Norms of valvular regurgitation in dogs. Mitral valve endocardiosis in dogs: stages, signs and treatment

Abbreviations:

CHF - cardiovascular failure, CHF - congestive heart failure, ECG - electrocardiographic study, ECHO - echocardiographic study, ACE inhibitors - angiotensin-converting enzyme inhibitors, SNK - capillary filling rate

In this article, we will continue the consideration of heart diseases, the most common in the practice of a veterinarian.

One of the most common cardiac pathologies in older dogs age group is endocardiosis of the atrioventricular valves, in particular the mitral valve. Frequency of occurrence this disease depends on the proportion of representatives different breeds in a particular region and on average accounts for 70% of heart pathologies in dogs.

Endocardiosis - myxomatous degeneration of atrioventricular valves of a non-inflammatory nature. This condition is also known as mucoid, myxomatous valvular degeneration, or chronic valvular fibrosis. The disease is characterized by the accumulation of glucosaminoglycans and fibrosis of the leaflets and tendon strings.

According to autopsy studies of Buchanon, Buchanan, (1979), valve pathology has the following distribution: 62% endocardiosis of the mitral valve only; 1% only tricuspid; 33% - both.

Predisposition:

The highest predisposition and early onset of the disease was noted in Cavalier King Charles Spaniel dogs. Polygenic inheritance is assumed with the influence of sex and age. Representatives of such breeds also belong to the risk group: toy and miniature poodle, miniature schnauzer, chihuahua, Pomeranian, Fox Terrier, Cocker Spaniel, Pekingese, Boston Terrier, Miniature Pinscher, Whippet. Of more large breeds endocardiosis can occur in Dalmatians, German Shepherds, Ridgebacks.

Pathophysiology:

The development of this disease includes the progression of two pathological processes: valve degeneration and mitral regurgitation.

Valvular degeneration. The primary defect is abnormal valve contractions, which lead to leaflet prolapse, which in turn increases pressure on the leaflets directly (improper leaflet closure) and indirectly (increased regurgitant flow). Regurgitation and pressure on the valve causes endothelial dysfunction and activates fibroblast growth, leading to subendothelial glycosaminoglycan deposition and fibrosis. In the future, these processes entail violations of the valve structure and an increase in regurgitation, and increased pressure due to prolapse and changes in the structure of the valves lead to rupture of the tendon strings (chords), aggravating the degree of regurgitation. In the final stage, the valve is a thin, fibrous and narrowed leaflets, mainly with signs of rupture of the tendon strings.

Mitral regurgitation and congestive heart failure. Valve damage progresses, causing insufficient closure of the leaflets, leading to regurgitation, the severity and development of which directly depends on the degree and speed of heart valve damage. As a result of compensatory mechanisms, there is an expansion of the atrium and ventricle, eccentric hypertrophy, as well as an increase in strength, frequency of contraction and activation of neurohormonal systems. In turn, ventricular dilatation further increases regurgitation, provoking secondary valvular insufficiency.

As the disease progresses, compensation for regurgitation is no longer possible, resulting in a decrease in cardiac output and increased venous pressure followed by pulmonary edema (left-sided CHF) or ascites (right-sided CHF). Pulmonary hypertension may develop as a consequence of left-sided heart failure.

Symptoms:

With the development of endocardiosis, the most frequent symptoms is a cough (sometimes the dog coughs up a little white foam, which it swallows back), shortness of breath appears, intolerance to physical exertion, the animal may become restless at night due to difficulty breathing when lying down. There may be fainting due to physical activity or excitement, as well as when coughing (cough syncope) or associated with supraventricular tachyarrhythmia.

Coughing fits become more frequent, especially after drinking or exercise. A persistent diffuse pulmonary edema giving crepitus or moist rales on auscultation. Gradually, not only the left, but also the right side of the heart is affected, which leads to the expansion of peripheral veins, liver enlargement, and ascites. Atrial stretch and myocardial degeneration is often the cause of premature atrial contraction or paroxysmal tachycardia.

It should be noted that this disease can be asymptomatic for several years.

Clinical examination:

On auscultation of a dog without clinical symptoms reveal:

– Systolic click (early stage): high-pitched, sharp sound between S1 and S2 heart sounds. This sound is often mistaken for an additional heart sound (causing the occurrence of a gallop rhythm).

– Apical systolic murmur of the mitral or tricuspid valve.

– Mild, early or late cholosystolic murmur (grades 1-2/6) corresponding to moderate to severe regurgitation.

Examination of a dog with CHF reveals:

– Loud heart murmur (level 4-6/6).

– Weakening of the 1st tone.

- Most often, supraventricular arrhythmias are detected. Atrial fibrillation indicates a severe form of the disease with a poor prognosis.

– Weak pulse on femoral artery and pulse deficit.

– Increased CNS and mucosal pallor (Fig. 1).

– Tachypnea, respiratory distress and orthopnea.

– Wheezing when breathing, sometimes obvious pulmonary edema.

- Pink foam in the nostrils and nasopharynx in acute, severe pulmonary edema (fulminant CHF).

- Ascites and swelling of the jugular veins (with right-sided heart failure).

Rice. 1. Pale mucous membranes

Electrocardiographic study

On electrocardiographic examination, there are various signs depending on the stage of the disease. An increase in the left atrium is characterized by dilated and bifurcated P waves (P-mitrale) (Fig. 2, 3). An increase in the left ventricle may be manifested by an increase in the voltage of the R wave in the 2nd lead, a left-sided shift electrical axis hearts. With the development of dystrophic changes in the myocardium, extended, jagged QRS complexes can be recorded. Unfortunately, ECG is an insensitive method for making a diagnosis, but the most effective test for determining arrhythmias. The presence of tachyarrhythmia, atrial fibrillation, or ventricular depolarization (Fig. 4) on an ECG usually indicates a severe course of the disease.

Rice. 2. P wave expansion

Rice. 3. Expansion and notching of the P wave

Rice. 4. Single left ventricular extrasystole

X-ray examination

In endocardiosis, the size of the heart varies from normal to left-sided or generalized cardiomegaly (Fig. 5, 6). An increase in the left atrium in the lateral projection is indicated by a dorsal displacement of the distal quarter of the trachea and splitting of the main bronchi; dorsoventral projection shows accentuation of the angle between the main bronchi; a double shadow at the six o'clock position, where the caudal margin of the atrium continues outside the left ventricle, and the left atrial appendage protrudes at the one to three o'clock positions. With the development of left-sided heart failure, the pulmonary veins are wider than the accompanying pulmonary artery; Air bronchograms are typical, but not pathognomonic, of cardiogenic pulmonary edema. In general, congestion and edema are perihilar, throughout the lung field, eventually showing changes.

Rice. 5. Lateral projection. Severe cardiomegaly with expansion of the shadow of the heart in the craniocaudal direction and with a displacement of the trachea dorsally

Echocardiographic study:

Two-dimensional echocardiographic scanning reveals eccentric hypertrophy of the left ventricle, dilatation of the left atrium (the degree of dilatation depends on the stage of the disease), significant deformation and thickening of the mitral valve leaflets (with severe disease), rupture of the tendon filaments (rare complication). Significant mitral valve prolapse and an echo from a ruptured tendon filament, rupture of the left atrial wall (a rare complication), a moderate amount of effusion in the pericardial cavity, and a significantly dilated left atrium are determined.

When scanning in M-mode, eccentric hypertrophy of the left ventricle is noted, an increase in end-diastolic size without thickening rear wall, hyperkinesia of the interventricular septum with volume overload, the average value of the shortening fraction is 40%, which decreases in the final stage of the disease - myogenic dilatation.

Complications of endocardiosis:

The most severe complications of endocardiosis are left atrial rupture and avulsion of the chord. In particular, atrial rupture can lead to the rapid development cardiogenic shock with a lethal outcome.

Differential diagnosis:

Scroll differential diagnoses includes: congenital mitral valve dysplasia, mitral regurgitation secondary to primary cardiomyopathy (DCMP), infective endocarditis mitral valve, systemic hypertension.

Forecast:

In the SVEP study, conducted on Cavalier King Charles Spaniel dogs that had a heart murmur in the absence of heart enlargement, the median time to onset of symptoms of heart failure was well over 3 years. The article by Borgarelli et al (2008) showed that in a more mixed group of dogs with mitral regurgitation that did not suffer from clinical manifestations of heart disease, less than 50% of such animals died from complications of this disease during the period of dynamic observation.

Treatment:

Asymptomatic stage (modified AHA/ACC stage B)

• Owner education (information about the disease and early symptoms of heart failure)
• Measurement blood pressure blood
• Plain chest x-ray (/-ECG) and re-examination annually
• Maintain normal body weight/condition
• Regular physical activity of low or moderate intensity
• Avoid intense physical activity
• Avoid salty foods; consider diets with moderate salt restriction
• Administering an ACE inhibitor to asymptomatic patients showing progressive cardiomegaly may slow deterioration, but this hypothesis has not yet been fully proven.

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

• Furosemide if needed
• Amlodipine
• ACE inhibitors
• Pimobendan (may be used with or without ACE inhibitors)
• /-digoxin (indicated for atrial tachyarrhythmias, including fibrillation)
• /- additional diuretics (spironolactone, hypothiazide)
• Antiarrhythmic therapy if necessary
• Limitation of physical activity
• Home monitoring of respiratory rate (/- heart rate)
• Severe symptoms of acute congestive heart failure
• Oxygen Support
• Furosemide (higher doses, parenteral)
• Amlodipine?
• Vasodilator therapy
• Antiarrhythmic therapy if needed
• /- positive inotropes
• Once the patient is stabilized, oral pimobendan/-digoxin therapy may be used.
• /- bronchodilator
• Thoracocentesis for large pleural effusions

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

• increase dose/frequency of furosemide; if necessary, they can be reduced within a few days after the symptoms subside
• increase dose/frequency of ACE inhibitor (from 1 to 2 times a day)
• increase the dose of the second diuretic
• thoracocentesis or abdominal centesis if necessary
• antiarrhythmics if needed
• sildenafil for secondary pulmonary hypertension (eg 1-2 mg/kg every 12 hours)
• trial treatment with a bronchodilator or antitussive

Patient monitoring:

In asymptomatic dogs, x-rays are taken when the first murmur is detected and then every 6 to 12 months thereafter to check for progressive cardiomegaly.

The frequency of re-examination of animals treated for heart failure depends on the severity of the disease and on the presence of complicating factors.

Patients with newly diagnosed or decompensated congestive heart failure should be evaluated more frequently. After an episode of congestive heart failure, once a week during the first month of treatment; repeat chest x-ray and ECG at first weekly check-up and at subsequent visits if any changes are observed on general physical examination.

Dogs with chronic heart failure whose symptoms are well controlled may be evaluated less frequently, usually several times a year.

Conclusions:

Endocardiosis is the most common heart disease in dogs. small breeds, which indicates the need and importance of a planned cardiac examination, even in asymptomatic patients. This is especially true for representatives of the Cavalier King Charles Spaniel breed, in which the genetic nature of the disease has been proven. Early referral to a specialist timely diagnosis and appropriate treatment will slow down the development of the disease and thereby improve the quality of life of the animal.

In this article we will talk about a very common cardiac disease dogs, which representatives of small breeds are susceptible to, is mitral valve endocardiosis.

What is mitral valve endocardiosis?

Endocardiosis, or myxomatous degeneration of the mitral valve, is a chronic disease that is characterized by changes in the valvular apparatus of the heart in dogs. Not only the mitral valve separating the left atrium and left ventricle, but also the tricuspid valve between the right atrium and ventricle can be subject to change.

Most often, dogs of such breeds as Spitz, Yorkshire Terrier, Toy Poodle, Chihuahua, Toy Terrier, Dachshund, Pekingese, Miniature Schnauzer, Fox Terrier, Cavalier King Charles Spaniel, Cocker Spaniel and many other dwarf and medium breeds (usually up to 15-20 kg by weight).
It should be noted that the disease occurs in chronic form and may take years to develop. Endocardiosis manifests itself from the age of 5 summer age, but more often changes begin from 8 to 12 years.

The causes of the disease are not clearly known. There is an opinion about hereditary factor. The process of collagen degeneration starts (collagenopathy, chondrodystrophy). Therefore, very often in a sick animal with endocardiosis, pathologies associated with the trachea can also be detected in parallel.

Stages of endocardiosis:

• Stage 1 - small scattered areas of nodules at the ends of the leaflets
• Stage 2 - nodules increase in size, their number increases, they merge
• Stage 3 - further fusion of nodules, plaque-like formations are found, the valves thicken, they become less elastic, the tendon filaments are affected, ultimately the entire valvular apparatus
• Stage 4 - the valves are compressed, bent, the tendon threads may break, the valves resemble a parachute.

Due to the deformation of the valves, they begin to pass an excess volume of blood back into the left atrium, the latter stretches and pressure increases in it. All this leads to compression of the main left bronchus and the classic "heart" cough. In addition, due to high blood pressure in the left atrium, pressure in the pulmonary veins rises, which leads to left-sided heart failure. As a result, stagnation occurs in the pulmonary circulation and pulmonary edema occurs. On final stages The development of the disease can also affect the right half of the heart. In the future, this will lead to pulmonary hypertension, or to the accumulation of fluid in abdominal cavity(ascites).

Symptoms of endocardiosis that should not be ignored:

• Cough is the very first and feature, which owners notice in their pet, but very often ignore, referring to a cold or "choking on something." Cough occurs at night or early in the morning. It may be associated with pulling on the leash or emotional arousal. But do not forget that cough, as a symptom, can manifest itself in many other diseases.
• Reduced endurance to physical exertion - on a walk in the usual mode, the dog quickly gets tired, stops, it needs more time to recover.
• Shortness of breath - the dog begins to breathe very often even during rest or sleep.
• Fainting (syncope) - can manifest itself in the form of a fall of the animal for a few seconds, a pose on its side with limbs stretched forward is characteristic. Fainting may be due to severe cough or due to violation heart rate. If such syncope is frequent, there is a risk of sudden death
• Decreased appetite, cachexia (weight loss) - multiple organ failure against the background of reduced cardiac output.

Diagnosis of endocardiosis.

To diagnose endocardiosis, a veterinary cardiologist needs to conduct a series of examinations:

• Careful history taking
• Auscultation of the heart and chest
• ECHOCG
• Radiography
• Blood test (biochemical, electrolytes, general clinical)

Depending on the stage and development of the disease is selected individual treatment: ACE inhibitors, aldosterone antagonists, diuretics, positive inotropes, antiarrhythmics, PDE-5 inhibitors, metabolic agents. Sometimes you have to resort to an oxygen chamber and pumping out the effusion from the abdominal cavity (abdominocentesis).

Unfortunately, it is impossible to cure endocardiosis, but if you adhere to strictly prescribed therapy, you can eliminate the symptoms (cough, shortness of breath, lethargy, etc.), improve the quality of life for your pet, help the “weakened” heart cope with its functions, thereby protecting other organs from insufficiency of their blood supply.

Prognosis: from favorable and cautious to unfavorable, it all depends on the stage of the disease and how the animal "responds" to therapy.

MITRAL VALVE ENDOCARDIOSIS, CASE STUDY

Govorina Nadezhda Gennadievna

c6th year student, faculty of biotechnology and veterinary medicine, IGSHA,

G. Irkutsk

Ludypov Tsydenzhap Ludypovich

scientific supervisor, doctor veterinary sciences, professor of IGSKhA,

G. Irkutsk

Relevance of the topic. Mitral valve endocardiosis is one of the most common pathologies in older dogs. It is believed that dachshunds, terriers, spaniels, as well as Pekingese and bulldogs (chondrodystrophic breeds), and other dogs of medium and dwarf breeds are most predisposed to the disease.

Often veterinarians observe several pathologies in the same patient with endocardiosis: prolapse intervertebral disc, collapse of the trachea, rupture of the anterior cruciate ligament, etc.

Endocardiosis is characterized by degenerative changes in the chords and leaflets of the mitral valve. As the disease progresses, dogs are characterized by the occurrence of failure of the bicuspid valve located between the left atrium and ventricle. Loose closure of the valve leaflets at the time of systolic contraction of the ventricle leads to the appearance of a reverse blood flow (regurgitation) directed to the left atrium.

Reasons above pathological process not yet fully elucidated, but a typical change in the structure connective tissue. The most likely age for the onset of this disease is 7-12 years. In 10% of dogs, the problem begins to progress from the age of 5. The genetic heritability of the pathology is obvious.

aim of this work is the diagnosis and treatment of an animal with endocardiosis.

Materials and research methods. The work was carried out on the basis of the Irkutsk city veterinary polyclinic and at the Irkutsk State Agricultural Academy in 2011. A dog with a pathology of the cardiovascular system was investigated electrocardiographically, radiographically, echocardiographically. For the treatment of a sick animal, drugs of the group were used: ACE inhibitors, loop and potassium-sparing diuretics, corticosteroids, metabolic drugs.

Research results.

On November 7, 2011, a dog (dachshund, 8 years old, nicknamed “Boniface”) was admitted to the polyclinic. According to the owner of the animal in May 2011, there was a cough with a frequency of 3-5 times a day and a duration of 30 seconds or more after feeding and exercise. No other abnormalities were observed in the dog. host with therapeutic purpose gave the dog "Bromhexine" ½ tab. 2 times a day for 10 days. After this episode, the frequency of coughing was reduced to 1-2 times a day. IN veterinary clinic did not apply.

1 week before going to the clinic (i.e., 11/1/2011), the dog's coughing frequency increased sharply (15-20 times a day), shortness of breath appeared on movement, and increased thirst. Appetite is good.

A clinical examination revealed noise in the mitral valve area - 3 degrees, tachycardia, T - 37.5, pale mucous membranes, CNC (capillary filling rate) - 2 seconds, pressure in the femoral artery was palpated, crepitus in the hilar lobes of the lung.

Instrumental research:

1.Radiography chest organs: enlargement of the left atrium, increase in the distal quarter of the trachea, radical pulmonary edema, initial pulmonary hypertension. Buchanan's ratio 12.5.

Rice. 1. Chest x-ray

2.ECG: sinus tachycardia, left atrial enlargement (Pmitrale)

Rice. 2. Electrocardiography

3.Echo KG: left atrial enlargement, left ventricular enlargement, ejection fraction 45%, grade 3 mitral regurgitation, initial pulmonary hypertension.

Fig.3. echocardiography

4.Blood analysis:

Table. 1

Blood analysis

Name	Norm	Actually
red blood cells
Hemoglobin, g/l
Leukocytes
Stab, %
Segmented, %
Eosinophils
Basophils
Lymphocytes
Monocytes
Urea
Creatinine
Bilirubin total
total protein
Alkaline phosphatase
Cholesterol
Triglycerides

Based on the anamnesis, clinical examination, radiography, electrocardiography, echocardiography and complete blood count, the following diagnosis was made: mitral valve endocardiosis.

The diagnosis is differentiated from:dilatory cardiomyopathy, congenital disease hearts , X chronic disease respiratory tract, pneumonia , pulmonary embolism , lung neoplasia (tumor).

Treatment: V this case used a combination of several medicines. ACE inhibitors - "Renitek" 5 mg x 10 kg. animal weight 2 p. per day, all the time. Diuretics - "Furosemide" - 4 mg / kg x 2 r. per day, "Spironolactone" - 25 mg / kg x 2 r. in a day. Metabolic therapy - Mildronate 250 mg. 1 caps. x 1 time per day. Corticosteroids - Prednisolone 2 mg/kg x 1 per day.

After 3 days of treatment, the cough was significantly reduced (attacks during stress). Canceled corticosteroids (prednisolone).

After 7 days of treatment, the dog's condition is stable, coughing 2 times a day, the mucous membranes are pale pink, the pulse on the femoral artery is well filled.

Further tactics: drink drugs constantly (the disease is chronic, not completely cured), for examination by a doctor and correction of treatment after one month, limit the dog in the load, follow a diet, inform the owners (discuss the progressive nature of the disease). follow the manifestation clinical signs drug intoxication. If signs of intoxication appear, stop further giving of drugs and immediately notify the veterinarian.

Discussion of the results of the study. Mitral valve endocardiosis is systemic disease. Proliferation and deposition of mucopolysaccharides within the subendothelial spongiform layer leads to thickening, distortion (stretching), and hardening of the atrioventricular (AV) valves; in particular, the swelling is nodular in nature (in the form of nodes), usually adhesions appear when the entire valve is affected and the adjacent chords are often affected.

AV valve decompensation causes regurgitation, high atrial pressure, reduced cardiac output, activation of compensatory mechanisms (sympathetic nervous system, RAAS (renin-angiotensin-aldosterone system), and atrial natriuretic factor), and congestive heart failure.

Volume overload leads to progressive ventricular dilatation, rigidity, and impaired ventricular function; as a result, congestive insufficiency and insufficiency due to reduced blood outflow develop.

With the rupture of the atrial walls of the vessels, acute cardiac tamponade may also develop.

Degenerative changes in the chordae (chordaetendineae) lead to distortion, stretching, weakening, and rupture, causing valvular instability and increased regurgitation.

Due to the greater load on the heart associated with the need to maintain normal blood pressure in pathological conditions, the heart muscle significantly increases in volume due to the thickening of the muscle wall. And, acquiring a spherical shape, the heart begins to put pressure on the trachea passing in the immediate vicinity. And the cough reflexogenic zones located on the trachea are not able to figure out that in this case there is no need to cough, and send a signal to the brain. The intensity of the cough at the same time increases gradually (along with an increase in the size of the heart). That's why this pathology must be differentiated from clinically similar pathologies such as dilated cardiomyopathy. With dilated cardiomyopathy, echocardiography shows an expansion of the cavity of the left and right ventricles with a decrease in myocardial contractility, an increase in pressure in pulmonary artery, atrial expansion, arrhythmia.

Chronic airway disease and pneumonia can be differentiated on x-ray by a characteristic pattern. bronchial tree, as well as during auscultation (wheezing, crepitus, grinding in the affected lobes of the lung).

Congenital heart disease and pulmonary embolism are differentiated by the Doppler method during echocardiography.

Tumors of the lungs are visualized on x-ray, according to characteristic pathological areas in the chest cavity.

As we see when carrying out instrumental diagnostics we can differentiate mitral valve endocardiosis from other pathologies and prescribe an effective treatment.

Rationale for treatment. The main drugs in the treatment of this disease will be: ACE inhibitors (angiotensin-converting enzyme), they inhibit the action of angiotensin-converting enzyme, stabilize the level of bradykinin, slow down the absorption of sodium and water. As a result of the impact on the renin-angiotensin system, ACE inhibitors have a pressure-lowering effect, which positively affects the performance and "life span" of the myocardium. Loop diuretics: "Furasemide" at a dose of 2-4 mg / kg x 2 r. in a day. It acts on the terminal part of the distal tubule of the nephron, reduces preload and afterload on the heart, eliminates congestion during internal organs and peripheral edema.

Potassium-sparing diuretics: "Spironolactone" (Veroshpiron) at a dose of 2-5 mg / kg per day. IN distal parts nephron, it prevents the retention of sodium and water by aldosterone, suppresses the potassium excretion effect and block side effects"furosemide".

Metabolic preparations: in this case, we prescribed "Mildronate", it restores the balance between the delivery and need of cells for oxygen, eliminates the accumulation of toxic metabolic products in cells, protecting them from damage; has a tonic effect on the body of the animal.

Corticosteroids: prednisolone, it limits the migration of leukocytes to the area of ​​inflammation, has a catabolic effect in the lymphoid tissue, thereby has an anti-inflammatory effect in the lungs and reduces cough. This drug is used in a short course, no more than 3-5 days.

This complex therapy showed positive results in the treatment of mitral valve endocardiosis, reduces myocardial remodeling and prolongs the life of the patient.

Conclusions: endocardiosis of the mitral clan is a common pathology of dogs, and the observation of the owners, timely and comprehensive examination this problem contributes to the detection of the disease on early stages, which in turn makes it possible to choose a more effective treatment regimen, improve the quality and life expectancy of the animal.

Bibliography:

1. Martin M., Corcoran B. Cardiorespiratory Diseases in Dogs and Cats, Trans. from English. S. L. Cheryatnikova. - M.: "Aquarium Print", 2010. - 496 p.
2. Encyclopedia "Andiag" - Cycle cardiology [Electronic resource]: Endocardiosis of atrioventricular valves. Date of last update: 15:28 05/03/2010 URL: http://www.edliny.ru/encyclopedia/355.html.

Characteristics.
It is expressed in the incomplete closure of the valve leaflets and, as a result, the reverse flow of blood in the atrium. Of the acquired heart diseases, this is the second most common pathology.

Etiopathogenesis.
The etiology of these lesions is unknown, but the increasing incidence and severity of the disease with age, in the absence of signs of inflammation, support a degenerative process called endotheliosis.
If in a broad sense these changes in the valves can be considered a rheumatoid disease, then etiologically they cannot be compared with human rheumatoid endocarditis, since the effect of bacterial pathogens has not been proven. Mitral valve insufficiency, which is based on true bacterial endocarditis, is very rare in dogs. In such cases, simultaneous damage to the aortic valves occurs.
Valve leaflet lesions begin with fragmentation of elastic fibers and fibroplasia. The deposition of mucopolysaccharides in the subendothelial and fibroelastic layers increases. On the free edges of the valves, solid nodular thickenings are formed, which determine the contracture of the valves with the impossibility of complete closure. As a result of these changes, there is a reverse flow of blood into the atria.
The intensification of the reverse blood flow leads to overstretching of the walls of the atria, which further increases the divergence of the valves. From the crowded atria during diastole, an increased amount of blood enters the ventricles of the heart, which creates an increased load and causes hypertrophy, and subsequently expansion of the ventricles. The entire structural complex of atrioventricular valves is involved in the process, microscopic intramural myocardial infarctions of the left ventricle develop. As an outcome, extrasystole or paroxysmal tachycardia may occur.

breed predisposition.
AV valve insufficiency can be found in any dog, but occurs predominantly in small to medium breed dogs.

Floor. Males get sick more often and more severely than females.

The disease is manifested by mitral valve insufficiency in 75% of cases, less often by a combination of mitral and tricuspid valve insufficiency and only sometimes by one tricuspid valve insufficiency.
Isolated mitral lesion is especially common in male Cocker Spaniels, and tricuspid valve lesion in dachshunds.

Clinical signs.
The picture of the disease in atrioventricular valve insufficiency some time after the asymptomatic period is quite characteristic. Decompensation of mitral valve insufficiency occurs with the appearance of signs of blood stagnation in the pulmonary circulation.
A chronic cough develops, sometimes with shortness of breath and cyanosis, worse at night or when the animal is excited. The animal stands with its head held high and elbows wide apart. During coughing fits, the dog expectorates a little white or slightly blood-colored foam, which is immediately swallowed. New bouts of coughing can provoke squeezing of the trachea with a collar or palpation of the organ. With decompensated tricuspid valve insufficiency, signs appear that indicate blood stagnation in the systemic circulation. Note peripheral edema, expansion of peripheral veins, enlargement of the liver and spleen, ascites (Fig. 30), hydrothorax, cardiac cachexia. The addition of arrhythmia is indicated by cases of loss of consciousness by animals. Then a non-rhythmic, accelerated pulse with an increased push or a pulse deficit is determined.

Susceptibility: Dogs, Cats

Clinic:
Auscultation
This pathological condition in dogs produces a familiar sound with variable intensity, characterized by the following:
Localization in space: 5-7 intercostal space, parasternally on the left ...
Localization in time: mostly protosystolic, but sometimes holosystolic
Its soft regular specific "outboard engine" type sound
In fact, these characteristics must be taken seriously with some caution, because objects have many variations:
· Since the intensity is very significant (5/6 - 6/6) the auscultatory field is very extensive on the left and right even to the caudal lobes of the lungs, thus making the main localization very delicate.
Since valvular fibrosis is accompanied by parietal hyperkinesia, prolapse or rupture of the cord, the tone of the noise can be completely different: musical, such as dry friction, rough sounds, any outside the norm.

General clinic:
1. Abdominal distension;
2. Abnormal behavior, aggression, change in habits;
3. Anorexia (lack of appetite, refusal to eat);
4. Arrhythmia, irregular heart sounds;
5. Ascites, accumulation of fluid in the abdominal cavity;
6. Auscultation: Abnormal lung or pleural sounds, rales: wet and dry, whistles; 7. Fast fatiguability at physical load;
8. galloping rhythm;
9. Hepatosplenomegaly, splenomegaly, hepatomegaly;
10. Dyspnoe (difficulty breathing, shortness of breath);
11. Distension of peripheral veins, jugular distension;
12. Intra-abdominal masses;
13. Cough;
14. Congestion of the oral mucosa, erythema, redness, hyperemia;
15. Fainting, syncope, convulsions, collapse;
16. Propulsion, inability to rise;
17. Pulse deficit, absence of pulse;
18. Vomiting, regurgitation, emesis;
19. Heart murmurs;
20. Mucous membranes - cyanosis;
21. Tachycardia, increased heart rate;
22. Tachypnea, increased frequency respiratory movements, polyp, hyperpnea;
23. Oppression (depression, lethargy);
24. Perceptible precordial flicker;
25. ECG: Atrial fibrillation (atrial fibrillation);
26. ECG: Atrial expansion (atrial expansion);
27. ECG: Atrial (atrial) premature (premature) tone;
28. ECG: Wandering pacemaker;
29. ECG: Ventricular (ventricular) tachycardia, multifocal or monofocal;
30. ECG: Ventricular (ventricular) premature (premature) tone, multifocal or monofocal;
31. ECG: Absence of "p" wave;
32. ECG: Sinus Arrhythmia;
33. ECG: Sinus tachycardia;
34. ECG: Third degree, complete atrioventricular block;
35. ECG: Enlargement of the ventricles (ventricular expansion), left, right or bilateral;

The diagnosis is made on the basis of auscultation and radiography. Above the fields of the atriventricular valves, a uniform systolic high- or mid-frequency noise of the fourth or fifth degree of intensity is heard.
If pulmonary edema occurs, crepitating moist rales are auscultated throughout the field, as well as the accent of the second heart sound (hypertension in the pulmonary artery). Additional symptom indicating insufficiency of the tricuspid valve is the pulsation of the jugular veins.

X-ray.
On lateral radiographs, the silhouette of the heart appears enlarged and rounded due to the expansion of the ventricles. The heart lies wide base on the chest. An increase in the left atrium is indicated by bronchial symptom(Y-shaped silhouette) formed by the main bronchus elevated dorsally by this atrium, and a change in the angle of the trachea relative to thoracic spine. The left atrium looks like a wedge where the overflowing pulmonary veins empty into it.
With an enlarged right atrium, the silhouette of the trachea is pushed a little anteriorly. The caudal vena cava is denser and wider than normal. In the dorsoventral projection, the hypertrophied atria are visible at the base of the heart in the form of separate shadows and are displaced: the left one is from the 2 o'clock position to the 4 o'clock position; right - from "II hours" to "9".

TREATMENT
First of all, it is recommended to reduce the weight of the animal and limit the load. In the case of a compensated defect of the atrioventricular valves, light loads are acceptable; in case of decompensation, their complete restriction is necessary.
Dietary recommendations are also of some importance: a salt-free diet, feeding the animal only once a day in the morning and a sufficient amount of masa, which, with a good appetite of the animal, completely covers its need for potassium.
Potassium supplements are given to dogs with anarexia.
With cachexia, it is recommended to increase the caloric content of the diet due to carbohydrates and fats.
Digoxin is prescribed for life at a dose of 0.022 mg/kg, minus the weight associated with ascites and obesity. The dose of the drug is divided into two doses. The effect is expected in 5-7 days. The appointment of digoxin is limited in case of kidney failure. In this case, digitoxin is more acceptable.
The second important component of therapy is the vasodilator prazosin. It reduces resistance peripheral vessels, as a result, the venous blood flow to the heart decreases and the work of the heart is facilitated. It is administered orally at a dose of 0.1-0.5 mg 2-3 times a day, but always against the background of digitalis therapy.
In the presence of congestion in the lungs and systemic circulation, eufillin (which helps to remove sodium from the body) and furosemide are additionally prescribed.
In the case of pulmonary edema, all appointments are performed intravenously, if possible, inhalation with oxygen and alcohol vapor is carried out, bloodletting and anesthesia are performed.
With hydrothorax and ascites in a hospital, thoracocentesis or laparocentesis is performed with the removal of fluid from the cavities.
The fight against arrhythmia is necessary for more than late stages. As an antiarrhythmic agent, quinidine sulfate is administered orally at a dose of 11 mg/kg every 6 hours until the arrhythmia attacks are permanently eliminated. In case of remission, the next examination of the animal is done after 4-6 months.

FORECAST
From the moment the disease is discovered, lifelong therapy is necessary. Upon termination of treatment, decompensation phenomena quickly recur. If ascites, hydrothorax, cardiac cachexia occur, the prognosis is unfavorable.

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