What is hypertrophic cardiomyopathy in cats. Treatment of HCM in cats

In HCM, abnormal movement of the anterior leaflet occurs mitral valve increased pressure in the left atrium. A decrease in the elasticity of the ventricular wall and a decrease in its volume causes insufficiency of diastolic function. The ventricle is unable to fully fill, which leads to a decrease in stroke volume. Increased pressure in the pulmonary veins, as a result - congestion in the pulmonary circulation and cardiogenic pulmonary edema.

The goal of therapy for such a disease is to slow down the processes of myocardial remodeling and prevent catastrophes. This pathology cannot be cured. But knowing about its presence, you can prevent the process of exacerbation - this is the creation of optimally comfortable conditions external environment, this is the absence of "travel", this is the absence of unjustified stress. Medical support is prescribed for life. As for the issue of repeated examinations, if a pathology is detected, then most often the cardiologist of our center recommends not to make unjustified trips. An additional examination is possible if symptoms of other diseases appear or if clinical HCM is active.

  • — always have in your mobile phone the number of the cardiologist of the center 050 213 34 68 —

    Maine Coon cardiomyopathy

    In veterinary clinics, alarm bells are heard every now and then. Owners in a panic ask: “Save my cat! Something terrible is happening to him. He screams from severe pain and cannot move. The hind legs, one or both at once, do not bend, they are extended like sticks. The muscles have hardened like wood, and the cat won’t even let you touch them.”

    In these cases, the score really goes not even for hours, but for minutes. Spasmodic palsy is a symptom of blockage in the femoral arteries. The cause is a clot of clotted blood - a thrombus. It is like a cork tightly stuck in the place where the main trunk of the aorta branches into two vessels going to each of hind legs cat. Blood stops flowing to the muscles, and after about two hours, the irreversible process of their death begins. In this case, the cat experiences unbearable pain. Let's remember how painful it is when you serve your leg, and it gradually begins to tingle with needles and pull. If you take action very quickly, then the cat can be helped. He is going to have a deep abdominal surgery. blood vessels in order to get to the clot and restore blood circulation. Then comes the long postoperative period when damaged muscles atrophy and are replaced by scar tissue. But the attack can happen again at any moment...

    Where did the blood clot come from in the cat's vessels? Straight from a cat's heart! Here we come close to the topic of our conversation.

    Insidious disease - Hypertrophic cardiomyopathy, in English is called Hypertrophic Сardiomyopathy, and its abbreviation looks like this - HCM. It begins gradually, without obvious symptoms. In the final stage, the affected heart looks larger than normal. Hence the name (hypertrophy - increase).

    If you look at the heart through the prism of a microscope and all the scientific knowledge accumulated to date, it is possible to distinguish three layers in its wall. Two of them are thin, but very necessary, make up the shells: the outer one is the epicardium and the inner one is the endocardium. The entire remaining thickness of the heart wall is occupied by its main engine - muscle mass. Penetrating deeper, we see individual fibers and even the fact that they are striated with transverse stripes, like a T-shirt. This is a striated musculature, similar to skeletal, that sets the whole body in motion. But its fibers are not arranged linearly, but are pierced by jumpers, making up a network where each individual element is connected to others.

    Analyzing the finest structure of the heart muscles, one can see that they owe their movement to special protein molecules - actin and myosin. The easiest way to describe them is as logs laid on rolls. Actin forms small, round molecules arranged in long chains. Myosin, on the contrary, has a long filament and a "head" - an active element that provides sliding along the actin chain.

    When a defective gene is unable to produce enough myosin, the heart tends to compensate for this loss. Muscle fibers begin to thicken. Histological data show that in true or congenital HCM, the size of the cardiomyocytes themselves increases - muscle cells hearts. And it turns out a colossus on clay feet. These huge swollen muscles have no important component for their work - myosin, and, accordingly, they contract worse and worse. With age, changes in the heart muscle accumulate. It loses its tone, mobility and elasticity. Bulky cells lead to hypertrophy (thickening) of the entire heart wall, especially in the left ventricle. The left side of the heart is responsible for the circulation of the whole body, the so-called large circle, and the right half is responsible for the movement of blood in the lungs - the small circle. If normally the wall of the right ventricle has a thickness of 1.5 mm, and the left one is about 2 times more - 3-5 mm, then in a hypertrophied left ventricle the wall reaches up to 9 mm. Accordingly, the cavity of the ventricle itself decreases, which should contain a certain volume of blood. Let's add here a sluggish clumsy muscle, and it becomes clear that the movement of blood slows down noticeably. The impulse at the huge heart is weakened, the one-time release of blood is reduced.

    The first signs of heart failure in affected cats may be shortness of breath, especially after exercise, fatigue, cyanosis of the skin and mucous membranes. Some cats are just trying to take care of themselves: they sleep more, less and are reluctant to move. After active play or during times of stress, such as moving, shortness of breath may occur. Movement is noticeable chest which is not normally observed. The cat breathes with its mouth open, like a dog. Sometimes there is a noise in the breath, which definitely does not happen in a healthy cat. unnatural color(pale or with blue) can be seen on the skin of the nasolabial mirror, on the mucous membrane of the gums and on inner surface auricle. It indicates a lack of oxygen in the blood.

    With further uncontrolled development of the disease, pulmonary edema and fluid accumulation in the chest cavity occur, leading to death.

    When the left ventricle ceases to cope with its work, “chokes”, then the part of the heart lying in front of it, the left atrium, suffers first of all. From constant excess pressure, it stretches, blood stagnates in it. Not getting into the weakened ventricle in time, it whirls around in whirlwinds. Under such conditions, blood coagulation mechanisms are triggered and clots form. They are attached to the wall of the atrium, but can easily come off and become the very blood clots - invisible, but sure killers. A blood clot can go to the lower part of the body and clog any artery - in the kidneys, intestines, liver, hind legs, causing partial or irreparable harm. If a thrombus enters carotid arteries in the brain, sudden death occurs without visible previous signs.

    And the biggest joke of HCM is that a young cat can lead an active lifestyle up to irreversible changes heart muscle. First and last symptom this pathology becomes a sudden death from pulmonary edema or thromboembolism.

    Hypertrophy of the heart walls can be caused by the presence of another disease - arterial hypertension (high blood pressure). In this case, one speaks of non-hereditary secondary HCM. Let's develop this topic a bit. Hypertension in humans is understood as an increase in total pressure in the systemic circulation. It is associated, as a rule, with a spasm of peripheral vessels or their narrowing, for example, as a result of the deposition of cholesterol plaques. Both changes increase with age, so hypertension is considered to be an age-related disease. Something similar happens in dogs, so many of the developments of humanitarian medicine apply to them. But in cats, the circulatory system is arranged in such a way that their vessels remain elastic up to advanced age, and the cholesterol that they receive at any age and in large quantities with meat food does not have a noticeable effect on them. In addition, the loads domestic cat are so minimal and stress so rare that she has no reason for classical hypertension. However, secondary feline HCM exists and is caused by the same hereditary factors. Suppose that the entrance to the aorta in a cat is narrowed - this is a congenital condition. The left ventricle is forced to make uncharacteristic efforts to push blood into a small hole. The muscles of the left ventricle sway, as in gym. However, any athlete can overstrain from excessive load. But the heart cannot stop, it is forced to work 24 hours a day. A similar process can occur in the right half of the heart with the difference that the symptoms of the disease will be more pronounced in the lungs. Symptoms are similar: exercise intolerance, sudden thromboembolism, pulmonary edema, hydrothorax, death at a young age.

    The difference is that the amount of myosin in the heart muscle remains at a normal level, and the heart wall increases not due to giant muscle fibers, but as a result of an increase in the number of normal cardiomyocytes. These differences can only be seen under a microscope. This means that the final diagnosis is made only after the death of the cat.

    There is no doubt that primary or secondary HCM is one of the most common cardiac diseases leading to sudden death among young cats. Breeding experience purebred cats and the observation of "familial" HCM confirms its hereditary nature. But like any disease, it has its own history of discovery, study, ups and downs.

    The mechanisms of HCM development have long been studied in humans. The changes are caused by mutations in the genes that code for the proteins responsible for contraction of the heart muscle. One of the main candidate genes is MYBPC3 (myosin binding protein C). The product of the MYBPC3 gene is myosin-binding protein, which is necessary for the proper functioning of the heart muscle. The first studies of HCM in cats, ironically, were carried out on representatives of the Maine Coon breed. And it was in Coons suffering from this heart disease that a decrease in the amount of myomysin protein, encoded by the MYBPC3 gene, was recorded. At the same time, the disease immediately received the epithet "breed-specific". Despite the fact that HCM has been found in many cat breeds (Ragdoll, Scottish Fold, Ocicat, British, American Shorthair, Bengal), as well as outbred crosses, it is Maine Coon breeders and owners who are particularly concerned about this pathology.

    The history of cardiomyopathy, as a hereditary disease, began its history not so long ago. In 1999, American Maine Coon breeder Dr. Katherine M. Meers hypothesized that HCM is an autosomal dominant mutation and is inherited with 100% penetrance. The latter means that all carriers of the defective gene will show signs of the disease.

    The dominant nature of the anomaly suggests that the presence of even one mutant allele may be sufficient for the development of the disease. Then in the journal Human Molecular Genetics in 2005, an article by the same researcher was published entitled "Protein C mutation associated with cardiac myosin in Maine Coon cats with familial hypertrophic cardiomyopathy."

    Since the diseased cats showed a progressive reduction in myosin-binding protein C, the MYBPC3 gene was chosen for study by the researchers. A direct DNA analysis was performed and a single altered base pair (G to C) was found at codon 31 (exon 3). In turn, this led to the replacement of the amino acid alanine (A) by proline (P) in the final protein. Computer analysis of the protein structure revealed the contraction of the alpha helix and the appearance in this region random turns that disrupt the structure and function of the protein. The mutation was named A31P. In addition, Meers found this mutation in every affected Maine Coon cat from the study group, either in a homozygous or heterozygous form. The analysis did not confirm the presence of a mutation in any healthy cat. This supported the original hypothesis of dominant inheritance and 100% penetrance.

    Possible genotypes were compiled.

    Hypertrophic cardiomyopathy in cats.

    In the ZVC Dingo, cats of the Scottish Fold and Maine Coon breeds are recommended to undergo an examination by a cardiologist before castration. What is it? whims of doctors or real threat Does heart disease exist?

    Hypertrophic cardiomyopathy is the most common cardiac pathology in the feline family. This is a primary heart disease characterized by thickening of the wall of the left ventricle, with a simultaneous decrease in its cavity. In most cases, thickening of the interventricular septum develops simultaneously.

    A number of studies have identified genetically inherited abnormalities that can lead to the development of HCM. A special predisposition to this disease is found in breeds: Maine Coon, British Shorthair and Scottish Fold.

    With HCM, abnormal movement of the anterior leaflet of the mitral valve occurs, increasing pressure in the left atrium. A decrease in the elasticity of the ventricular wall and a decrease in its volume causes insufficiency of diastolic function. The ventricle is unable to fully fill, which leads to a decrease in stroke volume. The pressure in the pulmonary veins increases, as a result - congestion in the pulmonary circulation and cardiogenic pulmonary edema.

    In cats with HCM, as the disease progresses, compensatory mechanisms (primarily an increase in heart rate) are depleted and clinical symptoms begin to appear.

    In the practice of our clinic, the clinical manifestation of this disease occurred after the following reasons:

    - for no reason (the conditions of detention, feeding did not change, there were no stress factors) 35%. Animals are usually older than 6 years

    — surgical interventions conducted in clinics where there are no conditions for examination, the use of anesthetics without a protocol. fifty %. Mostly patients after sterilization, castration.

    - change in conditions of detention ( fever and air humidity, moving, repairs, fright) 15%. Regardless of age, in the summer, with a pronounced pathology of the myocardium.

    The main symptoms are shortness of breath, lethargy, fainting, often sudden death.

    Violation of normal blood flow in the left atrium leads to the risk of thrombosis and, as a result, to ATE (arterial thromboembolism). In particular, ATE of the abdominal part of the aorta in the area of ​​its bifurcation will manifest itself as suddenly developing paresis, paralysis hind limbs, tachypnea, absence of pulsation of the femoral artery.

    It is almost impossible to recognize the presence of a disease without examination before such critical manifestations. A cat may experience fatigue, but whoever has seen the British knows that they sleep in a healthy form for 22 hours a day.

    A definite diagnosis of HCM can only be made based on the results of an ultrasound of the heart. Minor and controversial abnormalities can certainly be detected by ECG and chest x-ray, but they are not conclusive when making such a diagnosis.

    The most informative, the so-called expert method in the diagnosis of hypertrophic cardiomyopathy is echocardiography (our clients often call it ultrasound of the heart). It allows you to identify myocardial hypertrophy, namely: thickening of the interventricular septum and hypertrophy rear wall left ventricle (more than 6.0 mm in the diastolic phase), as well as a decrease in the cavity of the left ventricle.

    In addition, echocardiography makes it possible to assess the contractility of the ventricular myocardium.

    The goal of therapy for such a disease is to slow down the processes of myocardial remodeling and prevent catastrophes. This pathology cannot be cured. But knowing about its presence, you can prevent the process of exacerbation - this is the creation of optimally comfortable environmental conditions, this is the absence of "travel", this is the absence of unjustified stress. Medical support is prescribed for life. As for the issue of repeated examinations, if a pathology is detected, then most often the cardiologist of our center recommends not to make unjustified trips. An additional examination is possible if symptoms of other diseases appear or if clinical HCM is active.

    The outcome of the disease in patients admitted to us with a severe clinical manifestation of HCM (pulmonary edema) in most cases (95%) is favorable. Therapeutic doses furosemide and oxygen therapy returned the animal to normal state. Unreasonable (in the absence of a chest x-ray, echocardiography) treatment of such animals with all kinds of cardio drugs, unfortunately, can lead to death.

    If you are the owner of a cat of the indicated breed, we recommend:

    - undergo an examination to identify this pathology

    - get advice from a cardiologist on self-help in an emergency

    - at the first sign of difficulty breathing, fainting, blue mucous membranes, immediately contact our branch at Politboytsov 20A, where there is an equipped resuscitation unit and the possibility of diagnosing on echocardiography.

    – not examined animals should not be taken out of the city. Most often, during the summer period, the period of rest on the sea coast, taken away cats cannot receive qualified assistance.

    – always have in your mobile phone the number of the cardiologist of the center 050 213 34 68

    • Feline Cardiomyopathy Comparison of Feline Cardiomyopathy

    Myocardial disease is the most common form of heart disease in cats. All myocardial diseases can lead to the development of congestive heart failure.

    Three types of cardiomyopathy

    1. Dilated cardiomyopathy (DCM): Feline dilated cardiomyopathy is caused by a lack of taurine (although some cases may be idiopathic). With DCM, eccentric hypertrophy develops in the muscular wall of the heart and contractility decreases, which leads to a decrease in cardiac output. Today, DCM is rare, as taurine is added to commercial cat food.

    2. Hypertrophic cardiomyopathy is common in cats. In hypertrophic cardiomyopathy, concentric hypertrophy develops in the ventricular wall, which is characterized by thickening of the ventricular wall. The pumping function of the heart is good, but it cannot relax normally during diastole. In addition, thickening of the ventricular wall leads to malposition of the AV valves, so the animal may develop mitral valve insufficiency. Dynamic obstruction of the aortic outlet tract may occur against the background of systolic movement of the mitral valve forward. Stenosis can occur in mid/late systole, so it usually doesn't cause problems.

    3. Restrictive cardiomyopathy occurs when too much fibrous tissue in the endocardium, myocardium, or subendocardial tissues. Endocardial fibrosis is the most common cause. Fibrosis usually leads to diastolic dysfunction. The elasticity of the heart decreases, it cannot adequately fill and perform a pumping function. The heart must be filled with more high pressure than normal, leading to higher diastolic pressure. This leads to increased capillary pressure and pulmonary edema or pleural effusion.

    Clinical signs: most cats present with acute heart failure, even though their heart disease has developed over years. Heart disease develops slowly, and the activity of cats gradually decreases. Most owners do not notice this exercise intolerance. When the edema or effusion becomes severe, cats experience a sharp deterioration in the condition.

    1. Dyspnea due to pulmonary edema or pleural effusion.

    2. During auscultation, noises are often heard from the left or from right side chest. Cats often have a gallop rhythm, but the heart rate can be so high that the gallop rhythm is difficult to hear.

    3. An x-ray examination can show atrial enlargement (enlargement of the left or both atria). In the case of DCM, the ventricles also enlarge. In hypertrophic cardiomyopathy and sometimes in restrictive cardiomyopathy, the dorsoventral heart may be shaped like a valentine's heart.

    Forecast: in cats, cardiomyopathy is difficult to identify. These cats may respond poorly to drug therapy and live only a few days, or may respond well to drug therapy and live for many years. The prognosis depends on the response to therapy and the owner's ability to treat the cat.

    Treatment

    The immediate goal is to stabilize and support the animal with heart failure. After the animal is stabilized, further diagnostics are carried out and supportive drugs can be switched. Try to stabilize the animal without causing too much dehydration and hypotension (minor tolerable), as both of these disorders can lead to kidney failure. It is better to dehydrate and then rehydrate than to let the animal die of chronic heart failure. A. Introduction of oxygen. If the animal is unstable due to dyspnea, oxygen is administered to the animal by insufflation or by placing it in oxygen chamber. If the animal experiences a lack of oxygen, then first provide it with oxygen, and then carry out diagnostics.

    Principles of drug therapy

    1. Before the introduction of any drug, first determine:

    a. Purpose of treatment? It is necessary to control arrhythmias, increase myocardial contractility, reduce systemic resistance against which the heart ejects blood (afterload), and reduce hydrostatic capillary pressure.

    b. How to evaluate the effectiveness of drug therapy? For example, if attempts are being made to relieve congestion in the lungs, the respiratory rate should be monitored and repeated x-rays taken.

    c. Signs that will indicate that it is necessary to stop the drug? It may be necessary to decide to discontinue the drug if no result has been obtained within the first 24 hours, depending on the severity and immediate danger.

    The drug is discontinued if it reduces heart rate or myocardial contractility too much, or if vomiting or anorexia occurs during its use.

    2. If possible, start with monotherapy. Some time after the start of the drug administration, its effectiveness is evaluated. If the goal is not achieved, its administration is stopped, the dose is changed, or another drug is additionally prescribed. Make only one change at a time and allow enough time for the changes to take effect. Evaluate before and after each change.

    3. Avoid multiple drugs if possible, as this often leads to anorexia, especially in cats.

    4. In severe heart failure, it may be necessary to administer several drugs.

    SPECIAL DRUGS

    A. First choice diuretics:

    1. Furosemide (2-8 mg/kg) is usually the first choice. Its dose depends on the condition of the animal. Furosemide - relatively safe drug. Unfortunately, in heart failure, the forward movement of blood is reduced, therefore, the blood supply to the kidneys is impaired. As a result, furosemide may not be as effective as in animals with normal renal perfusion. The effectiveness of Lasix is ​​assessed by monitoring the respiratory rate and its nature, urinary excretion and using X-rays.

    a. In severe cases, therapy should be aggressive. Initially, furosemide is prescribed at a dose of 8 mg / kg IV every hour until the respiratory rate drops to 50-60 per minute. Then, 5 mg / kg is administered every 2-4 hours until the respiratory rate falls below 50. Then they switch to a maintenance dose. In cats, start at 4 mg/kg. It is very important to administer the drug intravenously first, since after an intravenous injection, the effect occurs after 5 minutes, while with an intramuscular injection, it appears after 30 minutes, and when administered orally, after an hour. These animals are likely to experience dehydration. Dogs will have an appetite and recover water balance immediately after preload reduction. Cats may need to be rehydrated first before they develop an appetite and start drinking on their own. The prognosis is poor if the animal is already dehydrated and has heart failure.

    b. After establishing the initial control dose of furosemide, begin its gradual reduction to the lowest possible maintenance dose. You may need to additionally prescribe another drug, such as enalapril.

    2. Angiotensin converting enzyme inhibitors (ACE inhibitors - captopril, enalapril, lisonopril) act by inhibiting the RAAS. Their overall effect is to reduce water retention and vasodilation. Therefore, their mechanism of action is associated with a reduction in preload as well as afterload. Other ACE inhibitors include benazepril and lisonopril.

    a. ACE inhibitors are not prescribed to animals with kidney disease. If there is suspicion that the animal may develop renal dysfunction, a biochemical blood test is performed before the administration of the drug, and then five days after the start of the drug administration. In most animals, renal dysfunction develops within 4-5 days after the start of the administration of ACE inhibitors.

    B. Venodilators increase venous capacity, thus reducing preload.

    Nitroglycerin ointment can be applied to skin covering in the area of ​​the ears or gums. The dose is 0.6 cm per 7 kg every 4-6 hours. The drug should be applied with gloves and in no case should it be given home to the owner!

    C. Positive inotropic drugs increase myocardial contractility and are very effective in myocardial insufficiency (determined by measuring shortening fraction). Often, when overloaded by volume, the shortening fraction does not decrease (normally, the shortening fraction in dogs is 34-40%).

    1. Digoxin is a weak inotropic drug. It is better to appoint at arrhythmias.

    2. Dopamine (5-10mcg/kg/min) and dobutamine (2-10mcg/kg/min) are good positive inotropic agents but have only a modest effect on the heart in myocardial insufficiency. These catecholamines are better than epinephrine and isoproterenol in the treatment of heart failure, as both of these drugs increase heart rate.

    At high doses, dopamine and dobutamine can also increase heart rate. Dopamine is much cheaper than dobutamine (dobutamine lowers pulmonary venous pressure). All catecholamines have a short half-life and must be administered as a constant rate infusion.

    D. Arterial dilators are used to reduce afterload. May cause hypotension. Use only nitroprusside and hydralazine if direct measurement is possible blood pressure. Do not use drugs that dilate arterial vessels in case of pressure overload (for example, with subaortic stenosis).

    1. Nitroprusside has a strong hypotensive action. When this drug is administered, an artery catheterization is necessary to continuously monitor blood pressure. Just a few drops of the drug can cause significant changes in blood pressure.

    2. With the introduction of hydralazine inside, the effect of the drug develops only after 30 minutes. Hydralazine also causes hypotension.

    3. Angiotensin converting enzyme inhibitors (ACE inhibitors), such as enalapril (0.5 mg/kg 2 times a day) or captopril (3 times a day), are used to a greater extent due to the diuretic effect; also have a weak dilating effect on the arteries.

    4. Amlodipine (a calcium channel blocker like diltiazem and nifedipine) causes arterial dilatation.

    E. Antiarrhythmic drugs digoxin, propranolol and lidocaine.

    Animals should be fed a salt-restricted diet. Treats should also contain minimal amount salt.

    Physical activity in animals with cardiomyopathy: physical activity provokes the appearance clinical signs but does not contribute to the progression of clinical signs. You can advise the owner not to limit the cat's movements, as the animal will do it itself.

    Ying S. Complete reference small animal veterinary medicine

    Sourced from www.icatcare.org

    Hypertrophic cardiomyopathy- a disease in which there is a thickening (or hypertrophy) of the wall of the ventricle of the cat's heart. As a result, the internal volume of the ventricle (the main chamber of the heart) decreases, which leads to a decrease in the amount of blood pumped per contraction.

    Hypertrophic cardiomyopathy is the most common form of heart disease in cats and can lead to heart failure. thromboembolism, and sometimes even to the sudden death of a cat.

    The genetic nature of hypertrophic cardiomyopathy in cats.

    Hypertrophy (thickening) of the walls can be secondary, that is, caused by some other disease (for example, hyperthyroidism or hypertension), but, in most cases, is idiopathic (without an established cause) and is considered primary disease- disease of the heart.

    Most cases of hypertrophic cardiomyopathy in humans have a genetic basis. Currently, more than 130 genetic mutations have been identified that cause a predisposition to develop this disease. There is evidence to suggest that many cases of hypertrophic cardiomyopathy in cats are also genetic.

    Specific genetic mutations identified for cats representing the Maine Coon and Ragdoll breeds. Mutations in the genes responsible for the production of the corresponding proteins in heart cells - MYBPC3 (from the English "cardiac myosin binding protein C" - cardiac myosin-binding protein), were found in cats of both these breeds suffering from hypertrophic cardiomyopathy. Although, it should be noted that mutations for each breed are different, in addition, similar mutations were found in cats of other breeds.

    Research is ongoing to identify other mutations that may contribute to the development of the disease not only in Maine Coons and Ragdolls, but also in other breeds of cats (for example, Norwegian Forest and Sphynx), among which the prevalence of hypertrophic cardiomyopathy is also increased.

    It is believed that the presence of defective genes increases the risk of developing hypertrophic cardiomyopathy in cats. Since chromosomes are always found in pairs in DNA, there is an increased risk in homozygous cats (with defective genes on each of the paired chromosomes) compared to heterozygous cats (one normal and one defective chromosome).

    The defective genes are the same in Maine Coon and Ragdoll cats, with some studies showing that at least 30-40% of affected cats carried one or both of the defective genes. However, the relationship between the presence of a mutation in the genes and hypertrophic cardiomyopathy is not unambiguous. Although the presence of a defect increases the risk of developing the disease, hypertrophic cardiomyopathy is not observed in all cats of these breeds that carry the defective genes. It is likely that there are other (as yet unidentified) gene defects, as well as environmental and biological factors affecting the development of hypertrophic cardiomyopathy in cats.

    Diagnosis of hypertrophic cardiomyopathy in cats.

    Measurement of the thickness of the walls of the chambers of the heart, carried out by ultrasound, can reveal hypertrophic cardiomyopathy in a cat. The matter is complicated by the fact that in some cats suffering from hypertrophic cardiomyopathy, ultrasound does not show abnormalities in the state of the heart in cases where the changes do not become serious. In such cases, special genetic tests are also needed for diagnosis. Such tests are now available in many veterinary clinics.

    For representatives of cat breeds such as Maine Coon and Ragdoll, for which hypertrophic cardiomyopathy is not uncommon, it is important to identify genetic predisposition to the disease. Ideally, cats of these breeds should be examined using both an ultrasound scan of the heart and genetic tests on blood samples or mouth swabs in specialized laboratories to accurately determine the genetic status of the animal.

    Prevention of hypertrophic cardiomyopathy in cats.

    It is recommended not to breed cats with confirmed hypertrophic cardiomyopathy with partners for whom genetic tests have shown positive result on both chromosomes (homozygous for this defect), since kittens will inevitably inherit the defect. The risk of disease in this case will be very high.

    The question of participation in selection of cats with a positive heterozygous status (one normal gene and one mutant) should be carefully considered. Such cats will inevitably pass on the defect to some part of their kittens. Although when choosing cats for breeding, there are many various factors, high prevalence clinical form Hypertrophic cardiomyopathy caused by gene defects in cat breeds such as the Maine Coon and Ragdoll means that one must be very careful in selecting such animals. to gradually reduce the presence of defective genes in these breeds, thus reducing the risk of developing hypertrophic cardiomyopathy.

    Hypertrophic cardiomyopathy in cats can manifest itself at any age, so a single cardiac ultrasound showing the absence of abnormalities is not a guarantee that there is no problem. Cardiologists recommend an annual echocardiogram for cats involved in breeding programs. It also makes sense to periodically examine cats no longer bred, as this may allow the identification of possible carriers of the defect among their offspring.

    In some countries, when registering breeding cats, along with the genetic status, the results of ultrasound are also indicated with comments from a veterinary cardiologist. Such information allows you to better select pairs for breeding cats.

    Hypertrophic cardiomyopathy in cats.

    Hypertrophic cardiomyopathy

    Hypertrophic cardiomyopathy (HCM) in cats dangerous disease, which occurs as a result of excessive thickening of the heart muscle. With thickening of the heart muscle, the myocardium loses its ability to relax, which leads to a decrease in the volume of circulating blood. This leads to disruption of the heart and, as a consequence, to the development of heart failure.

    HCM is among the most common heart diseases in cats.

    Causes

    The exact cause of hypertrophic cardiomyopathy has not yet been named. However, risk groups have been identified among the following cat breeds:

    – ragdoll

    - Maine Coon

    – sphinx

    - Scottish fold

    - British and American Shorthairs

    - Persian

    - Norwegian forest

    It is no coincidence that the Ragdoll and Maine Coon breeds are in the first place on this list. In these breeds, specific genes responsible for the occurrence of HCM have been identified. Currently, Ragdoll and Maine Coon cats can be tested for the presence of a dangerous gene.

    Hypertrophic cardiomyopathy is very insidious disease. The first symptom of this disease can be thromboembolism, pulmonary edema, and even death. Sometimes in the early stages of the disease, shortness of breath and fatigue may occur.

    The most common complication associated with HCM is thromboembolism. It can occur suddenly, against the background of apparent well-being. Blood clots arising as a result of the disease can block vital vessels in the animal's body. The femoral arteries are most often blocked. In this case, the first symptom of the disease is sudden paralysis pelvic limbs with severe pain syndrome. The cat screams, cannot stand on its hind legs.

    In these cases, your pet's life depends on the speed of circulation in veterinary clinic.

    Diagnostics

    Since HCM is very difficult to treat on late stages, then the disease should be detected as soon as possible. The sooner treatment is started, the greater the chance of a good prognosis.

    Methods for diagnosing HCM are as follows:

    - echocardiography (ultrasound examination of the heart)

    - chest x-ray

    – electrocardiography

    Echocardiography allows not only to detect the disease at an early stage, but also to understand whether there is a risk of its occurrence in the future. It is highly desirable for representatives of breeds that are at risk to undergo examination data even in the absence of visible symptoms of the disease. This is especially true for animals that will receive anesthesia.

    tribal breeding

    Animals in which the diagnosis of HCM is confirmed are withdrawn from breeding, in order to avoid the spread of this pathology.

    ICD

    Hypertrophic cardiomyopathy in cats

    Recently, the owners' treatment of cats in extremely serious condition (weakness, shortness of breath, paralysis of the pelvic limbs), pulmonary edema has become more frequent. And also the cases of death of animals from pulmonary edema after planned surgical measures (castration and sterilization) have become more frequent.

    What is the cause? The answer, as a rule, in these cases is HYPERTROPHIC CARDIOMYOPATHY.

    Hypertrophic cardiomyopathy (HCM) is a disease characterized by hypertrophy (thickening) of the wall of the left and/or occasionally right ventricle. Hypertrophy is often asymmetric, predominantly affecting the interventricular septum. Characterized by an irregular, chaotic arrangement of muscle fibers in the myocardium. zheludok

    HCMP is the most common cause heart failure, arterial thromboembolism and sudden death in cats.

    Hypertrophic cardiomyopathy can be primary or secondary.

    Primary HCM is a hereditary disease. Occurs - this disease is more common and is caused by mutations in the genes encoding the synthesis of myocardial contractile proteins.

    There are breeds that are predisposed to developing HCM. These are Maine Coons, Ragdolls, Sphynxes, British and American Shorthairs, Scottish Folds, Norwegian Forest Cats and some others. That is, kittens inherit this disease from their parents, and by the age of 1-3 years they may develop signs of heart failure. However, this is not a guarantee that your outbred Murka cannot have this pathology, what if her grandmother sinned with a British or Persian cat? kotje

    In secondary HCM, changes in the myocardium (heart muscle) develop under the influence of other diseases (for example, with hyperthyroidism). In such animals, signs of heart failure may develop either at a very old age, or not have time to develop at all.

    A distinctive feature of this disease is the significant complexity of early diagnosis. In a cat with HCM, the presence of the disease may present for the first time with pulmonary edema and/or death. That is, the signs will not develop for a long time and gradually, they will not be noticed by the owner, but severe manifestations of the disease will immediately and sharply develop.

    Often signs of heart failure (mostly shortness of breath - rapid breathing and/or breathing open mouth) a cat or a cat begins to demonstrate after stress, which is either transporting an animal or visiting a veterinary clinic for some reason not originally related to heart disease. Only a small percentage of owners of cats diagnosed with HCM can recall noticing that the cat was breathing heavily after exercise (provoked by the owner or another animal of the game). At the same time, the insidiousness of this pathology lies in the fact that during examination, auscultation, and even on a chest x-ray, in the absence of complaints, more than half of the animals with HCM may not have any abnormalities.

    The mechanism of development of this pathology lies in the fact that as the heart muscle thickens, the volume of the left ventricle decreases, because of this, the volume of blood pumped through it decreases. Because of this, in turn, pressure in the left atrium rises, it increases, pressure in the vessels of the lungs rises, and then, in later stages, pulmonary edema and / or hydrothorax develops (accumulation of free fluid in pleural cavity).

    It is possible to know reliably whether a cat has HCM or not only with echocardiography (ultrasound of the heart). Examination, auscultation, X-ray, ECG are additional research, and allow only to suspect that something was wrong.

    One of the frequent and extremely severe complications of HCM, which can appear against the background of the absolute apparent well-being of a cat, is thromboembolism (blockage of the vessel by a thrombus that has formed in the dilated left atrium). Most often, blockage occurs at the level of the femoral arteries, in which case the first symptom will be a sudden paralysis of the pelvic limbs and severe pain - the cat screams, drags its hind legs. In such cases, the count goes to hours, if not minutes. A very small percentage of patients recover, more often these are animals with mild symptoms. In a recovered animal, a relapse (a repetition of the situation) is highly likely in the coming months. Of course, the sooner the patient arrives at the veterinary clinic, the greater the chance of restoring blood flow.

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

    Echocardiography of a cat with no health complaints should be performed if:

    a) a cat of a risk group breed;

    b) you noticed that the cat is inactive or breathes through an open mouth after exercise;

    c) if one of the first two signs is combined with the fact that your pet needs general anesthesia.

    As mentioned above, the disease may not manifest itself in any way, the doctor at the appointment during examination before anesthesia does not reveal changes, while in a cat with HCM, general anesthesia can lead to serious complications in the form of pulmonary edema and death in the next hours or days after surgery. This applies primarily to young animals who have come to the clinic for castration. As a rule, these patients are about a year old, and the vast majority of those who were diagnosed with HCM showed no signs of the disease. The reason for conducting echocardiography in this case was either the doctor's alertness regarding the presence of HCM, or increased anxiety of the owners about the upcoming anesthesia. The detection of HCM in these animals is not absolute contraindication to general anesthesia, but it is more high degree anesthetic risk, this is a different approach to conducting general anesthesia, this is the need for a longer and more careful postoperative observation, the possibility of the owners in the coming days after the operation, in case of complications, urgently contact the clinic.

    We wish health to you and your pets!

    Deputy chief doctor veterinary center"Hope"

    Andreeva Ekaterina Alexandrovna.

    Cardiac pathologies in cats are classified as diseases of older age. The most common cardiomyopathies are myocardial lesions characterized by an increase in the size of the heart muscle. Of several varieties, hypertrophic cardiomyopathy (HCM) is more often diagnosed - an isolated myocardial lesion with hypertrophy (thickening) of the walls of the ventricles. Dilated cardiomyopathy (DCM) is also common, with pathological increase(dilation) of the heart chambers. The insidiousness of this disease is that it may not declare itself for a long time, suddenly falling on the pet with the full severity of symptoms. Therefore, the owner must be especially careful not to miss the first prerequisites. developing disease at your pet.

    Hypertrophic cardiomyopathy in cats is classified as primary or idiopathic. This means that she is independent disease that is not a complication or symptom of another disease. It presumably has a genetic nature, so it can be diagnosed in young individuals.

    In addition, in more rare cases, HCM may also be secondary. In this case, it appears as a consequence already an existing disease(diabetes, kidney dysfunction, thyroid disease).

    The mechanism of development of pathology

    Hypertrophy of the walls of the ventricles significantly impairs the work of the heart, which leads to stagnation of blood in the atria. Weak blood flow causes circulatory hypoxia ( oxygen starvation caused by circulatory disorders). Due to spasm of peripheral vessels, the risk of thrombosis increases. If left untreated, the disease can lead to heart failure, dangerous arrhythmias, and even death.

    Depending on the localization, HCM of the right or left ventricle is distinguished. In cats, lesions of the left ventricle and interventricular septum are more common.

    The pathological process slows down growth muscle tissue that forms the contractile system of the heart. The body compensates for this deficiency connective tissue thickening the walls of the myocardium. A kind of scars appear on the heart, reducing the size of the heart chambers. For the same reason, the elasticity of the organ also decreases.

    Reasons for the development of the primary form

    American researchers found that the primary nature of the disease is due to hereditary factor. They also concluded that cats and cats of the Maine Coon and Ragdoll breeds are most predisposed to pathological mutations. Later, the following breeds were added to the risk group for the incidence of primary hypertrophic myocardiopathy: Persian, Sphynx and Abyssinian.

    Currently, the fact that the presence of mutations in the genes increases the likelihood of the disease is considered proven, although the number of affected cats with defective genes was only 40% of the total number that took part in the study. Therefore, it is possible that there are also other hereditary disorders that increase the likelihood of the onset of the disease.

    The genetic nature of HCM is confirmed by cases of the disease of both parents and their children. It is based on inherited mutations in the genes responsible for the production of the myosin protein, which is responsible for the contractile function of the myocardium.

    The secondary (acquired) nature of the disease is caused by mutations of the same genes that occur under the influence of various adverse factors. environment and as a result of improper care.

    Causes of the secondary form of the disease

    Cats of the following breeds are susceptible to secondary forms of the disease: British Shorthair, Siamese, Russian Blue and Siberian. Secondary cardiomyopathy can develop in them as a complication of a whole series of ailments.

    1. Diseases of the heart and lungs:

    • congenital pathologies of the myocardium (bovine heart);
    • infectious diseases of the heart muscle;
    • arterial hypertension;
    • pneumonia of a different nature.

    2. Metabolic disorders:

    • amyloidosis (violation of protein metabolism, characterized by pathological deposition in the tissues of the amyloid protein);
    • hemochromatosis or pigmented cirrhosis (a liver disease that leads to impaired iron metabolism in the body).

    3. Endocrinological diseases:

    • acromegaly (abnormal production of growth hormone);
    • hyperthyroidism (overactive thyroid gland).

    4. Malignant neoplasms: lymphoma ( oncological disease lymphatic system).

    In addition, the provoking factors may be the wrong conditions for keeping the animal:

    • effects of prolonged stress.
    • Deficiency of essential trace elements in the diet. This is especially true for the amino acid taurine. Her enough has a beneficial effect on the heart muscle, reduces the load on the heart, protects the heart tissue from damage.
    • Chronic intoxication, the source of which can be long-term drug therapy, exposure to household chemicals, infection with helminths.

    Symptoms of the disease

    Hypertrophic cardiomyopathy is often characterized by a prolonged absence of symptoms. This course is explained by the good compensatory ability of the heart at a young age. But gradually the heart ceases to cope with the load, and in short time severe symptoms develop. If treatment is not started on time, the animal will not live long.

    Therefore, it is very important for the owner to take action as soon as he notices the first warning signs:

    • lethargy, loss of interest in outdoor games, hypodynamia. Body temperature may be lowered;
    • breathing problems, shortness of breath;
    • suffocation, fainting, signs of hypoxia begin as the disease becomes more severe;
    • blanching of mucous membranes. Over time, they acquire a bluish tint;
    • reflex cough during attacks of suffocation;
    • a characteristic posture of lack of air: the animal stands with its paws apart and its neck stretched out;
    • pulmonary edema, accumulation of fluid in the pleural cavity;
    • paralysis of the hind legs can occur in severe stages, as a symptom of severe thromboembolism;
    • sudden death of the animal may be the only symptom of the disease if it proceeded in latent form without obvious symptoms.

    Diagnosis of the disease

    The veterinarian makes a preliminary diagnosis while listening to heart sounds. The basis is systolic murmurs, disturbances heart rate(arrhythmias) and gallop rhythm (three-part rhythm, indicating myocardial insufficiency). Clarifying diagnostics includes instrumental research heart muscle:

    1. Chest x-ray. It will allow you to see pathologically dilated cardiac chambers and pleural effusion in the presence of pulmonary reactions.
    2. Electrocardiography is needed in order to detect the presence of arrhythmias and tachycardia. At this stage, the diagnosis of HCM can already be made.
    3. Ultrasound examination of the heart is the most informative method. It is needed in order to identify how thickened the wall of the myocardium. It is possible to determine the amount of blood flow and the presence of blood clots in the arteries.

    Cats with high risk diseases. It is determined using special genetic tests that help to see the individual predisposition of the individual.

    Treatment of the disease

    A complete cure of the disease can only come as a result of surgical intervention. Conservative treatment It is aimed at strengthening the heart muscle and reducing the load on it as much as possible. This will extend the life of the animal and improve its quality of life. Great importance has drug therapy, although it is equally important to take some care in keeping and caring for a sick animal.

    Medical therapy

    Cats with this disease receiving adequate treatment usually live quite a long time.

    Usually, the treatment regimen is based on drugs that reduce the load on the heart:

    1. Beta-blockers (Atenolol, Propranolol) reduce the number of contractions per unit of time, thereby reducing the organ's need for oxygen. Prevent arrhythmias.
    2. Calcium channel blockers (Diltiazem) by reducing the heart rate, help the hypertrophied wall of the myocardium to relax and partially recover.
    3. ACE inhibitors (enalapril) are used to treat heart failure and reduce high blood pressure.
    4. Diuretics (furosemide) are used to prevent congestion in the body, as the likelihood of pulmonary edema or pleural effusions is high.

    In the event that diuretics are not effective enough, excess fluid is removed from the body surgically, by puncturing the chest, in the area where there is an accumulation of pleural effusion.

    Content Features

    Particular attention during the care of a sick animal should be given to the following points: stressful situations, restriction of physical activity and therapeutic diet.

    Therapeutic diet

    To prevent congestion in the body, the animal is offered a salt-free diet. It helps maintain normal blood pressure.

    The diet must include medicinal feed with the amino acid taurine, which can also be given orally. This will significantly reduce the load on the animal's heart and prevent the development of heart failure and other unpleasant symptoms.

    Preventive measures

    It is difficult to prevent the primary form of the disease. Individuals at risk of such hereditary pathologies, it is recommended not to allow for breeding in order to exclude the possibility of the appearance of offspring with this pathology.

    Owners of Maine Coon and Ragdoll cats are advised to conduct a special test for their pets to determine its genetic status. Prevention of the secondary form of HPCM should be carried out throughout the life of the animal. It includes the following main steps:

    • regular preventive examinations in a veterinary clinic;
    • drawing up a balanced diet with a sufficient content of trace elements that strengthen the heart muscle (potassium, magnesium) and the amino acid taurine;
    • training the heart muscle by stimulating motor activity;
    • prevention of stressful situations.

    The owner can independently assess the condition of his pet. To do this, he must independently determine how many beats per minute his heart makes. A weakened pulse on the femoral artery (less than a hundred beats per minute) may indicate that the animal has heart failure or thromboembolism (blockage of large arteries).

    Hypertrophic cardiomyopathy in cats is a fairly common disease. Most effective measures helping to delay its onset or even prevent it altogether - constant prevention and early diagnosis. Therefore, these measures should never be neglected. In this situation, it is important not to waste time.