Mitral valve endocardiosis, also called myxomatous degeneration of the heart valves, can affect the mitral valve, which separates the left atrium and left ventricle, and the tricuspid valve on the right side of the heart. Most often - 60% of cases of damage to the mitral valve, 33% - degeneration of both valves, and 6% - only the tricuspid valve.

Endocardiosis of the mitral valve in dogs is an organic disease; during its course, degenerative changes occur in the structure of the connective tissue that makes up the chords and leaflets of this bicuspid valve. First, small nodules appear, which enlarge and connect with each other, eventually forming growths and plaques.

The tendinous strings or chords of the valve also become thicker and coarser. The valve itself thickens, becomes deformed, and its flaps no longer close tightly. A pathology of the mitral valve occurs; it does not cope well with its function, passing a stream of blood from the ventricle into the atrium (mitral regurgitation). This is how heart failure develops with all the ensuing consequences.

It must be said that mitral valve endocardiosis in dogs progresses very slowly, as the body uses powerful compensatory mechanisms to ensure efficient functioning of the heart and blood vessels.

It is believed that the disease debuts no earlier than the age of five, but usually the owners consult a doctor when the disease is already causing visible changes in the health of the four-legged animal. The older the dog, the more often endocardiosis is found in it.

Dogs of toy and medium-sized breeds are susceptible to this disease: dachshunds, toy poodles, Pomeranians, Chihuahuas, Cavalier King Charles spaniels. Large breeds include German Shepherds.

Mitral valve endocardiosis in dogs: symptoms

A disease such as mitral valve endocardiosis in dogs develops over years, but at first it does not make itself known. Only during preventive or routine examinations, for example before vaccination, can a doctor hear a heart murmur.

Cough is one of the main signs of this disease. Initially it occurs after exercise and feeding. Subsequently, the frequency of coughing increases. A cough occurs because the enlarged left atrium puts pressure on the bronchus, from which reflex signals go to the brain, which provokes a cough.

An enlarged abdomen and ascites are a consequence of heart failure, stagnation of blood in the systemic circulation, especially in the hepatic veins. The liquid component of the blood penetrates through the vessels into the abdominal cavity and accumulates there, which can be seen in the dog’s swollen belly.

Increased water consumption -

The dog's appetite usually does not suffer and remains good despite the illness.

Complications of mitral valve endocardiosis in dogs

With further progression of chronic heart failure, congestion in the lungs, intestines, and internal organs increases, which weakens their functioning. Under conditions of blood stagnation, bacteria inhabiting the mucous membranes are activated, thereby provoking the development of inflammatory processes in the lungs, bronchitis, and gastroenterocolitis.

Mitral valve endocardiosis in dogs: diagnosis

When diagnosing mitral valve endocardiosis in dogs, the doctor will listen to the dog’s heart and lungs, identify typical heart murmurs, and prescribe blood tests: general and biochemical. An X-ray examination is mandatory, in which you can see an enlarged shadow from the left atrium and ventricle, upward displacement of the bronchus due to pressure of the left atrium, pulmonary edema, congestion in the pulmonary veins, and an enlarged liver. Echocardiography can effectively identify a number of pathological changes in the heart.

Causes of endocardiosis in dogs

The causes of the disease are unclear, but the possibility of a hereditary nature has been suggested.

Type 1-2 - characterized by small lesions on the valves, which are small nodules on the free edges.

Type 3-4 - the nodules become larger and merge into plaques, which leads to thickening and deformation of the valves. The excess tissue causes the valve to bulge (prolapse) toward the atrium.

Thus, the mitral valve of insufficiency closes at the moment of systole (contraction) of the left ventricle and part of the stroke volume of blood flows back into the left atrium, cardiac output into the aorta decreases. The disease develops, the left atrium stretches and the pressure in it increases. Pulmonary hypertension develops.

The main complications are rupture of tendon strings, infective endocarditis, the occurrence of blood clots on the valve with the development of thromboembolism.

Initial development of the disease

But the onset of the disease significantly advances the appearance of its first symptoms. Cardiac ultrasound examinations of almost any older at-risk dog can detect signs of endocardial disease, but owners may not always notice the symptoms. As a rule, the first symptoms of endocardiosis appear after the age of 6 years, and the disease subsequently progresses with age.

The course of the disease has individual characteristics for each individual dog. Therefore, it is impossible to predict how the disease will manifest itself in the distant future, just as it is impossible to predict the speed of its development. Therefore, it is so important not only to identify the disease in a timely manner, but also to understand the characteristics of its course in a particular pet. The prescribed treatment is determined by the stage of the disease and the patient's condition.

Diagnosis of endocardiosis includes a complex of different methods and approaches. First of all, the veterinarian personally examines the dog. Modern high-quality equipment cannot replace the hands, eyes, ears and head of a doctor. Important information can be obtained through a conversation with the owner, examination of the dog, auscultation - listening to the heart, its sounds, noises and wheezing, as well as palpation and percussion (that is, feeling with fingers and gently tapping them).

Of the diagnostic methods, echocardiography (ECHO), which is an ultrasound examination of the heart using a special Doppler mode, plays a significant role. No other method is capable of providing such a quantity of data on the hemodynamic and anatomical individual characteristics of the heart.

ECG (electrocardiography), which is a technology for studying the electrical activity of the heart, is also widely used. Used to determine arrhythmias (heart rhythm disturbances) that may complicate the course of the underlying disease.

Cardiac pathology can trigger pathological processes and lead to diseases of other organs, primarily the liver, kidneys and brain. Due to the fact that endocardiosis is typical specifically for older animals, this category of patients often suffers from other diseases. Diagnosis of associated illnesses is sometimes carried out through a blood test.

Symptoms of respiratory diseases are often similar to symptoms of heart disease, in particular, signs of heart failure. For example, cough can be associated with both heart disease and respiratory tract diseases. The strength of the cough, its duration and other features can only suggest its cause, but it is impossible to make an accurate diagnosis without instrumental research. For this purpose, an X-ray method of examining the chest is used.

Symptoms of endocardiosis in dogs

At the initial stage, symptoms are not pronounced, but as the disease progresses, clinical signs become more noticeable.

CHF is classified according to the degree of development of symptoms. There are four functional classes of CHF.

• 1 functional class. Symptoms are absent or appear during severe psycho-emotional and physical stress.
• 2 functional class. Symptoms may appear with moderate exercise, but do not appear at rest.
• 3 functional class. Symptoms occur with moderate exercise and rarely at rest.
• 4 functional class. Symptoms appear at rest, and moderate physical activity leads to a sharp increase in symptoms.

Endocardiosis is a chronic degenerative valve disease in which the valve thickens and becomes deformed. This pathology almost never occurs in cats. The most commonly affected valves are the mitral (left) and tricuspid (right) valves in dogs. Isolated endocardiosis of the tricuspid valve is extremely rare.

Mitral valve endocardiosis may be hereditary. As a rule, it occurs in older dogs of small and medium breeds. Vulnerable breeds include dachshunds, poodles, cocker spaniels, and Yorkshire terriers. Degenerative collagen nodules form on the valve leaflets, which deform the leaflets.

The latter do not close tightly and allow reverse blood flow (so-called regurgitation occurs) from the ventricle to the atrium. The atrium stretches and increases in size. This stage of compensatory increase in atrial volume allows most patients to remain without symptoms of CHF for quite a long time.

With further progression of the disease, clinical signs of CHF appear: cough, exercise intolerance, shortness of breath, the risk of developing pulmonary edema - a condition that poses a serious threat to life. Various arrhythmias can complicate the disease. With severe endocardiosis, sudden rupture of the chords and even rupture of the atrium wall can occur, leading to death within a very short time.

According to the severity of regurgitation and the development of symptoms, 4 stages of mitral valve endocardiosis (MV) are divided:

• Stage 1. The MV is deformed, but the atrium is not enlarged. The animal has no clinical symptoms.
• Stage 2. The atrium and ventricle are slightly enlarged. There are no symptoms.
• Stage 3. Increased pressure in the left atrium. Moderate congestion in the lungs. The leading symptom is cough.
• Stage 4. Decreased pumping function of the heart. High risk of pulmonary edema. An increase in the size of the liver is often observed, and there may be ascites (free fluid in the abdominal cavity).

This disease has a very long asymptomatic period.

The main clinical signs are cough, shortness of breath (more than 30 breath/min), cyanosis/anemia of the mucous membranes, fainting (sudden, short-term loss of consciousness), general weakness, exercise intolerance, weight loss, ascites.

The most common symptoms of endocardiosis in dogs are coughing (in some cases with white foam that the dog swallows back), shortness of breath and exercise intolerance. Sometimes the dog becomes restless at night due to difficulty breathing when lying down. Also, in some cases, fainting occurs during physical activity or excitement, when coughing (so-called cough fainting) or associated with supraventricular tachyarrhythmia.

An increase in coughing attacks is observed after drinking and physical activity. Sustained diffuse pulmonary edema develops, leading to moist rales. Over time, damage develops not only to the left, but also to the right side of the heart, this entails dilation of peripheral veins, ascites, and enlargement of the liver. Due to myocardial degeneration and atrial stretching, premature contraction of the atria often occurs - paroxysmal tachycardia.

The peculiarity of this disease is that it occurs without symptoms for the first few years.

Holosystolic murmur when listening to the heart is more pronounced in the upper left part (between the 4th and 6th left ribs) and is typical for those patients who have mitral regurgitation. This noise can travel in all directions. Mild regurgitation is often inaudible or is heard exclusively in early systole (in this case, a protosystolic murmur occurs).

Physical activity or emotional arousal often leads to an increase in the intensity of soft noises during mitral regurgitation. In further stages of the disease, a more pronounced murmur is noted, but in those dogs that have massive regurgitation and severe heart failure, the murmur is soft or completely inaudible. In some cases it resembles a musical tone.

Some animals with chronic mitral valve disease have a mid-late systolic clicking sound, with or without a murmur. A galloping sound is sometimes heard in the upper left side of the heart in dogs with advanced disease. Tricuspid regurgitation usually causes a holosystolic murmur, which is heard more clearly in the left upper part of the heart.

Pulsation of the jugular vein, vibration of the chest on the right in the area symmetrical to the location of the heart on the left, as well as features of the noise heard in the projection of the tricuspid valve help to differentiate the radiating noise of mitral regurgitation from the noise of tricuspid insufficiency in the right half of the chest.

Pulmonary sounds when listening can be both normal and pathological. Harsh, intense breathing and crepitation sounds heard at the end of inspiration (most clearly heard in the ventral fields) occur with pulmonary edema. Due to rapidly developing pulmonary edema, expiratory and inspiratory wheezing and shortness of breath develop.

Some dogs with mitral regurgitation have abnormal pulmonary sounds, which are caused largely not by heart failure itself, but by concomitant respiratory disease. Sinus tachycardia is common in dogs diagnosed with congestive heart failure.

Diagnosis and prognosis of the disease

To accurately determine the animal’s condition, it is necessary to undergo a comprehensive cardiological examination. It includes anamnesis, physical examination, chest x-ray, echocardiography, and electrocardiogram.

The prognosis for life in dogs is quite variable and can range from several months to several years, depending on the stage of the disease, response to therapy and the owner’s willingness to carry out long-term therapeutic treatment. Treatment of CHF usually consists of strictly following an individually selected regimen of medications (pills).

Endocardiosis in dogs is a chronic degenerative disease of the atrioventricular valves. Also in the literature, this disease may be called myxomatous or mucoid valve degeneration.

In most cases, this disease occurs in dogs and most often affects males, who may have a more rapid progression of the disease.

The most vulnerable breeds at risk are the Cavalier King Charles Terrier, dachshunds, pugs, French bulldogs, poodles, chihuahuas, Yorkshire terriers, fox terriers, Spitz dogs, cocker spaniels, etc. It is believed that a dog that can be lifted with one hand is predisposed to atrioventricular diseases valves

Large breed dogs can also have this heart pathology, but in them it proceeds according to a different principle.

Most often the mitral valve is affected, less often the mitral and tricuspid valves, and even more rarely the tricuspid valve.

Causes of endocardiosis in dogs

The causes of the disease are unclear, but the possibility of a hereditary nature has been suggested.

There is a classification of AV valve endocardiosis:

Type 1-2 - characterized by small lesions on the valves, which are small nodules on the free edges.

Type 3-4 - the nodules become larger and merge into plaques, which leads to thickening and deformation of the valves. The excess tissue causes the valve to bulge (prolapse) toward the atrium.

Thus, the mitral valve of insufficiency closes at the moment of systole (contraction) of the left ventricle and part of the stroke volume of blood flows back into the left atrium, cardiac output into the aorta decreases. The disease develops, the left atrium stretches and the pressure in it increases. Pulmonary hypertension develops.

The main complications are rupture of tendon strings, infective endocarditis, the occurrence of blood clots on the valve with the development of thromboembolism.

Symptoms of endocardiosis in dogs

This disease has a very long asymptomatic period.

The main clinical signs are cough, shortness of breath (more than 30 breath/min), cyanosis/anemia of the mucous membranes, fainting (sudden, short-term loss of consciousness), general weakness, exercise intolerance, weight loss, ascites.

Diagnosis of endocardiosis in dogs

Inspection

Skin turgor and constitution are assessed. Color of mucous membranes, capillary refill rate. Presence of shortness of breath. Dyspnea is usually expiratory, i.e. on exhalation, short. Volume of the abdominal cavity.

Palpation

The pulse is felt in the femoral artery; it has a rapid rise and reduced filling or pulse deficiency. The frequency and rhythm of heart contractions and the intensity of the apical impulse are assessed. The percussion method determines the presence of free fluid in the abdominal and thoracic cavity.

Auscultation

When auscultating the lungs, harsh breathing and moist rales are heard. Auscultation of the heart reveals a holosystolic murmur, a murmur behind the first sound. There may be an increase in tone II, III (gallop sound). Mesosystolic click, sinus arrhythmia.

Electrocardiography (ECG)

Signs of left ventricular and left atrium hypertrophy. P – mitrale (increase in the P wave), expansion of the QRS complex, left-sided displacement of the EOS, increase in the amplitude of R. Signs of ipretrophy of the right atrium and right ventricle may occur. P – pulmonale (high tooth P), right-sided displacement of the EOS. Deep S wave (right ventricular overload). Rhythm disturbances - supraventricular extrasystoles, ventricular extrasystoles, atrial fibrillation.

Echocardiography (EchoCG)

There is damage to the mitral/tricuspid valve, thickening, nodularity, and hypercontrast of the valves. Rupture of tendon threads. Secondary signs are enlargement of the ventricles and/or atria. Hypertrophy of the free wall of the left ventricle. Mitral regurgitation. Systolic prolapse. The contractility fraction may be reduced.

Endocardiosis in a dog. EchoCG

Radiography

X-rays are used to assess the size of the heart and determine the enlargement of the left atrium and left ventricle. Enlargement of the right side of the heart is also possible. The significantly enlarged left atrium compresses the main bronchus. Cardiosternal contact increases. Congestion in the pulmonary veins is visualized. With interstitial pulmonary edema, the structure of the vessels is smoothed, and with alveolar edema, “cotton-wool” darkening occurs. Determine the presence of hydrothorax. In the abdominal cavity, pay attention to the liver; if there is stagnation in the systemic circulation, there will be hepatomegaly (liver enlargement) and ascites.

Endocardiosis in a dog. Radiography

Calculation coefficients are carried out:

1. Cardiothoracic index (CTI)
2. Buchanan coefficient.

Holter monitoring

A method by which daily monitoring of heart function is carried out.

Treatment of endocardiosis in dogs

Treatment is prescribed by a doctor depending on the stage of the disease, clinical signs and research results.

1. ACE inhibitors (enalapril, benazepril)
2. Diuretics (furosemide, spironolactone)
3. Cardiac glycosides (digoxin), in the presence of a permanent form of atrial fibrillation.
4. Pimobendan (Vetmedin, Hartmedin)
5. Calcium channel blockers (diltiazem)
6. Beta-blockers (metoprolol, nebivolol, etc.)
7. Load limitation
8. Diet.

In a city apartment, dog lovers are increasingly choosing representatives of miniature breeds. And rarely do the happy owners of a baby think about the diseases characteristic of this breed. Meanwhile, we can identify a whole group of diseases characteristic of small dogs. As a cardiologist, I would like to talk about a heart disease called Endocardiosis.

Endocardiosis is a disease of the heart valves that is common in small breed dogs. Most often, dogs in the so-called risk group suffer from this disease. These are Pekingese, Toy Terriers, Chihuahuas, Spitz, Yorkshire Terriers, Poodles, Dachshunds, Spaniels, Pugs, French Bulldogs. Damage to the valves is less common in large dogs, especially the terrier group, but, as a rule, the disease is not aggressive and rarely leads to serious consequences. As for dwarf breeds, there is a certain tendency: the lower the weight, the more common Endocardiosis is and, as a rule, it is more severe.

Endocardiosis is a disease of the second half of life and does not occur in young animals.

What is Endocardiosis? The heart is a kind of pump, consisting of 4 chambers, whose task is to ensure continuous blood flow. Valves are located between the chambers of the heart; their task is to allow blood to pass in only one direction. With endocardiosis, these valves gradually thicken and become deformed, stop closing tightly and begin to let blood pass in the opposite direction. The pressure in the chambers of the heart gradually increases. This automatically leads to increased pressure and stagnation in the upstream vessels. So, if the valve, which is located between the left atrium and the left ventricle, is changed, stagnation of blood develops in the pulmonary veins, which can lead to pulmonary edema. This is a life-threatening condition; if the animal is not given timely help, it may die. If there is pathology of the valve between the right atrium and the ventricle, ascites develops - accumulation of fluid in the abdominal cavity, this also requires treatment.

It has been noticed that in approximately 70% of cases, the valve located in the left side of the heart suffers. At 5% - the valve is on the right side. In 25%, both valves are affected. The clinical picture observed in Endocardiosis is also connected with this. Among the symptoms that the owner may notice, the most common are rapid breathing (shortness of breath), increased fatigue, an enlarged abdomen, and sometimes fainting. These signs may be present all together or separately. The most common symptom that develops earlier than others is shortness of breath. It is very important to pay attention to your dog’s breathing rate; normally, at rest, it does not exceed 27 per minute. If you notice rapid breathing in your pet, which is not associated with heavy physical activity, but appears after minor exertion or is observed at rest, you should immediately consult a veterinarian.

However, the disease begins to develop long before the first symptoms appear. In almost every dog ​​from the risk group of the older age group, an ultrasound examination of the heart can reveal signs of Endocardiosis, but owners do not always notice the symptoms of the disease. Usually, the first signs of Endocardiosis can be noticed after 6 years, and the disease progresses with age. Each dog has individual characteristics of the course of the disease. Despite the same physical and biological laws occurring in the body, it is impossible to predict in detail how the disease will behave in the long term and at what speed it will develop. Therefore, it is so important not only to detect the disease in a timely manner, but also to understand how it progresses in a given animal. Treatment is prescribed depending on the stage of the disease and the patient’s condition.

A combination of different methods and approaches is used to diagnose Endocardiosis. First of all, the doctor examines the animal. Not even the most modern device can replace the eyes, hands and head of a doctor. A lot of information can be gleaned from a conversation with the owner, examination, auscultation (listening to heart sounds, murmurs, wheezing), palpation and percussion (as in medical language palpating and gentle tapping with fingertips are called). A preliminary diagnosis is made already at the stage of examining the patient; further, special diagnostic methods can confirm the diagnosis and identify the features of the course.

First of all, we should mention Echocardiography (ECHOkg) - this is a study of the heart using ultrasound using a special Doppler mode. No other research method provides so much information about the anatomical and hemodynamic (hemodynamics - the movement of blood through the chambers of the heart and vessels) features of the heart.

In addition to Echocardiography, everyone knows such a research method as ECG (Electrocardiography). This is a way of recording the electrical activity of the heart. It is used to detect arrhythmia (heart rhythm disturbance) that may complicate the course of the underlying disease.

Heart pathology itself can trigger a cascade of pathological processes and cause diseases of other organs. Often such target organs are the kidneys, liver, and brain. In addition, Endocardiosis is more common in older animals; concomitant diseases are often detected in this category of patients. To diagnose concomitant pathologies, in some cases a blood test is required.

Respiratory tract diseases often have symptoms similar to heart failure. For example, a cough may be associated with both heart disease and respiratory tract pathology. Based on the strength, duration, and other features, the origin of the cough can be assumed, but it cannot be accurately diagnosed! To make a diagnosis in such cases, an X-ray examination of the chest is required.

What to do if you are the owner of a cute dog at risk? Do not panic! Knowledge is power!

The first visit to a cardiologist should be scheduled at age 6, even if you do not notice any abnormalities in your dog’s condition. Remember, it is necessary to identify the disease as early as possible! It may be too early to start treatment, but after the study, the doctor will definitely tell you when the next time it is necessary to check your friend’s heart, so as not to “miss” the disease.

Observe the animal's breathing. Learn to count your dog's resting breathing rate. If the disease has been identified, this very simple test will tell you when the animal's condition begins to deteriorate and you should make an unscheduled visit to the doctor.

If your animal is already receiving treatment, pay very close attention to all the recommendations of the veterinary cardiologist. Therapeutic cooperation between doctor and patient is very important; this is the key to good mutual understanding and successful treatment. Don’t be afraid to ask again if you don’t understand something. If for some reason you do not trust the doctor, do not self-medicate, look for another doctor. However, I would like to warn that changing clinics and doctors too frequently does not bring benefit to the patient or the desired effect.

Many owners ask: could they provoke the development of the disease? Endocardiosis is a genetically determined disease that does not depend on the conditions of keeping and feeding the animal. However, obesity can aggravate the disease. Maintaining a dog's normal weight is the most important responsibility of the owner!

Regarding the treatment of Endocardiosis: currently, the surgical method of replacing heart valves is not used in veterinary practice; treatment is carried out therapeutically. Treatment is aimed at eliminating the symptoms of heart failure, improving quality of life and increasing its duration. Of course, we cannot cure this disease, but we can help the animal and prolong its life!

/ Canine mitral valve endocardiosis (degenerative disease of the atrioventricular valves).

Canine mitral valve endocardiosis (degenerative disease of the atrioventricular valves).

Photo from Clinician's Brief magazine

Article from the book “Textbook of Veterinary Internal Medicine” Fourth Edition, 2009

Translation from English Vasiliev AV

Chronic degenerative atrioventricular valve disease is the most common cause of heart failure in dogs. This condition is also known as canine mitral valve endocardiosis, mucoid or myxomatous valve degeneration, or chronic valvular fibrosis. Because clinically significant degenerative valvular disease is rare in cats, this article will focus on chronic valvular disease in dogs. The mitral valve is the most commonly damaged valve, but degenerative changes are also found in the tricuspid valve in many dogs. However, isolated degenerative tricuspid valve disease is rare. Thickening of the aortic or pulmonary valve occasionally occurs in older animals, but rarely causes more than mild regurgitation.

Etiology and pathophysiology

The cause of canine mitral valve endocardiosis is unclear, but it is likely hereditary. The most frequently affected dogs are small to medium-sized breeds, middle-aged and older. The prevalence and severity of the disease increases with age. About a third of small breed dogs over 10 years of age suffer from this disease. The most vulnerable breeds include the Toy and Miniature Poodle, Miniature Schnauzer, Chihuahua, Pomeranian, Fox Terrier, Cocker Spaniel, Pekingese, Boston Terrier, Miniature Pinscher, Whippet and Cavalier King Charles Spaniel. A particularly high prevalence and early onset of the disease was noted in the Cavalier King Charles Spaniel, in which polygenic inheritance is assumed to be influenced by sex and age. This is reflected in the fact that the overall prevalence of mitral regurgitation murmurs and degenerative valve disease is similar in male and female dogs, but in males there may be a more rapid progression of the disease. Some large breed dogs are also affected and the prevalence of the disease may be higher in German Shepherds.

Multiple factors may be involved, including collagen degeneration, increased valvular stress, and endothelial function. Pathological changes in valves with endocardiosis of the mitral valve of dogs develop gradually with age. Early lesions appear as small nodules on the free edges of the valve; they become larger and merge into plaques, which thicken and deform the valve. Histological changes are described as myxomatous degeneration. Collagen within the damaged leaflets degenerates and acidic mucopolysaccharides and other substances accumulate within the leaflets, leading to nodular thickening, deformation and weakening of the valve, as well as its tendon strings. Excess tissue between the chordal insertions often bulges ( prolapse) like a parachute or balloon towards the atrium. Mitral valve prolapse may be important in the pathogenesis of this disease, at least in some breeds.

The damaged valve gradually begins to leak, since its valves are definitely not co-opted. As the lesions progress, valvular insufficiency (regurgitation) becomes clinically evident. Endocardial fibrosis may form; and, in patients with advanced disease, partial or even complete atrial rupture. Chronic valvular insufficiency is also associated with intramural coronary arteriosclerosis, microscopic intramural myocardial infarctions, and focal myocardial fibrosis. The length of time over which these changes cause clinical myocardial dysfunction is unclear; however, impairment of myocardial contractility occurs late in this disease. Interestingly, older dogs without valvular disease also have similar vascular lesions.

Pathophysiological changes in canine mitral valve endocardiosis are associated with volume overload on the damaged side of the heart after the valve (or valves) become less efficient. Regurgitation usually develops slowly over months and years. Mean atrial pressure remains fairly low during this time, except in situations with a sudden increase in the volume of regurgitation (eg, chord rupture). As valve degeneration progresses, more and more blood flows inefficiently back into the atrium from the ventricle, reducing blood flow into the aorta. Compensatory mechanisms increase blood volume to meet the body's circulatory needs, including increased sympathetic activity, decreased vagal tone, and activation of the renin-angiotensin-aldosterone system. . The amount of natriuretic peptide increases; higher concentrations of sedial natriuretic peptide are associated with marked left atrial enlargement and severe congestive heart failure. The damaged ventricle and atrium enlarge to accommodate the increased volume of regurgitation and provide the required stroke volume of the heart; In an attempt to normalize the resulting stress on the heart walls, eccentric myocardial hypertrophy develops.

These compensatory changes in heart size and blood volume allow most dogs to remain asymptomatic for long periods of time. Massive left atrium enlargement may develop before any signs of heart failure appear, and some dogs never show clinical signs of heart failure. The tolerability of the disease is influenced by the rate of progression of regurgitation and its degree. stretching of the atria and contractility of the ventricles. A gradual increase in atrial, pulmonary venous and capillary hydrostatic pressure stimulates a compensatory increase in pulmonary lymphatic flow. Overt pulmonary edema develops when the pulmonary lymphatic system is insufficient. Tricuspid regurgitation may be severe enough to cause right-sided congestive heart failure. Increased pulmonary vascular pressure secondary to chronic left-sided congestive heart failure may also contribute to the development of right-sided heart failure.

Ventricular pumping function is maintained fairly well until late in the disease in many dogs, even in the presence of significant signs of congestion. However, chronic volume overload reduces myocardial contractility over time. The mechanism of myocardial dysfunction may involve free radical damage as well as neurohormonal activation. Reduced contractility increases ventricular dilatation and valvular regurgitation and therefore may exacerbate congestive heart failure. Assessment of left ventricular contractility in animals with mitral regurgitation is complicated by the fact that the most commonly used clinical indices (eg. echocardiographic shortening fraction, ejection fraction) overestimate contractility. Echocardiographic assessment of the end-systolic volume index may be useful. This index suggests that myocardial function is normal or slightly decreased in most dogs with canine mitral valve endocardiosis. Other echo/Doppler indices may also help assess left ventricular systolic and diastolic function.

Complicating factors

Although canine mitral valve endocardiosis usually progresses slowly, certain complicating factors can precipitate the development of acute clinical signs in dogs with compensated disease (Table 1). For example, tachyarrhythmias may be severe enough to cause decompensation of congestive heart failure, syncope, or both. Frequent atrial extrasystoles, paroxysmal atrial tachycardia, or atrial fibrillation can reduce ventricular filling time and cardiac output, increase myocardial oxygen demand, and increase pulmonary congestion and edema. Ventricular tachyarrhythmias also occur, but more rarely.

Sudden rupture of pathologically altered chordae tendineae rapidly increases the volume of regurgitation and can provoke rapidly developing pulmonary edema within a few hours in a previously compensated or even asymptomatic dog. Symptoms of low cardiac output may also occur. Sometimes a torn chorda tendineum is an incidental finding (on echocardiogram or autopsy), especially if it is a second or third order chord. Massive enlargement of the left atrium can cause compression of the left main bronchus and stimulate persistent cough, even in the absence of congestive heart failure. In addition, massive enlargement of the left (or right) atrium can lead to partial or complete rupture of the wall. Rupture of the atrium wall usually causes cardiac tamponade; Apparently this complication occurs more often in male miniature poodles, cocker spaniels and dachshunds. In most of these cases there is severe valve pathology, massive enlargement of the atrium and, often, a torn chordae tendineus of the first order.

Clinical manifestations

Canine mitral valve endocardiosis may not cause clinical symptoms for several years, and some dogs never develop symptoms of heart failure. In those dogs that have these symptoms, they represent decreased exercise capacity and evidence of pulmonary congestion and pulmonary edema. Reduced exercise tolerance and cough or tachypnea on exertion are the most common initial complaints among owners. As pulmonary congestion increases and interstitial edema develops, the respiratory rate increases. Cough is more common at night or early in the morning, and also with increased activity. Severe pulmonary edema results in obvious respiratory distress and usually a wet cough. Symptoms of severe pulmonary edema may develop gradually or acutely. Intermittent episodes of symptoms of pulmonary edema, alternating with periods of compensated heart failure over months and years, are common. Episodes of transient weakness or acute collapse (syncope) may occur due to arrhythmias, cough, or atrial rupture. Symptoms of tricuspid regurgitation, usually overshadowed by symptoms of mitral regurgitation, include ascites; respiratory distress due to pleural effusion and, rarely, swelling of the subcutaneous tissues. Abdominal congestion can cause gastrointestinal symptoms.

Holosystolic murmur, best heard in the area of ​​the apex of the heart on the left (from the fourth to the sixth intercostal space on the left) is typical for patients with mitral regurgitation. Noise can travel in any direction. Mild regurgitation may be inaudible or the murmur may be caused only in early systole (protosystolic). Exercise or excitement often increases the intensity of the soft murmurs of mitral regurgitation. . Louder murmurs are associated with advanced disease, but in dogs with massive regurgitation and severe heart failure, the murmur may be soft or even inaudible. Sometimes the noise can be similar to a musical tone. Some dogs with chronic mitral valve disease have a mid-to-late systolic clicking sound, with or without a murmur. S3, a galloping sound, may be heard at the left apex in dogs with advanced disease. Tricuspid regurgitation typically produces a holosystolic murmur, better heard at the right apex. Features that help differentiate the murmur of tricuspid regurgitation from the radiating murmur of mitral regurgitation on the right parts of the chest, include pulsation of the jugular vein, vibration of the chest above the projection of the apex of the heart on the right and features of the noise in the projection of the tricuspid valve.

Pulmonary sounds may be normal or abnormal. Accented, harsh breathing and crepitus sounds at the end of inspiration (especially in the ventral fields of the lungs) are observed with the development of pulmonary edema. Rapidly developing pulmonary edema causes widespread inspiratory and expiratory wheezing and shortness of breath. Some dogs with mitral regurgitation have abnormal lung sounds caused by concurrent pulmonary or airway disease rather than congestive heart failure. Dogs with congestive heart failure are prone to sinus tachycardia; dogs with chronic lung disease often have sinus arrhythmia and a normal heart rate. Pleural effusion causes decreased pulmonary sounds ventrally.

On physical examination, there may be no other abnormalities or they may be insignificant. Peripheral capillary perfusion and arterial pulse strength are usually normal, although pulse deficits may occur in dogs with tachyarrhythmias. Palpable vibration of the chest in the projection of the heart is detected with loud (grade 5-6/6) noises. Stretching of the jugular vein and its pulsation are not characteristic of isolated mitral regurgitation. In animals with tricuspid insufficiency, jugular venous pulsation is observed during ventricular systole; it is more obvious after physical or emotional stress. Distension of the jugular vein occurs due to increased filling pressure of the right side of the heart. Jugular vein pulsation and distension are more obvious with cranial abdominal compression (positive hepatojagular reflux). Ascites or hepatomegaly may be evident in dogs with congestive right-sided heart failure.

Diagnostics

Radiography

Chest x-rays of canine mitral valve endocardiosis usually reveal some degree of left atrium and left ventricular enlargement that progresses over months to years. As the size of the left atrium increases, dorsal displacement of the main bronchus may occur. Marked enlargement of the left atrium causes compression of the left main bronchus. Fluoroscopy may demonstrate dynamic collapse of the main bronchus during coughing or even quiet breathing in such animals. Extreme enlargement of the left atrium can develop over time, even without clinically obvious heart failure. Enlargement of the right heart to varying degrees occurs with chronic tricuspid regurgitation, but it may be masked by changes in the left heart and lungs associated with concurrent microvascular dysplasia.

When left-sided congestive heart failure occurs, pulmonary venous congestion and interstitial pulmonary edema occur; this may be followed by progressive interstitial and alveolar pulmonary edema. Although cardiogenic pulmonary edema in dogs is typically hilar, dorsocaudal, and bilaterally symmetrical, some dogs exhibit an asymmetrical distribution. The presence and severity of pulmonary edema does not necessarily correlate with the degree of cardiomegaly. Acute, severe regurgitation (eg, chordae tendineus rupture) may cause severe edema in the presence of minimal left atrial enlargement. Conversely, slowly progressive mitral regurgitation may cause marked left atrial enlargement in the absence of congestive heart failure. Early symptoms of right-sided heart failure include distension of the caudal vena cava, visualization of lines between the lung lobes, and hepatomegaly. Overt pleural effusion and ascites occur in advanced heart failure.

Electrocardiography

The ECG may be suggestive of enlargement of the left or both atria and left ventricle, although it is often within normal limits. Dogs with severe tricuspid regurgitation sometimes show signs of right ventricular enlargement. Arrhythmias, especially sinus tachycardia, supraventricular premature beats, paroxysmal or persistent supraventricular tachycardia, ventricular premature beats, and atrial fibrillation are often detected in dogs with severe disease. These arrhythmias may be present in decompensated congestive heart failure, weakness, or syncope.

Echocardiography

Echocardiography reveals increased atrial and ventricular size secondary to atrioventricular valve regurgitation. This increase can be pronounced, depending on the degree of volumetric overload. Increased movements of the interventricular septum and the free wall of the left ventricle are observed with mitral regurgitation, when contractility is not impaired, the shortening fraction is high and the value of the mitral-septal separation index is reduced. Although the size of the ventricle in diastole increases, the systolic size remains normal until the onset of myocardial failure. Determination of the end-systolic volume index can help assess myocardial function. The thickness of the ventricular wall in canine mitral valve endocardiosis is usually normal. With severe tricuspid regurgitation, paradoxical movement of the interventricular septum can occur simultaneously with dilatation of the right atrium and right ventricle. Pericardial fluid (blood) is observed when the left atrium is ruptured and cardiac tamponade may be apparent. Small amounts of fluid in the pericardium may also add to the symptoms of right-sided congestive heart failure.

Damaged valve leaflets are thickened and may appear knotty. Smooth thickening is characteristic of a degenerative disease (endocardiosis). Conversely, rough and irregular valve vegetations are characteristic of bacterial endocarditis; however, differentiation between them may not be possible using echocardiography alone. Systolic prolapse, involving one or both valve leaflets, is common in degenerative atrioventricular valve disease. A torn chorda tendineus or leaflet tip is sometimes seen moving toward the atrium during systole. The direction and extent of the disrupted blood flow can be seen using color Doppler. The size of the area of ​​impaired blood flow provides a rough estimate of the severity of regurgitation.

The converging flow assay (PISA) is considered by some to be a more accurate way to assess the severity of mitral regurgitation. Other Doppler techniques can be used to assess ventricular systolic and diastolic function. The maximum flow velocity during tricuspid regurgitation indicates whether pulmonary hypertension is present and how severe it is.

Clinicopathological findings

Clinical laboratory findings may be normal or reflect changes associated with congestive heart failure or a concurrent noncardiogenic disorder. Other diseases that cause symptoms similar to those that develop with congestive heart failure include tracheal collapse, chronic bronchitis, bronchiectasis, pulmonary fibrosis, pulmonary neoplasia, pneumonia, pharyngitis, heartworm disease, dilated cardiomyopathy, and bacterial endocarditis.

Treatment and prognosis

Drug therapy for canine mitral valve endocarditis is used to control symptoms of congestive heart failure, maintain cardiac function, and correct excessive neurohormonal activation that contributes to the development of the disease. Drugs that reduce left ventricular size (eg, diuretics, vasodilators, positive inotropes), may reduce the volume of regurgitation by reducing the size of the mitral annulus. Drugs that promote arterial vasodilation increase cardiac output and reduce the volume of regurgitation by lowering systemic blood pressure. As the disease progresses, frequent re-evaluation and treatment adjustments become necessary. In many dogs with severe mitral regurgitation, clinical compensation can be maintained for months or years with adequate treatment. Although symptoms of congestive heart failure develop gradually in some dogs, others experience acute onset of severe pulmonary edema or syncope. Intermittent episodes of decompensation in dogs receiving long-term treatment for congestive heart failure can often be successfully managed. Treatment should take into account the patient's clinical status and the nature of the complicating factors. Surgical interventions such as mitral annulus repair, other valve repair techniques, and mitral valve replacement may be used in some patients, but are not widely available.

Asymptomatic atrioventricular regurgitation

Dogs that do not show clinical signs of the disease are generally not indicated for drug therapy. There is currently limited convincing evidence that ACE inhibitors or other drugs slow the onset of symptoms of congestive heart failure in asymptomatic dogs. It is also unclear whether dogs with severe cardiomegaly may benefit from drugs that correct pathological remodeling.

It is important to educate the owner about the disease process and early symptoms of congestive heart failure. It is probably wise to avoid high-salt diets, reduce body weight in obese dogs, and avoid prolonged intense exercise. A moderately salt-restricted diet may be beneficial. Periodic reassessment (eg every 6-12 months) of heart size and function is advisable, and also blood pressure. Other pathologies also need to be corrected.

Congestive heart failure with mild or moderate symptoms.

When clinical symptoms are observed due to emotional or physical activity, various treatment modalities are used (Table 2). The degree of aggressiveness of therapy is influenced by the severity of clinical symptoms and the nature of complicating factors. When it is unclear whether respiratory symptoms are caused by early congestive heart failure or a non-cardiogenic disease, a trial of furosemide therapy is indicated ( eg 1-2 mg/kg orally 2-3 times a day). With cardiogenic pulmonary edema, improvement usually occurs quickly.

Furosemide is used to treat dogs with radiographically documented pulmonary edema and/or severe clinical signs. If the edema is severe, higher doses and more frequent administration are used. Once symptoms of failure are controlled, the dose and frequency of furosemide are gradually reduced to the lowest effective dose and frequency used in chronic therapy. Furosemide monotherapy (without ACE inhibitors or other drugs) is not recommended for long-term treatment of heart failure.

ACE inhibitors are commonly recommended for the treatment of mitral valve endocardiosis in dogs with initial symptoms of heart failure. The ability of these drugs to modulate neurohormonal responses to heart failure appears to be their main advantage. Chronic therapy with ACE inhibitors may improve exercise capacity and reduce cough and dyspnea, although it is unclear whether they increase life expectancy in affected dogs.

Pimobendan is also increasingly used to treat moderate to severe congestive heart failure. This drug has positive inotropic, vasodilator, and other effects. Its beneficial effects may exceed those of ACE inhibitors, although they are often used together. Digoxin, with or without pimobendan, is often used adjunctly in the treatment of congestive heart failure secondary to severe mitral regurgitation. The baroreceptor sensitizing effect of digoxin may be more beneficial than its weak positive inotropic effect. Marked left ventricular enlargement, apparent decreased myocardial contractility, or recurrent episodes of pulmonary edema despite treatment with furosemide and other drugs are indications for the use of digoxin. Digoxin is also indicated for rate control heart rate in dogs with atrial fibrillation and as an antiarrhythmic drug for the treatment in some cases of frequent atrial premature contractions or supraventricular tachycardia. To prevent its toxicity, moderate doses and measurement of serum concentrations are required.

Moderate salt restriction (eg diets for dogs with kidney disease or for old dogs) is recommended at the onset of the disease. Further salt restriction can be achieved with diets designed for dogs with heart failure. Limiting exercise is important if there are symptoms of congestive heart failure. During the chronic, compensated stage, regular, mild to moderate intensity exercise (without causing excessive respiratory effort) is recommended. . Vigorous exercise is not recommended. Antitussive therapy may be useful in dogs without pulmonary edema but with a persistent cough caused by compression of the main bronchus by the left atrium (eg hydrocone bitartrate, 0.25 mg/kg orally 2-3 times daily or butorphanol 0 .5 mg/kg orally 2-4 times a day).

Severe congestive heart failure

Severe pulmonary edema and shortness of breath at rest require urgent treatment. Aggressive diuretic therapy with parenteral furosemide (eg, 2–4 mg/kg IV every 1–4 hours initially), oxygen support, and cage confinement is initiated as early as possible. Careful handling is important because additional stress may precipitate cardiac and respiratory arrest. Chest x-rays and other diagnostic procedures are delayed until the animal's respiratory system is more stable.

Vasodilator therapy is also indicated. If adequate monitoring equipment is available, intravenous sodium nitroprusside can be used to rapidly dilate the veins and arteries; however, blood pressure should be closely monitored to prevent hypotension. Another option is oral hydralazine. Its direct and rapid arterial vasodilating effect increases blood movement and reduces regurgitation; however, oral administration may cause stress. A reduced dose is used in animals already receiving ACE inhibitors. Amlodipine is an alternative arterial vasodilator, but it has a much slower onset of action. Topical nitroglycerin may also be used in an attempt to reduce pulmonary venous pressure by direct venodilation.

If positive inotropic therapy is indicated, pimobendan (or digoxin) can be started (or continued if previously prescribed) as soon as acute dyspnea subsides. Digoxin may have a beneficial effect in the presence of paroxysmal atrial tachycardia or atrial fibrillation. Although it will take several days to reach therapeutic blood concentrations with oral maintenance doses, intravenous digitalization is not recommended in most cases. Diltiazem or beta blockers may be prescribed instead of (or in addition to) digoxin if supraventricular tachyarrhythmia requires treatment. Dogs that require more intensive inotropic support or that have persistent hypotension may be given intravenous dobutamine, dopamine, or amrinone.

Adjunctive therapy often includes mild sedation to reduce anxiety (eg butorphanol or morphine). Bronchodilators (theophylline, aminophylline) may be useful if bronchospasm is caused by severe pulmonary edema; these drugs may help support respiratory muscle function, although the effectiveness of this is unclear.

Thoracentesis is indicated in dogs with moderate to large volumes of pleural effusion to improve pulmonary function. Ascites that impairs respiratory function should also be addressed. In some cases, treatment of ventricular tachyarrhythmias is necessary. Careful monitoring is important to adjust treatment and identify drug toxicity or side effects (eg azotemia, electrolyte abnormalities, hypotension, arrhythmias).

Once the initial condition is stabilized, prescriptions are adjusted over several days or weeks to determine optimal long-term therapy. Furosemide is titrated to the lowest doses (and longest intervals) that control symptoms of congestive heart failure. Prescription of ACE inhibitors is recommended for continuation of therapy if hydralazine or sodium nitroprusside were used as the initial vasodilator. Since the effect of the initially prescribed hydralazine wears off gradually, the first dose of the ACE inhibitor should be 2 times less than the standard starting dose (i.e., 0.25 mg /kg orally). Treatment with ACE inhibitors can be started at a standard dose a short time after discontinuation of the sodium nitroprusside infusion.

Long-term treatment of the refractory form of the disease

When congestive heart failure due to canine mitral valve endocardiosis becomes refractory, therapy is intensified or adjusted according to the individual needs of the patient. Recurrent pulmonary edema in some animals responds to an increased dose of furosemide and limited mobility for several days. The dose of furosemide can then be reduced to the previous one or be slightly higher, if possible. The dose of ACE inhibitors should be as high as possible, if this has not been done previously (for example, enalapril should be given not once, but twice a day).

Pimobendan and/or digoxin may be added if this has not been done previously. The dose of digoxin is not increased above the standard dose, unless subtherapeutic blood concentrations are established. Spironolactone can be additionally used if this has not been done previously. This aldosterone antagonist may reduce the severity of recurrent refractory pulmonary edema or effusions, as well as have beneficial effects on myocardial remodeling. Other diuretics with different mechanisms of action or the combination of spironolactone with hydrochlorothiazide may be useful.

Continuous monitoring is important, especially renal function and serum electrolyte concentrations. Restriction of salt in the diet may be increased. If doses of ACE inhibitor and furosemide are already maximal, low doses of hydralazine (eg.

0.25 to 0.5 mg/kg orally 2 times a day) or amlodipine (eg 0.005 to 0.2 mg/kg orally 1 time a day), and blood pressure should be monitored.

Intermittent tachyarrhythmias may contribute to the development of decompensated congestive heart failure, as well as episodes of transient weakness or syncope. Syncope caused by coughing, atrial rupture, or other causes of decreased cardiac output may also occur. Despite the periodic recurrence of symptoms of congestive heart failure, many dogs with chronic atrioventricular valve regurgitation can enjoy a good quality of life for several years after the first symptoms of heart failure appear.

Patient monitoring and reassessment

For long-term therapy to be successful, the owner must be educated about the disease process, the clinical symptoms of deficiency, and the medications needed to control them. As the disease progresses, adjustments in treatment are necessary (eg, adjusting the doses of medications used or adding additional ones). Some common potential complications of chronic degenerative atrioventricular valve disease can cause decompensation (Table 1). Monitoring at home is important to identify early signs of decompensation. Respiratory (+/- cardiac) rate levels can be monitored periodically while the dog is quietly resting or sleeping; a persistent increase in them may signal early decompensation.

Asymptomatic dogs should be re-evaluated at least annually as part of a routine cardiac protection program. The frequency of re-evaluation of dogs being treated for heart failure depends on the severity of the disease and the presence of complicating factors. Dogs with newly diagnosed or decompensated congestive heart failure should be assessed more frequently (over a period of days to weeks) until their condition is stable. Dogs with chronic heart failure whose symptoms are well controlled may be evaluated less frequently, usually several times a year. Medication support, the dog’s attitude to treatment, medications and doses received, and diet should be discussed with the owner at each appointment.

A general physical examination, with particular attention to cardiovascular parameters, is important at each visit. If arrhythmias or unusually low or high heart rates are detected, an ECG is indicated. When an arrhythmia is suspected but not detected on a routine ECG, an ambulatory ECG (eg, 24-hour Holter monitoring) may be indicated. The rate and pattern of breathing are also recorded; a chest x-ray is advisable if abnormal lung sounds are heard or if the owner reports cough, other respiratory symptoms, or an increased resting respiratory rate. Other causes of cough should be considered if neither pulmonary edema nor venous stasis is seen on radiography and if the resting respiratory rate is not increased. Compression of the left main bronchus by the enlarged left atrium may stimulate a dry cough. Antitussives are helpful, but should only be prescribed after other causes of cough have been ruled out.

Echocardiography may demonstrate chordal rupture, progressive cardimegaly, or worsened myocardial function. Frequent monitoring of serum electrolyte concentrations and renal function is important. Other routine blood and urine tests should also be performed periodically. Digoxin blood concentrations in dogs receiving it should be measured 7-10 days after initiation of treatment or dose adjustment. Additional measurements are recommended if symptoms of digoxin toxicity are detected or if kidney disease or electrolyte imbalance (hypokalemia) is suspected.

The prognosis in dogs that exhibit clinical signs of canine mitral valve endocardiosis is quite variable. With adequate therapy and careful management of complications, some dogs do well for more than four years after the first symptoms of heart failure appear. Some dogs die with the first episode of rapid pulmonary edema. Life expectancy for most symptomatic dogs ranges from a few months to several years.

Table 1
Potential complications of canine mitral endocardiosis

Causes of acute pulmonary edema

• arrhythmias
  • frequent atrial extrasystoles
• paroxysmal atrial/supraventricular tachyarrhythmia
  • atrial fibrillation
  • frequent gastric tachyarrhythmias
  • exclude toxicity of drugs (eg digoxin)
• rupture of chordae tendineae
• iatrogenic fluid overload
  • Excessive volumes of intravenous fluid or blood given
  • liquids high in sodium
• Prescribing an inappropriate or unpredictable drug
• insufficient treatment for this stage of the disease
• increased heart work
  • physical effort
  • anemia
  • infection/sepsis
  • hypertension
  • diseases of other organs (eg lungs, kidneys, liver, endocrine system)
  • increased temperature and humidity of the environment
  • excessively cold external environment
  • other environmental stressors
  • high salt intake

Causes of decreased cardiac output or weakness

• arrhythmias (see above)
• rupture of chordae tendineae
• syncope due to cough
• left atrial rupture
  • intrapericardial bleeding pericardial tamponade
• increased myocardial work (see above)
• secondary right-sided heart failure
• myocardial degeneration and poor contractility

table 2
Guidelines for the treatment of canine mitral endocardiosis

Asymptomatic stage (modified AHA/ACC stage B)

• Owner education (information about the disease and early symptoms of heart failure)
• Standard cardiac support
  • blood pressure measurement
  • plain chest x-ray (+/- ecg) and re-examination annually
  • maintaining normal body weight/conditioning
  • regular low- to moderate-intensity physical activity
  • avoid intense physical activity
  • heartworm testing and prevention in endemic areas
• Treat other existing diseases
• Avoid salty foods; consider diets with moderate salt restriction
• Consider ACE inhibitors if there is significant left atrial (+/- left ventricular) enlargement; adjunctive treatment to correct neurohormonal activation may or may not be clinically beneficial

Symptoms of heart failure are mild or moderate (modified AHA/ACC stage C, chronic)

• Same as for the asymptomatic stage, and
• Furosemide, if necessary
• ACE inhibitors (or pimobendan)
• Pimobendan (can be used with or without ACE inhibitors)
• +/- digoxin (indicated for atrial tachyarrhythmias, including fibrillation)
• +/- additional diuretics (spironolactone, hydrochlorothiazide)
• Antiarrhythmic therapy if necessary
• Completely limiting physical activity until symptoms improve
• Moderate salt restriction
• Home monitoring of respiratory rate (+/- heart rate)

Severe symptoms of acute congestive heart failure

• Oxygen support
• Caging and careful handling
• Furosemide (higher doses, parenteral)
• Vasodilator therapy
• Consider intravenous sodium nitroprusside, or
• Oral hydralazine or amlodipine, +/- topical nitroglycerin
• +/- butorphanol or morphine
• Antiarrhythmic therapy if necessary
• +/- positive inotropes:
• If myocardial insufficiency is established, intravenous administration of drugs can be used
• Once the patient has been stabilized, therapy with pimobendan +/- oral digoxin may be used.
• +/- bronchodilator
• Thoracentesis for large collections of pleural effusion

Treatment for chronic relapsing or refractory heart failure (modified AHA/ACC stage D)

• Ensure that treatment for stage C is administered at optimal doses and intervals, including furosemide, ACE inhibitors, pimobendan and/or digoxin, spironolactone
• Rule out systemic arterial hypertension, arrhythmias, anemia and other complications
• Increase dose/frequency of furosemide; if necessary, they can be reduced over a few days after symptoms have subsided
• Forced restriction of mobility until symptoms subside
• Add pimobendan if not prescribed
• Increase the dose/frequency of the ACE inhibitor (from 1 to 2 times a day)
• add digoxin if not prescribed; monitor its serum concentration; increase dose only if subtherapeutic concentration is established
• Add (or increase dose) a second diuretic (eg, spironolactone, hydrochlorothiazide)
• Additional afterload reduction (eg amlodipine or hydralazine); monitor blood pressure
• Further limiting salt intake; Make sure your drinking water is low in sodium
• Thoracentesis or abdominal centesis if necessary
• Eliminate arrhythmias if present
• Consider treatment with sildenafil for secondary pulmonary hypertension (eg, 1-2 mg/kg every 8-12 hours)
• Consider a trial of a bronchodilator or cough suppressant

Endocardiosis is a heart valve disease common in small breed dogs. It is the latter who constitute the risk group for this disease. These breeds include Toy Terriers, Pekingese, Spitz, Chihuahuas, Poodles, Yorkshire Terriers, Spaniels, Dachshunds and French Bulldogs. Less commonly, this disease affects large dogs, mainly the terrier group, but in them it usually occurs less aggressively than in small dogs, and only in rare cases does it cause serious consequences. With regard to dwarf breeds, the following correlation is observed: the smaller the weight of the dog breed, the more often representatives of this breed develop endocardiosis and the more severe this disease is in them.

General idea of ​​the disease

Endocardiosis is a disease exclusively of the second half of a dog's life; it does not occur in young animals.

What is endocardiosis essentially? The heart is a biological pump, consisting of 4 chambers in dogs, as in humans, and providing continuous blood flow. Between its chambers there are valves that allow blood to flow in only one direction. During endocardiosis, these valves gradually become deformed, thicken, and no longer close tightly enough, beginning to let blood back through. As a result, the pressure inside the heart gradually increases. This leads to stagnation of blood and increased pressure in the vessels located near the heart.

In particular, changes in the valve located between the left ventricle and the left atrium lead to stagnation of blood in the veins of the lungs, which causes pulmonary edema. Pulmonary edema is a life-threatening condition and if not treated promptly, the dog can die. If there is pathology of the valve between the right ventricle and the right atrium, ascites occurs - a pathological accumulation of fluid in the abdominal cavity, which also requires treatment.

About 70% of cases of the disease affect only the valve located on the left side of the heart. Only 5% of cases of the disease affect only the right valve, another 25% of cases are associated with damage to both valves. Clinical manifestations of endocarditis are associated with this. The most frequently noted symptoms by dog ​​owners are shortness of breath, rapid breathing, abdominal enlargement, increased fatigue, and fainting. All of these symptoms may appear at once, or one or more of them. The most common symptom, appearing earlier than others, is shortness of breath. You should pay close attention to your dog's breathing rate, which normally should not exceed 27 breaths per minute at rest. If you notice rapid breathing that is not associated with increased physical activity, you should immediately contact a veterinarian.

Initial development of the disease

But the onset of the disease significantly advances the appearance of its first symptoms. Cardiac ultrasound examinations of almost any older at-risk dog can detect signs of endocardial disease, but owners may not always notice the symptoms. As a rule, the first symptoms of endocardiosis appear after the age of 6 years, and the disease subsequently progresses with age.

The course of the disease has individual characteristics for each individual dog. Therefore, it is impossible to predict how the disease will manifest itself in the distant future, just as it is impossible to predict the speed of its development. Therefore, it is so important not only to identify the disease in a timely manner, but also to understand the characteristics of its course in a particular pet. The prescribed treatment is determined by the stage of the disease and the patient's condition.

Diagnosis of endocarditis includes a complex of different methods and approaches. First of all, the veterinarian personally examines the dog. Modern high-quality equipment cannot replace the hands, eyes, ears and head of a doctor. Important information can be obtained through a conversation with the owner, examination of the dog, auscultation - listening to the heart, its sounds, noises and wheezing, as well as palpation and percussion (that is, feeling with fingers and gently tapping them). Preliminary diagnosis is carried out at the stage of examining the dog, then the diagnosis is confirmed and individual characteristics of the course of the disease are identified using special diagnostic methods.

Of the diagnostic methods, echocardiography (ECHO), which is an ultrasound examination of the heart using a special Doppler mode, plays a significant role. No other method is capable of providing such a quantity of data on the hemodynamic and anatomical individual characteristics of the heart.

ECG (electrocardiography), which is a technology for studying the electrical activity of the heart, is also widely used. Used to determine arrhythmias (heart rhythm disturbances) that may complicate the course of the underlying disease.

Cardiac pathology can trigger pathological processes and lead to diseases of other organs, primarily the liver, kidneys and brain. Due to the fact that endocardiosis is typical specifically for older animals, this category of patients often suffers from other diseases. Diagnosis of associated illnesses is sometimes carried out through a blood test.

Symptoms of respiratory diseases are often similar to symptoms of heart disease, in particular, signs of heart failure. For example, cough can be associated with both heart disease and respiratory tract diseases. The strength of the cough, its duration and other features can only suggest its cause, but it is impossible to make an accurate diagnosis without instrumental research. For this purpose, an X-ray method of examining the chest is used.

Actions to take if you have a risky breed

What to do if you become the owner of a cute dog of a “risky” breed? First of all, don't panic.

It is necessary to schedule the first visit to a veterinarian-cardiologist after the dog reaches 6 years of age, even if there are no pathologies in its condition. It is necessary to detect the disease as early as possible. It is likely that it will be too early to start treatment, but after the examination, the veterinarian will definitely inform you when exactly your pet’s heart will need to be checked again, so as not to “miss” the disease.

You should observe your dog's breathing, learning to count its frequency at rest. If the disease has been identified, such an extremely simple study will determine the moment when the pet’s condition worsens, after which a visit to the veterinarian will be necessary.

If your dog is already undergoing treatment, you must be extremely attentive to the recommendations of your veterinarian-cardiologist. In general, cooperation between the patient and the doctor plays a vital role and is a guarantee of effective treatment. Don't be afraid to ask if something is unclear. If for any reason the veterinarian is not trustworthy, you should not self-medicate, it is better to look for another veterinarian. But it should be noted that frequent changes of doctors worsen the effectiveness of treatment.

Many owners wonder: can the dog owner himself provoke the development of this disease? The answer here is negative, since endocardiosis is a genetically determined disease and does not depend in any way on the conditions in which the dog is kept. But a factor such as dog obesity can lead to aggravation of the disease. Therefore, maintaining the correct weight of the pet is an important responsibility of the owner.

To treat endocardiosis, there are currently no surgical methods to replace heart valves, so treatment is carried out exclusively by therapeutic methods and is aimed at eliminating the manifestations of heart failure, improving the quality and length of life. This disease remains incurable, but veterinary medicine can help the pet and make its life longer.

Predisposition

The highest predisposition to this disease and its earliest onset were noted in the Cavalier King Charles Spaniel breed. Presumably there is polygenic inheritance, which is influenced by age and gender. The risk group also includes the following breeds: miniature poodle, chihuahua, miniature schnauzer, fox terrier, Pomeranian, Pekingese, cocker spaniel, whippet, miniature pinscher. Of the larger breeds, endocarditis occurs in German shepherds, Dalmatians and Ridgebacks.

Pathophysiology

The development of endocardiosis in dogs involves the progression of 2 pathological processes: mitral regurgitation and valve degeneration.

Valvular degeneration consists of its abnormal contractions, leading to protrusion of the leaflets, which causes an increase in pressure on the leaflets directly and indirectly. Regurgitation leads to endothelial dysfunction by promoting fibroblast growth and causing subendothelial deposition of glycosaminoglycans followed by fibrosis. Over time, all these processes lead to disruption of the valve structure, as well as to an increase in regurgitation, while high pressure as a result of prolapse and changes in the structure of the leaflets cause rupture of tendon strings (chordae), which aggravates regurgitation. At the final stage of the disease, the heart valve becomes a fibrous, narrowed valve, most often with rupture of the tendon strings.

The progression of valve damage leads to insufficiently tight closure of the valves and regurgitation, the development and severity of which is directly determined by the speed and degree of damage to the heart valves. Compensatory mechanisms lead to expansion of the ventricle and atrium, eccentric hypertrophy and an increase in the strength and frequency of heart contractions, as well as activation of neurohormonal systems. Ventricular dilatation at the same time increases regurgitation and leads to secondary valvular insufficiency.

As the disease progresses, compensation for regurgitation becomes impossible, leading to decreased cardiac output and increased venous pressure, as well as subsequent pulmonary edema or ascites. Pulmonary hypertension can result from left-sided heart disease.

Symptoms of canine endocardiosis

The most common symptoms of endocarditis in dogs are coughing (in some cases with white foam, which the dog swallows back), shortness of breath and exercise intolerance. Sometimes the dog becomes restless at night due to difficulty breathing when lying down. Fainting also occurs in some cases during physical activity or anxiety, during coughing (so-called cough fainting) or associated with supraventricular tachyarrhythmia.

An increase in coughing attacks is observed after drinking and physical activity. Sustained diffuse pulmonary edema develops, leading to moist rales. Over time, damage develops not only to the left, but also to the right side of the heart, this entails dilation of peripheral veins, ascites, and enlargement of the liver. Due to myocardial degeneration and atrial stretching, premature contraction of the atria often occurs - paroxysmal tachycardia.

The peculiarity of this disease is that it occurs without symptoms for the first few years.

Holosystolic murmur when listening to the heart is more pronounced in the upper left part (between the 4th and 6th left ribs) and is typical for those patients who have mitral regurgitation. This noise can travel in all directions. Mild regurgitation is often inaudible or is heard exclusively in early systole (in this case, a protosystolic murmur occurs).

Physical activity or emotional arousal often leads to an increase in the intensity of soft noises during mitral regurgitation. In further stages of the disease, a more pronounced murmur is noted, but in those dogs that have massive regurgitation and severe heart failure, the murmur is soft or completely inaudible. In some cases it resembles a musical tone.

Some animals with chronic mitral valve disease have a mid-late systolic clicking sound, with or without a murmur. A galloping sound is sometimes heard in the upper left side of the heart in dogs with advanced disease. Tricuspid regurgitation usually causes a holosystolic murmur, which is heard more clearly in the left upper part of the heart.

Pulsation of the jugular vein, vibration of the chest on the right in the area symmetrical to the location of the heart on the left, as well as features of the noise heard in the projection of the tricuspid valve help to differentiate the radiating noise of mitral regurgitation from the noise of tricuspid insufficiency in the right half of the chest.

Pulmonary sounds when listening can be both normal and pathological. Harsh, intense breathing and crepitation sounds heard at the end of inspiration (most clearly heard in the central fields) occur with pulmonary edema. Due to rapidly developing pulmonary edema, expiratory and inspiratory wheezing and shortness of breath develop.

Some dogs with mitral regurgitation have abnormal pulmonary sounds, which are caused largely not by heart failure itself, but by concomitant respiratory disease. Sinus tachycardia is common in dogs diagnosed with congestive heart failure. Dogs with chronic pulmonary disease often have sinus arrhythmia with a normal heart rate. Due to pleural effusion, lung sounds are weakened.

Clinical examination

During auscultation of a dog that is not currently showing any clinical signs, the following is revealed:

• systolic click (at an early stage): high pitch, the presence of a sharp sound between the heart sounds S1 and S2; this sound is often mistaken for an additional heart tone (which causes the appearance of a gallop rhythm);
• systolic apical murmur of the tricuspid or mitral valve;
• early or late soft holosystolic murmur, corresponding to moderate or severe regurgitation.

A complete examination of the dog reveals:

• loud heart murmur (levels 4-6/6);
• weakened 1st tone;
• ventricular arrhythmias, in particular atrial fibrillation, indicating a severe course of the disease and a poor prognosis;
• weak and rare pulse observed in the femoral artery;
• pallor of the mucous membranes;
• tachypnea, orthopnea, respiratory distress;
• wheezing, pulmonary edema;
• pink foam in the nostrils, as well as in the nasopharynx in the presence of acute and severe pulmonary edema;
• ascites, swelling of the neck veins (in case of right-sided heart failure).

Complicating factors

Canine endocardiosis is a slowly progressive disease, but certain factors can lead to acute symptoms in those dogs that have a compensated form of the disease. In particular, the severity of tachyarrhythmias may be strong enough to lead to decompensation of cardiac congestive failure. Paroxysmal atrial tachycardia, frequent atrial extrasystoles and atrial fibrillation can reduce the filling time of the cardiac ventricles, increase the need for oxygen in the heart muscle, and aggravate pulmonary edema. Ventricular tachyarrhythmias also occur, but they are less common.

Due to the sudden rupture of the chordae tendineae, which have undergone pathological changes, the volume of regurgitation quickly increases, which can lead to the rapid development of pulmonary edema - within a few hours in a completely devoid of any symptoms or a compensated dog. In addition, there are symptoms of heart failure. In some cases, a torn chorda tendineus is discovered by chance (on an echocardiogram), primarily when it is a chord of the 2nd or 3rd order.

Due to significant enlargement of the left atrium, compression of the main left bronchus sometimes occurs and a persistent cough is stimulated. This can occur even in the absence of heart failure. Also, a significant increase in the left or right atrium can lead to a complete or partial rupture of the wall, which leads to cardiac tamponade. This complication is most often observed in miniature poodles, dachshunds and cocker spaniels, especially in males.

Treatment and prognosis for endocardiosis

Drug treatment for canine endocardiosis is aimed at controlling the symptoms of congestive heart failure, supporting heart function, and correcting excessive neurohormonal activity that contributes to the development of the disease. Drugs that reduce the size of the left heart ventricle (diuretics) reduce the volume of regurgitation and the size of the fibrous mitral annulus. Drugs that promote arterial vasodilation increase cardiac activity and reduce the amount of regurgitation by reducing blood pressure.

The progression of the disease leads to the need for regular assessment of the dog’s condition, as well as periodic adjustments to treatment. In many dogs with severe mitral regurgitation, compensation is maintained for several years with proper treatment. Heart failure develops slowly in a significant proportion of affected dogs, while in other dogs there is severe, acute pulmonary edema.

Alternating episodes of decompensation in animals undergoing long-term treatment for heart failure can often be successfully reversed. When treating, it is necessary to take into account the clinical status of the animal and the factors that in a particular case complicate the course of the disease. Surgeries such as mitral annulus repair and other methods of mitral valve replacement and valve restoration may be used in some cases, but are not widely available.

About the author: Anna Aleksandrovna Maksimenkova

Practicing veterinarian in a private clinic. Directions: therapy, oncology, surgery. Read more about me in the "About Us" section.