue Doppler imaging techniques, are being increasingly used to characterize disease.

Hypertrophy of the papillary muscles can be pronounced and obliteration of the left ventricle in systole is observed in some cats. Increased echogenicity (brightness) of papillary muscles and subendocardial areas is usually a marker of chronic myocardial ischemia with resulting fibrosis. The shortening fraction of the left ventricle is usually normal or increased. However, some cats have mild to moderate left ventricular dilatation and reduced contractility (contraction fraction 23-29%; normal contractility fraction 35-65%). Occasionally, right ventricular enlargement and pleural or pericardial effusion are seen.

Cats with dynamic left ventricular outflow tract obstruction also often have either early closure of the aortic valve leaflets, as detected on M-mode examination. Doppler ultrasonography can demonstrate mitral regurgitation and turbulence in the left ventricular outflow tract, although positioning the ultrasound beam along the blood stream at maximum ventricular ejection velocity is often difficult and it is easy to underestimate the systolic gradient.

Left atrial enlargement can be mild to severe. Spontaneous enhancement (rotation, smoke echo) is seen within the enlarged left atrium in some cats. This is thought to be the result of blood stasis with cell aggregation and is a precursor to thromboembolism. Thrombosis is sometimes visualized within the left atrium, usually in its ear.

Other causes of myocardial hypertrophy must be excluded before idiopathic HCM is diagnosed. Thickening of the myocardium can also occur due to infiltrative disease. Variations in myocardial echogenicity or wall irregularity can be detected in such cases.

Excess connective tissue appears as bright, linear echoes within the left ventricular cavity.

Clinicopathological features

Cats with moderate to severe HCM have high concentrations of circulating natriuretic peptides and cardiac troponins. Congestive heart failure cats have been found to have varying degrees of elevated plasma concentrations of tumor necrosis factor (TNF).

Picture 1
Radiographic findings in feline HCM. Lateral (A) and dorsoventral (B) views showing left atrial enlargement and mild ventricular enlargement in a male domestic shorthair cat. Lateral © view in a cat with HCM and severe pulmonary edema

Figure 2
Electrocardiogram in a cat with HCM demonstrating infrequent ventricular extrasystoles and deviation electrical axis hearts to the left. Leads 1,2,3, speed 2.5 mm / sec. 1cm=1mV

Figure 3
Echocardiographic findings in feline HCM. M-mode image (A) at the level of the left ventricle in a seven-year-old male domestic shorthair cat. The thickness of the free wall of the left ventricle and the interventricular septum in diastole is approximately 8 mm. B-mode image (B) in the right parasternal position along the short axis of the left ventricle in diastole (B) and systole © in a male Maine Coon with hypertrophic obstructive cardiopathy. In (B), note hypertrophied and bright papillary muscles. In ©, note the almost complete obliteration of the left ventricular chamber in systole. IVS, interventricular septum; LV, left ventricle; LVW, left ventricular free wall; RV, right ventricle

Figure 4
A, Mid-systole M-mode echo image of the cat in Figure 3 (B and C). An anterior mitral leaflet echo is seen in the lumen of the left ventricular outflow tract (arrow) due to abnormal systolic movement of the anterior mitral leaflet towards the interventricular septum (SAM). B, M-mode echocardiogram at the level of the mitral valve, also showing SAM (arrows).

Ao, aorta; LA, left atrium; LV, left ventricle.

Figure 5
Color Doppler image during systole in a male domestic longhair cat with hypertrophic obstructive cardiopathy. Note the turbulent flow above the protrusion of the thickened interventricular septum into the lumen of the left ventricular outflow tract and the mild mitral valve regurgitation often associated with SAM. Right parasternal position along the long axis of the left ventricle. Ao, aorta; LA, left atrium; LV, left ventricle.

Figure 6
Echocardiogram obtained from the right parasternal position along the short axis of the left ventricle at the level of the aorta and left atrium in an old male domestic shorthair cat with restrictive cardiomyopathy. Note the marked left atrial enlargement and thrombus (arrows) within the atrial appendage. A, aorta; LA, left atrium; RVOT, right ventricular outflow tract

Treatment

Subclinical HCM

There is no consensus on whether (and how) asymptomatic cats should be treated. It is not clear whether the progression of the disease can be slowed down or life expectancy can be increased with the use of medications before the onset of clinical manifestations of the disease. According to anecdotal reports, some cats show increased activity and better health after treatment with beta-blockers or diltiazem if echographic abnormalities or arrhythmias are detected. When moderate or severe left atrial enlargement is detected, especially with spontaneous echo contrast, antithrombotic therapy is prudent.

Re-examination once or twice a year is usually desirable. Secondary Causes myocardial hypertrophy, such as systemic arterial hypertension and hyperthyroidism should be ruled out (or treated if present).

Clinically obvious HCM

The goal of therapy is to increase ventricular filling, reduce congestion, control arrhythmia, and prevent. Furosemide is used only at doses needed to control the symptoms of congestion. Moderate to severe accumulation of pleural effusion is removed by thoracocentesis while the cat is gently held in a sternal position. Cats with severe symptoms of congestive heart failure usually receive oxygen support, parenteral furosemide, and sometimes other drugs to control swelling (described in more detail later). Once initial treatment received, the cat needs to be kept calm. The respiratory rate is recorded initially and then assessed every 30 minutes or more often, but without causing additional distress to the cat. Placement of an intravenous catheter, blood sampling, radiography, and other tests and treatments should be deferred until the cat is more stable.

Ventricular filling is improved by slowing the heart rate and increasing cardiac relaxation. Stress and activity levels should be kept as low as possible. Although the calcium blocker diltiazem or beta-blockers have long been the mainstay of long-term oral therapy, ACE inhibitors may be of great benefit in cats with congestive heart failure. Further research is needed for optimal recommendations. The decision to use one drug or another depends on the echocardiographic or other findings in the individual cat or on response to treatment. Diltiazem is often used in the presence of severe symmetrical left ventricular hypertrophy. Beta-blockers are currently preferred in cats with left ventricular outflow tract obstruction, tachyarrhythmias, syncope, suspected myocardial infarction, or concomitant hyperthyroidism. ACE inhibitors can reduce neurohormonal activation and pathological myocardial remodeling. They are sometimes used as monotherapy or combined with diltiazem or a beta-blocker. Long-term therapy usually includes drugs to reduce the chance of arterial thromboembolism. Dietary sodium restriction is recommended as long as the diet is eaten well, but it is more important to prevent anorexia.

Certain drugs are generally undesirable for use in cats with HCM. This includes digoxin and other positive inotropic agents because they increase myocardial oxygen demand and may exacerbate dynamic left ventricular outflow tract obstruction. Any drugs that increase the heart rate are also potentially harmful because tachycardia decreases left ventricular filling time and predisposes to myocardial ischemia. Arterial vasodilators can cause hypotension and reflex tachycardia, and cats with HCM have a low preload reserve. Hypotension may also exacerbate dynamic left ventricular outflow tract obstruction. Although ACE inhibitors lower blood pressure, their vasodilatory effect is usually mild.

Diuretic therapy

Cats with severe pulmonary edema usually receive furosemide IM at 2 mg/kg every 1 to 4 hours first, prior to IV catheter placement, without undue stress to the cat. The frequency of respiratory movements and the severity of dyspnea are used to correct diuretic therapy. If breathing improves, treatment with furosemide can be continued at a reduced dose (1 mg/kg every 8-12 hours). Once pulmonary edema is controlled, furosemide is given orally and the dose is gradually titrated to the lowest effective level. The starting dose of 6.25 mg/cat every 8-12 hours may be tapered gradually over several days or weeks, depending on the cat's response to treatment. For some cats, dosing several times a week (or less) is sufficient, while others need to be given furosemide several times a day. Complications of excessive diuresis include azotemia, anorexia, electrolyte disturbances and poor filling of the left ventricle. If the cat is unable to rehydrate itself by oral fluid intake, careful parenteral fluid administration may be necessary (eg 15-20 ml/kg/day 0.45% isotonic solution, 5% aqueous solution glucose or other solutions with low content sodium).

Therapy for acute congestive heart failure

Nitroglycerin ointment can be used every 4 to 6 hours, although there are no studies on its effectiveness in this situation. The bronchodilatory and mild diuretic effects of aminophylline (5 mg/kg every 12 hours IM or IV) may be useful in cats with severe pulmonary edema provided it does not increase heart rate.

Butorphanol may be used to reduce anxiety. Acepromazine can be used as an alternative and may promote peripheral redistribution of blood due to its beta-blocking effect. Hypothermia may increase peripheral vasodilation. Morphine should not be used in cats. Aspiration of fluid from the airways and mechanical ventilation with positive end-expiratory pressure may be considered in critical cases.

ACE inhibitors. ACE inhibitors have beneficial effects, especially in cats with refractory heart failure. Inhibition of the renin-angiotensin system can reduce angiotensin-mediated ventricular hypertrophy. Inhibition of the renin-angiotensin system can reduce the size of the left atrium and the thickness of the interventricular septum in at least some cats. The most commonly used drugs in cats are enalapril and benazepril, although other inhibitors are also available.

Calcium channel blockers. Calcium channel blockers are thought to have beneficial effects in cats with HCM by modestly reducing heart rate and contractility (which reduces myocardial oxygen demand). Diltiazem promotes coronary vasodilation and may have positive influence for myocardial relaxation. Verapamil is not recommended due to its variable bioavailability and the risk of toxicity in cats. Amlodipine is primarily a vasodilator and is not used in HCM because it can induce reflex tachycardia and worsen the systolic ejection gradient.

Diltiazem is well tolerated in many cases. Long-acting diltiazem preparations are more suitable for long-term use, although serum concentrations may be variable. Dilacor (diltiazem) XR 30 mg/cat once or twice daily or Cardizem CD 10 mg/kg once daily are most commonly used.

Beta blockers. Beta-blockers may reduce heart rate and dynamic left ventricular outflow tract obstruction more potently than diltiazem. They are also used to suppress tachyarrhythmias in cats. Inhibition of the sympathetic system also results in a decrease in myocardial oxygen demand, which may be important in cats with ischemia or myocardial infarction. By inhibiting catecholamine-induced damage to cardiomyocytes, beta-blockers may reduce myocardial fibrosis. Beta-blockers may delay active myocardial relaxation, although the benefit of lowering the heart rate may be more important.

Atenolol is the most commonly used. Propranolol or other non-selective beta-blockers may also be used, but should be avoided until the pulmonary edema has resolved. Antagonism to beta receptors located in respiratory tract leading to bronchoconstriction is a complication when non-selective beta blockers in congestive heart failure. Propranolol (a fat-soluble drug) causes lethargy and appetite depression in some cats.

Occasionally, beta-blockers are added to diltiazem (or vice versa) in cats with chronic refractory insufficiency or to decrease the heart rate in atrial fibrillation. However, close monitoring is necessary to prevent bradycardia or hypotension in animals receiving this combination.

Chronic refractory congestive heart failure

Refractory pulmonary edema or pleural effusion is difficult to treat. Moderate or severe pleural effusion should be removed by centesis. Various treatment strategies can help slow the rate of abnormal fluid accumulation, including maximizing the dose (or adding) of ACE inhibitors; increasing the dose of furosemide to 4 mg/kg every 8 hours; increasing the dose of beta-blockers or diltiazem to increase heart rate control and adding verospirone with or without hydrochlorothiazide. Veroshpiron can be in the form of a flavored suspension for more accurate dosing. Pimobendan and digoxin may also be used to treat symptoms of refractory right-sided congestive heart failure in cats without left ventricular outflow tract obstruction and those with progressive left ventricular dilatation and end-stage systolic myocardial failure. Frequent monitoring is necessary, as azotemia and electrolyte disturbances may develop.

Forecast

Numerous factors affect the prognosis in cats with HCM, including the rate at which the disease progresses, the likelihood of thromboembolism and/or arrhythmias, and response to treatment. Asymptomatic cats with only mild to moderate left ventricular and left atrial enlargement often live normally for several years. Cats with marked left atrial enlargement and marked hypertrophy have more high risk development of congestive heart failure, thromboembolism and sudden death. Left atrial size and age (eg older cats) are negatively correlated with lifespan. The average life expectancy for cats with congestive heart failure is likely to be between 1-2 years. The prognosis is worse in cats with atrial fibrillation and refractory congestive heart failure. Thromboembolism and congestive heart failure give a cautious prognosis (median survival time 2 to 6 months), although some cats do well if the symptoms of congestive heart failure are controlled and there are no life-threatening heart attacks. important organs. Recurrent thromboembolism is common.

Treatment protocol for cats with HCM

Severe symptoms of acute congestive heart failure

• oxygen support
• minimizing contact with the patient
• furosemide (parenteral)
• thoracocentesis (if pleural effusion is present)
• heart rate control and antiarrhythmic therapy (if indicated)
• (you can use intravenous diltiazem, esmolol or (+/-) propranolol)
• +/- nitroglycerin (on the skin)
• +/- bronchodilators (eg aminophylline or theophylline)
• +/- sedation
• monitor: respiratory rate, heart rate and rhythm, blood pressure, kidney function, serum electrolytes, etc.

Symptoms of congestive heart failure are mild to moderate

• ACE inhibitors
• furosemide
• antiarrhythmic prophylaxis (aspirin, clopidogrel, heparin, low molecular weight heparin, or warfarin)
• load limitation
• restriction of salt in the diet, subject to its palatability

Treatment chronic form GKMP

• ACE inhibitors
• beta blockers (eg atenolol) or diltiazem
• furosemide (lowest effective dose and frequency)
• antithrombotic prophylaxis (aspirin, clopidogrel, heparin, low molecular weight heparin, warfarin)
• thoracocentesis if necessary
• +/- verospirone and/or hydrochlorothiazide
• +/- simultaneous application beta-blocker and diltiazem
• +/- additional antiarrhythmic therapy, if indicated
• monitoring respiratory rate (and heart rate if possible) at home
• limiting salt in the diet, if appropriate
• monitoring of kidney function, electrolytes, etc.
• correct other disorders (rule out hyperthyroidism and hypertension if not already done)
• +/- positive inotropic drugs (only if systolic function deteriorates without obstruction of the outflow tract of the left ventricle)