Dilation of the mitral valve in a dog is the most common pathology, the clinical signs of which are weak or absent altogether.

Mitral valve prolapse what is it?

Mitral valve in dogs located between the left atrium and the left ventricle. It controls in the diastole phase the unidirectional flow of arterial blood from the left atrium through the prescioventricular opening into the left ventricle. In systole, the valve closes under blood pressure when the left ventricle contracts and prevents blood from flowing back from the left ventricle to the left atrium. The valve consists of two leaves and is called a two-leaf valve. Heart valve disease is common in small breed dogs, especially the mitral valve in Yorkies.

Mitral valve prolapse

There are two main forms of mitral insufficiency: organic and relative. Organic insufficiency is characterized by gross morphological changes in the structure of the valve (wrinkling, deformation). Relative - characterized by insufficiency in the absence of morphological changes in the valve itself (mitral valve prolapse 1–2 degrees, expansion of the valve ring, rupture of tendon filaments, cardiomyopathy, etc.).

In infectious and other diseases of the heart, the valve leaflets can be deformed. Then the valve does not close completely, a hole remains between the leaflets and, as a result, the valve cannot completely prevent the backflow of blood. Part of the blood from the left ventricle of the heart goes back into the left atrium - the phase of organic failure begins. First, the left atrium hypertrophies, but due to the fact that its muscle layer is thin and not designed for heavy loads, decompensation soon occurs and the left atrium stretches and increases in size. Since all the blood from the lungs does not have time to pump out, there is an increase in pressure in the vessels of the lungs. At the same time, due to the large blood flow in the diastole phase into the left ventricle of the heart, it also hypertrophies, but over time its compensatory capabilities decrease and there is a failure of the left ventricle function. Ultimately, the load on the right parts of the heart increases and stagnation occurs in the systemic circulation.

During the period when the heart compensates for the failure of the mitral valve, the animal does not show any signs of heart failure, even with great physical exertion. Over time, with decompensation, shortness of breath appears on the background of exertion, then at rest, coughing fits.

Diagnosing mitral regurgitation in dogs

The main diagnostic methods are: clinical, radiographic and (ECHO KG). Auscultation reveals a systolic murmur in the projection of the apex of the heart. Radiographically determined an increase in the shadow of the atria with displacement of the trachea, congestion in the lungs. In the early stages of mitral insufficiency, the radiographic picture may be normal.

Early echocardiography usually detects mitral valve insufficiency using Doppler imaging. To use the determination of the severity of the insufficiency, color, CW and PW Doppler are used and are guided by a semi-quantitative assessment. In the later stages of the development of valve pathology, secondary ultrasound signs are determined in the form of an increase in the cavity of the left ventricle and left atrium, expansion of the valve ring, pulmonary hypertension, tricuspid valve insufficiency.

Treatment of mitral regurgitation

Conservative treatment of mitral valve insufficiency is the use of diuretic drugs (furosemide, lasix), ACE blockers and peripheral vasodilators.

Surgical treatment of mitral valve insufficiency. The main operations to restore the function of the mitral valve of the heart is.

This article will focus on a very common cardiac disease in dogs, which affects representatives of small breeds. mitral valve endocardiosis.

What is mitral valve endocardiosis?

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

Most often, dogs of such breeds as Spitz, Yorkshire Terrier, Toy Poodle, Chihuahua, Toy Terrier, Dachshund, Pekingese, Miniature Schnauzer, Fox Terrier, Cavalier King Charz 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 is chronic and can develop over the years. Endocardiosis manifests itself as early as 5 years of 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 the hereditary factor. Collagen degeneration process starts (collagenopathy, chondrodystrophy). Therefore, very often in a sick animal with endocardiosis, it is also possible to simultaneously detect pathologies associated with the trachea.

Endocardiosis stages:

• Stage 1 - small, scattered areas of nodules at the ends of the valve leaflets
• Stage 2 - the 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, tendon filaments are affected, ultimately the entire valve apparatus
• Stage 4 - the flaps are compressed, bent, tendon filaments may break, the valves resemble a parachute.

Due to the deformation of the valves, they begin to pass excess blood volume back into the left atrium, the latter stretching and increasing pressure in it. All this leads to compression of the main left bronchus and the classic "heart" cough. In addition, the increased pressure in the left atrium increases the pressure in the pulmonary veins, which leads to left-sided heart failure. As a result, stagnation occurs in the pulmonary circulation and pulmonary edema occurs. In the last stages of the development of the disease, the right half of the heart may also be affected. In the future, this will lead to pulmonary hypertension, or to the accumulation of fluid in the abdominal cavity (ascites).

Endocardiosis symptoms that cannot be ignored:

• Cough is the very first and characteristic symptom that owners notice in their pet, but very often ignore it, referring to a cold or "choked on something." The cough is noted at night or early in the morning. It can 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 activity - during a walk in the usual way, the dog quickly gets tired, stops, it needs more time to recover.
• Shortness of breath - the dog begins to breathe very quickly even while resting or sleeping.
• Fainting (syncope) - can manifest itself in the form of an animal falling for a few seconds, a position on the side with limbs extended forward is characteristic. Fainting can be due to severe coughing, or due to an irregular heart rhythm. If these faints are frequent, there is a risk of sudden death.
• Decreased appetite, cachexia (emaciation) - multiple organ failure against a background of reduced cardiac output of blood.

Diagnosis of endocardiosis.

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

• Careful history taking
• Auscultation of the heart and chest organs
• Echocardiography
• X-ray
• Blood test (biochemical, electrolytes, general clinical)

Depending on the stage and development of the disease, individual treatment is selected: ACE inhibitors, aldosterone antagonists, diuretics, positive inotropes, antiarrhythmics, PDE-5 inhibitors, metabolic agents. Sometimes you have to resort to an oxygen chamber and pumping 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 of your pet, help the "weakened" heart to 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.

/ 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 AV 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. Since clinically significant degenerative valve disease is rare in cats, this article will focus on chronic valve disease in dogs. The mitral valve is the most frequently and most severely affected, but degenerative changes are also seen in the tricuspid valve in many dogs. However, isolated degenerative tricuspid valve disease is rare. Thickening of the aortic or pulmonary valve sometimes occurs in older animals, but rarely causes more than mild insufficiency.

Etiology and pathophysiology

The cause of canine mitral valve endocardiosis is unclear, but a hereditary nature is likely. The most commonly affected dogs are small to medium sized breeds of middle age and older. The prevalence and severity of the disease increases with age. About a third of small breed dogs over 10 years old 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 with the influence of sex and age is expected.This is manifested in the fact that, in general, the 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 also get sick and the prevalence of the disease may be higher in German Shepherds.

Multiple factors, including collagen degeneration, increased stress on valve leaflets and endothelial function, can occur. Valve abnormalities in canine mitral valve endocardiosis develop gradually with age. Early lesions are small nodules on the free margins of the valve; they become larger, merge into plaques, which thicken and deform the valve. The 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 cords. Excessive tissue between the sites of chord attachment often protrudes. prolapse) as 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 flaps 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 valve insufficiency is also associated with intramural coronary arteriosclerosis, microscopic intramural myocardial infarction, and focal myocardial fibrosis. The length of time during which these changes cause clinical myocardial dysfunction is unclear; however, impaired myocardial contractility occurs late in this disease. Interestingly, older dogs without valvular disease also have similar vascular lesions.

Pathophysiologic changes in canine mitral valve endocardiosis are associated with volume overload of the damaged side of the heart after the valve (or valves) becomes less functional. Regurgitation usually develops slowly over months and years; mean atrial pressure remains fairly low during this time, unless there is a sudden increase in regurgitation volume (e.g. chord rupture). As valve degeneration progresses, more blood volume moves ineffectively back into the atrium from the ventricle, reducing blood flow to the aorta. Compensatory mechanisms increase blood volume to meet the body's circulatory needs, including increased sympathetic activity, decreased vagus tone, activation of the renin-angiotensin-aldosterone system ... The amount of natriuretic peptide increases; higher concentrations of chair natriuretic peptide are associated with marked left atrial enlargement and severe congestive heart failure. Damaged ventricle and atrium enlarge to accommodate increased regurgitation and provide the required stroke volume; in an attempt to normalize the resulting stress of 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 enlargement of the left atrium may develop before any symptoms of heart failure appear, and some dogs never show clinical symptoms of heart failure. The rate of progression of regurgitation, degree, affects the tolerance of the disease. 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. Explicit pulmonary edema develops when the capacity of the pulmonary lymphatic system is insufficient. Tricuspid failure 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 is reasonably well maintained until late in disease in many dogs, even with symptomatic congestion. However, chronic volume overload decreases myocardial contractility over time. The mechanism of myocardial dysfunction may include free radical damage as well as neurohormonal activation. Decreased contractility increases ventricular dilation and valvular regurgitation and therefore may exacerbate congestive heart failure. echocardiographic shortening fraction, ejection fraction) overestimate contractility. Echocardiographic evaluation of end-systolic volume index may be helpful. This index suggests that myocardial function is normal or slightly reduced in most dogs with canine mitral valve endocardiosis. Other echo / Doppler indices can also help assess left ventricular systolic and diastolic function.

Complicating factors

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

A sudden rupture of pathologically altered tendon chords 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 mid-stream output may also occur. Sometimes a torn chord tendon is an accidental finding (on echocardiogram or autopsy), especially if it is a second or third order chord. Massive enlargement of the left atrium can compress the left main bronchus and induce persistent cough, even in the absence of congestive heart failure. In addition, a massive increase in the left (or right) atrium can lead to partial or complete rupture of the wall. Rupture of the atrial wall usually causes cardiac tamponade; This complication appears to be more common in the male pygmy poodle, cocker spaniel and dachshund, most of which have severe valve abnormalities, massive atrial enlargement, and often a ruptured first-order notochord.

Clinical manifestations

Mitral valve endocardiosis in dogs 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 a decrease in exercise tolerance and manifestations of pulmonary congestion and pulmonary edema. Reduced exercise tolerance and coughing or tachypnea on exertion are the most common initial owner complaints. With increased pulmonary congestion and the development of interstitial edema, the respiratory rate increases. Coughs are more common at night or early in the morning, or with increased activity. Severe pulmonary edema leads to obvious respiratory distress and usually a wet cough. Symptoms of severe pulmonary edema can develop gradually or acutely. Intermittent episodes of pulmonary edema symptoms alternating with periods of compensated heart failure over months and years are common. Episodes of transient weakness or acute collapse (syncope) can occur due to arrhythmias, coughing, or atrial rupture. Symptoms of tricuspid regurgitation, usually overshadowed by those of mitral regurgitation, include ascites; respiratory distress due to pleural effusion; and, rarely, subcutaneous tissue edema. Abdominal congestion can cause gastrointestinal symptoms.

A holosystolic murmur, which is better heard in the apex region on the left (fourth to sixth intercostal space on the left), is typical of patients with mitral regurgitation. Noise can travel in any direction. Mild regurgitation may be inaudible or the cause of the murmur is only in early systole (protosystolic). Exercise or agitation 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 mild or even inaudible. Sometimes the noise can be similar to a musical tone. Some dogs with chronic mitral valve disease have a moderate to late systolic clicking sound, with or without noise. S3, a gallop sound, can be heard in the left apex of the heart in advanced dogs. Tricuspid regurgitation typically produces a holosystolic murmur, better heard in the right apex. Features that help differentiate the murmur of tricuspid regurgitation from radiating mitral regurgitation murmur in the right parts of the chest, include pulsation of the jugular vein, vibration of the chest over the projection of the apex of the heart on the right, and features of noise in the projection of the tricuspid valve.

Pulmonary sounds can be normal or abnormal. Accentuated, hard breathing and sounds of crepitus 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 pulmonary sounds caused by concurrent pulmonary or airway disease rather than congestive heart failure. Dogs with congestive heart failure tend to have sinus tachycardia; Dogs with chronic lung disease often have sinus arrhythmias and a normal heart rate. Pleural effusion causes ventral attenuation of pulmonary sounds.

On physical examination, other abnormalities may not be present or they are insignificant. Peripheral capillary perfusion and arterial pulse strength are usually normal, although a pulse deficit 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. Distension of the jugular vein and its pulsation are not characteristic of isolated mitral regurgitation. In animals with tricuspid insufficiency, pulsation of the jugular vein is observed during ventricular systole; it is more evident after physical or emotional stress. The stretching of the jugular vein occurs due to the increased filling pressure of the right heart. Jugular vein pulsation and distension are more evident with cranial abdominal compression (positive hepatojugular 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 show some degree of enlargement of the left atrium and left ventricle, which progresses over months or years. As the size of the left atrium increases, dorsal displacement of the main bronchus may occur. Severe enlargement of the left atrium causes compression of the left main bronchus. Fluoroscopy may show dynamic collapse of the main bronchus during coughing or even calm breathing in these animals. Extreme enlargement of the left atrium can develop over time, even without clinically evident heart failure. Right heart enlargement occurs to varying degrees in chronic tricuspid valve regurgitation, but it can be masked by changes in the left and lungs associated with concurrent microvascular dysplasia.

With the appearance of left-sided congestive heart failure, congestion in the pulmonary veins 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, asymmetric distribution is observed in some dogs. The presence and severity of pulmonary edema does not necessarily correlate with the degree of cardiomegaly. Acute, severe regurgitation (eg, tearing of the tendon chords) can cause severe edema in the presence of minimal left atrial enlargement. Conversely, slowly progressive mitral regurgitation can cause marked enlargement of the left atrium without congestive heart failure. Early symptoms of right-sided heart failure include distension of the caudal vena cava, visualization of lines between the lobes of the lungs, and hepatomegaly. Explicit pleural effusion and ascites occur in severe heart failure.

Electrocardiography

The ECG may suggest an increase in the left or both atria and left ventricle, although it is often normal. Dogs with severe tricuspid insufficiency sometimes show signs of right ventricular enlargement. Arrhythmias, especially sinus tachycardia, supraventricular premature beats, paroxysmal or persistent supraventricular tachycardia, ventricular beats, and atrial fibrillation are common in dogs with severe disease. These arrhythmias can occur with decompensated congestive heart failure, weakness, or syncope.

Echocardiography

Echocardiography reveals an increase in the size of the atria and ventricles secondary to atrioventricular valve failure. This increase can be pronounced, depending on the degree of volume overload. Enhanced movements of the interventricular septum and the free wall of the left ventricle are observed during 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 insufficiency. Determination of the end-systolic volume index can help in assessing myocardial function. Ventricular wall thickness is usually normal in canine mitral valve endocardiosis; in severe tricuspid regurgitation, paradoxical septal movement may occur concurrently with dilatation of the right atrium and right ventricle. Pericardial fluid (blood) occurs when the left atrium has ruptured and cardiac tamponade may be evident. A small amount of fluid in the pericardium may also complement the symptoms of right-sided congestive heart failure.

Damaged valve flaps are thickened and may look knotted. Smoothed thickening is characteristic of degenerative disease (endocardiosis). Conversely, rough and irregular valve vegetation is characteristic of bacterial endocarditis; however, it may not be possible to differentiate between them by echocardiography alone. Systolic prolapse, involving one or two valve leaflets, is common in degenerative disease of the atrioventricular valves. A torn notochord or leaf tip is sometimes seen moving towards the atrium during systole. The direction and extent of the impaired blood flow can be seen with color Doppler imaging. The size of the area of ​​impaired blood flow provides a rough estimate of the severity of the regurgitation.

The convergent flow method (PISA) is considered by some experts as a more accurate way to assess the severity of mitral regurgitation. Other Doppler techniques can be used to assess the systolic and diastolic ventricular function. The maximum flow rate during tricuspid regurgitation indicates whether there is pulmonary hypertension and how pronounced it is.

Clinicopathological findings

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

Treatment and prognosis

Medication for canine mitral valve endocardiosis is used to control the symptoms of congestive heart failure, maintain heart function, and correct excessive neurohormonal activation that contributes to the development of the disease Medications that reduce left ventricular size (e.g. diuretics, vasodilators, positive inotropics), can reduce the volume of regurgitation by decreasing the size of the mitral annulus. Drugs that promote arterial vasodilation, increase cardiac output and reduce regurgitation by lowering systemic blood pressure. As the disease progresses, frequent reassessment 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 develop acutely severe pulmonary edema or syncope. Intermittent episodes of decompensation in dogs receiving long-term treatment for congestive heart failure can often be successfully treated. Treatment should take into account the clinical status of the patient and the nature of complicating factors. Surgical procedures such as mitral anulus repair, other valve repair and mitral valve replacement techniques may be used in some patients but are not widely available.

Asymptomatic atrioventricular regurgitation

Dogs that do not show clinical symptoms of disease are generally not indicated for drug therapy. There is insufficient evidence to date that ACE inhibitors or other drugs delay 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 inform the owner of the disease process and early symptoms of congestive heart failure. It is probably wise to avoid high-salt diets, to reduce body weight in obese dogs, and to avoid prolonged intense exercise. A moderate salt restriction diet may be helpful. Periodic reevaluation (e.g. every 6-12 months) of heart size and function is desirable, and also blood pressure. Other pathologies also need to be corrected.

Congestive heart failure with mild to moderate symptoms.

When clinical symptoms are observed due to emotional or physical activity, various treatments 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 noncardiogenic disease, trial therapy with furosemide is indicated ( e.g. 1-2 mg / kg orally 2-3 times a day). With cardiogenic pulmonary edema, improvement is usually rapid.

Furosemide is used to treat dogs with radiographically confirmed pulmonary edema and / or severe clinical symptoms. If the edema is severe, higher doses and more frequent administration are used. Once symptoms of deficiency are controlled, the dose and frequency of furosemide administration 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 generally recommended for the treatment of mitral valve endocardiosis in dogs with early symptoms of heart failure, and their ability to modulate neurohormonal responses to heart failure appears to be their main advantage. Chronic therapy with ACE inhibitors can improve exercise tolerance, coughing and shortness of breath, although it is unclear whether these prolong life in affected dogs.

Pimobendan is also increasingly used to treat moderate to severe congestive heart failure. This drug has positive inotropic, vasodilatory, and other effects; its benefits may exceed those of ACE inhibitors, although they are often used together. Digoxin, with or without pimobendan, is often additionally used in the treatment of congestive heart failure due to severe mitral regurgitation. Digoxin's sensitizing effect on baroreceptors may be more beneficial than its mild positive inotropic effect. Marked left ventricular enlargement, apparent decrease in myocardial contractility, or recurrent episodes of pulmonary edema despite treatment with furosemide and other drugs are indications for digoxin. Digoxin is also indicated for frequency control. cardiac contractions in dogs with atrial fibrillation and as an antiarrhythmic drug for the treatment in some cases of frequent atrial premature beats or supraventricular tachycardia. To prevent its toxicity, moderate doses and measurement of serum concentration are required.

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

Severe congestive heart failure

Severe pulmonary edema and dyspnea 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 maintenance should be given as early as possible. Handling with caution is important because additional stress can trigger 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 veins and arteries; however, blood pressure must be closely monitored to prevent hypotension. Oral hydralazine is another option. Its direct and rapid arterial vasodilatory effect enhances blood flow and reduces regurgitation; however, oral administration can be stressful. 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 application of nitroglycerin can 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 the acute dyspnea has subsided. Digoxin may be beneficial in the presence of paroxysmal atrial tachycardia or atrial fibrillation. Although it will take several days to reach therapeutic blood levels with oral maintenance doses, intravenous digitalization is not recommended in most cases. Diltiazem or beta-blockers may be given in place of (or in addition to) digoxin if supraventricular tachyarrhythmia requires treatment. Dogs requiring more intense inotropic support or who have persistent hypotension may be given intravenous dobutamine, dopamine, and amrinone.

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

Thoracocentesis is indicated in dogs with moderate to large volume of pleural effusion to improve lung function. Ascytes that impair respiratory function should also be treated. In some cases, treatment of ventricular tachyarrhythmias is necessary. Close monitoring is important to correct treatment and detect drug toxicity or side effects (eg azotemia, electrolyte disturbances, hypotension, arrhythmias).

Once the initial state is stabilized, the appointments are adjusted over several days or weeks to find the optimal long-term therapy. Furosemide is titrated to the lowest doses (and longest intervals) that control the symptoms of congestive heart failure. Prescription of ACE inhibitors is recommended for continuation of therapy if hydralazine or sodium nitroprusside were used as initial vasodilators. Since the effect of initially prescribed hydralazine disappears gradually, the first dose of an 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 shortly after discontinuation of the sodium nitroprusside infusion.

Long-term treatment of the refractory form of the disease

When congestive heart failure in 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 increased doses 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 before (for example, enalapril should be given not once, but twice a day).

Pimobendan and / or digoxin may be added if not already done. The dose of digoxin is not increased above the standard dose, unless a subtherapeutic blood concentration is established. Spironolactone can be used additionally if not previously done. 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 a combination of spironolactone with hydrochlorothiazide may be helpful.

Constant monitoring is important, especially of renal function and serum electrolyte concentrations. Salt restriction in the diet can be increased. If the doses of ACE inhibitor and furosemide are already at their maximum, low doses of hydralazine (eg.

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

Intermittent tachyarrhythmias can 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 periodic recurrence of symptoms of congestive heart failure, many dogs with chronic AV 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 aware of the process of the disease, the clinical symptoms of deficiency and the drugs needed to control them. As the disease progresses, it is necessary to adjust the treatment (e.g. adjusting the doses of drugs used or adding additional drugs). Several common potential complications of chronic degenerative AV valve disease can cause decompensation (Table 1). Home monitoring is important in order to detect early symptoms of decompensation. Respiratory (+/- cardiac) rate levels can be monitored periodically when the dog is calmly resting or sleeping; a persistent increase in them may signal early decompensation.

Asymptomatic dogs should be reevaluated at least once a year in the context of a routine cardiac protection program. The frequency of reevaluation in dogs receiving treatment for heart failure depends on the severity of the disease and on the presence of complicating factors. Dogs with newly diagnosed or decompensated congestive heart failure should assessed more frequently (ranging from a few days to weeks) until they are stable. Dogs with chronic heart failure whose symptoms are well controlled may be evaluated less frequently, usually several times a year. Medication support, 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 essential at every visit. If arrhythmias or an unusually low or high heart rate are found, an ECG is indicated. When arrhythmia is suspected but not detected on a routine ECG, an ambulatory ECG (eg, Holter 24-hour monitoring) may be indicated. Respiratory rate and type are also recorded; chest x-ray is advisable if abnormal lung sounds are heard or if the wearer reports a cough, other respiratory symptoms, or an increased resting respiration rate. Other causes of cough should be considered if neither pulmonary edema nor venous congestion is detected on chest x-ray and if the resting respiratory rate is not increased. Compression of the left primary bronchus by an enlarged left atrium may stimulate a dry cough. Antitussives are helpful, but should only be given after other causes of cough have been ruled out.

Echocardiography may show chord rupture, progressive cardimegaly, or impaired myocardial function. Frequent monitoring of serum electrolyte concentrations and renal function is important. Other routine blood and urine tests should also be done periodically. Blood digoxin concentration in dogs receiving it should be measured 7 to 10 days after initiation of treatment or dose adjustment. Additional measurements are recommended if there are signs of digoxin toxicity or if kidney disease or electrolyte imbalance (hypokalemia) is suspected.

The prognosis in dogs in dogs that show clinical symptoms 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 a few years.

Table 1
Potential complications of canine mitral endocardiosis

Causes of acutely developed pulmonary edema

• arrhythmias
  • frequent atrial extrasystoles
• paroxysmal atrial / supraventricular tachyarrhythmia
  • atrial fibrillation
  • frequent ventricular tachyarrhythmias
  • eliminate the toxicity of drugs (e.g. digoxin)
• tendon chord rupture
• iatrogenic fluid overload
  • excess volumes of intravenous fluid or blood injected
  • high sodium liquids
• prescribing an unsuitable or unpredictable drug
• insufficient treatment for this stage of the disease
• increased work of the heart
  • physical effort
  • anemia
  • infection / sepsis
  • hypertension
  • diseases of other organs (e.g. lungs, kidneys, liver, endocrine system)
  • high temperature and humidity of the environment
  • excessively cold external environment
  • other stressful environmental influences
  • high salt intake

Causes of decreased cardiac output or weakness

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

table 2
Guidelines for the management of canine mitral endocardiosis

Asymptomatic stage (modified AHA / ACC stage B)

• Owner training (information on disease and early symptoms of heart failure)
• Standard Heart Support
  • blood pressure measurement
  • plain chest x-ray (+/- ecg) and re-examination annually
  • maintaining normal body weight / condition
  • regular physical activity of low or medium intensity
  • avoid intense physical activity
  • testing for heartworms and prevention of this disease in endemic areas
• Treat other existing medical conditions
• Avoid salty foods; consider moderate salt restriction diets
• Consider ACE inhibitors if there is marked left atrial enlargement (+/- left ventricle); adjunctive treatment to correct neurohormonal activation may or may not be clinically beneficial

Mild to moderate heart failure symptoms (AHA / ACC modified stage C, chronic)

• The same as for the asymptomatic stage, and
• Furosemide if needed
• 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 as needed
• Complete limitation of physical activity until symptoms decrease
• Moderate salt restriction
• Respiratory rate monitoring at home (+/- heart rate)

Severe symptoms of acute congestive heart failure

• Oxygen support
• Cage and careful handling
• Furosemide (higher doses, parenteral)
• Vasodilatory therapy
• Consider IV sodium nitroprusside, or
• Oral hydralazine or amlodipine, +/- topical nitroglycerin
• +/- butorphanol or morphine
• Antiarrhythmic therapy, if needed
• +/- positive inotropes:
• If myocardial insufficiency is established, intravenous drug administration may be used
• Once the patient is stabilized, pimobendan +/- oral digoxin therapy can be used
• +/- bronchodilator
• Thoracocentesis for large accumulation of pleural effusion

Treatment for Chronic Recurrent or Refractory Heart Failure (AHA / ACC Modified Stage D)

• Ensure stage C treatment is applied 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 the dose / frequency of furosemide; if necessary, you can reduce them within a few days after the symptoms have subsided
• Forced limitation of movement until symptoms abate
• Add pimobendan if not assigned
• Increase the dose / frequency of the ACE inhibitor (from 1 to 2 times a day)
• add digoxin if not prescribed; monitor serum concentration; increase dose only if subtherapeutic concentration is established
• Add (or increase the dose) a second diuretic (e.g. spironolactone, hydrochlorothiazide)
• Additional afterload reduction (e.g. amlodipine or hydralazine) monitor blood pressure
• Further limiting salt intake; make sure your drinking water is low in sodium
• Thoracocentesis or abdominal centesis as needed
• Eliminate arrhythmias if present
• Consider the need for sildenafil treatment for secondary pulmonary hypertension (eg 1-2 mg / kg every 8-12 hours)
• Consider trial treatment with a bronchodilator or antitussive drug

A healthy heart is a healthy body. This is an axiom both in medicine and in veterinary medicine. Unfortunately, there are many dangerous pathologies of the cardiovascular system, which, if not detected in time, lead to severe forms of heart failure. The only problem is that animals are not constantly examined, and therefore the same mitral valve endocardiosis in dogs is often detected already at those stages when the pathological process has gone too far.

This is a chronic disease of the atrioventricular valve, characterized by the gradual and irreversible development of degenerative changes in it. Statistics show that it is this pathology that is perhaps the most common cause, second only to various cases.

Process development stages

For the first time, all stages of the process were summarized, systematized and studied by Whitney's veterinarian, and this was back in 1974. There are four of them:

• On first stage the left atrium and ventricle do not change in any way, but small "nodules" appear on the mitral valve itself, that is, places of degenerative tissue changes.

• Second stage characterized by the fusion of lesions, and they begin to capture also the valve chords.

• When the disease reaches 3 degrees, on the valve itself there are numerous growths in the form of plaques, the chords are thickened and noticeably "coarser" than the norm. The thickness of the MC itself also increases significantly, and the flexibility decreases. The basal part of the valve is thickened and there may be areas of calcification (mineralization) and bleeding.

• Process 4 degrees characterized by the fact that the valve tissue undergoes rapid degradation, the shape of the latter is greatly distorted, the edges are folded. In severe cases, the chords break or completely lose their elasticity, which allows the valve to dangle when the ventricle contracts, like an open window vent. At this stage, the valve may resemble an open parachute in the sky.

Read also: Enterocolitis in dogs - signs and treatment of intestinal inflammation

Endocardiosis of the mitral valve alone occurs in 60% of cases, and with the participation of the mitral and tricuspid valve, the process proceeds in 30% of cases. The participation of only the mitral and aortic, only the tricuspid or aortic valves is a very rare phenomenon, as Buchanan wrote about in 1979. The older the dog is, the faster the pathological process develops.

Clinical signs

What are the symptoms of mitral valve endocardiosis in dogs? As a rule, in young animals, the signs of pathology grow slowly, since the compensatory capabilities of the organism are still active. The first clinical signs are always vague heart murmurs. Gradually they become pansystolic, that is, they are audible with any contraction of the heart.

Very often, until middle age, the clinic does not appear at all. But subsequently, the symptoms of acute heart failure begin to increase rapidly, which is especially clearly confirmed by the constant cough due to a large amount of effusion (congestion in the pulmonary circulation). It is important not to miss this moment, since it is at this stage that treatment urgently needs to be started. Note that cough often appears only at night or after minor physical exertion (in the early stages, then it will become permanent).

In the future, the disease rapidly progresses to acute left-sided heart failure, the first sign of which will be constant shortness of breath. In the case when the tricuspid valve is also involved in the process, there are signs of right-sided heart failure, expressed in rapid exhaustion, severe shortness of breath, ascites. When the situation becomes very difficult, fainting is not excluded.

Treatment

Typically, treatment for mitral valve endocardiosis in dogs is symptomatic and aimed at eliminating the most "gross" signs of heart failure. In the very early stages of the disease, that is, when a heart murmur just appears, but there are no other clinical signs, it is not required to treat the animal, since there is no sense from this. Even the theory of some veterinarians about limiting sodium intake in feed has not found real confirmation in practice.

Endocardiosis is a disease of the heart valves that occurs in small breed dogs. It is the latter that constitute the risk group for this ailment. These breeds include Toy Terriers, Pekingese, Spitz, Chihuahuas, Poodles, Yorkshire Terriers, Spaniels, Dachshunds and French Bulldogs. Less commonly, this disease affects large dogs, mainly groups of terriers, however, in them it usually proceeds less aggressively than in small dogs, and only in rare cases entails serious consequences. With regard to dwarf breeds, the following correlation is observed: the smaller the mass of the dog breed, the more often the representatives of this breed develop endocardiosis and the more severe this disease progresses in them.

General understanding of the disease

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

What is endocardiosis in essence? The heart is a biological pump, composed of 4 chambers in dogs, as in humans, and providing continuous blood flow. Between its chambers there are valves that allow blood to pass only in one direction. With endocardiosis, these valves are gradually deformed, thickened, cease to close tightly enough, starting to pass blood back. 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, a change in the valve located between the left ventricle and the left atrium leads to stagnation of blood in the veins of the lungs, which causes pulmonary edema. Pulmonary edema is a life-threatening condition and the dog can die if not treated promptly. In the presence of valve pathology 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 affect only the valve 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. The clinical manifestations of endocarditis are associated with this. The most common symptoms noted 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 that appears earlier than others is shortness of breath. You should look closely at your dog's breathing rate, which should normally 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 your veterinarian.

The initial development of the disease

But the onset of the development of the disease is much ahead of the onset of its first symptoms. When examining almost any dog ​​at risk of an older age by means of ultrasound of the heart, signs of endocardiosis can be detected, but the owners do not always notice the symptoms. As a rule, the first symptoms of endocardiosis appear after the age of 6 years, then the disease progresses with age.

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

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

Of the diagnostic methods, echocardiography (ECHOkg) plays a significant role, which is a study of the heart with ultrasound using a special Doppler mode. No other method is capable of providing such a large amount of data on the hemodynamic and anatomical individual characteristics of the heart.

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

Cardiac pathology is capable of starting pathological processes and causing diseases of other organs, primarily the liver, kidneys and brain. Due to the fact that endocardiosis is typical for older animals, this category of patients often suffers from other diseases. Diagnosis of concomitant ailments is sometimes done through a blood test.

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

Actions in the presence of a risky breed

What to do after becoming the owner of a cute dog of a "risky" breed? First of all, don't panic.

It is necessary to plan the first visit to the 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 it will be necessary to check your pet's heart again so as not to "miss" the disease.

Observe the dog's breathing by learning to count its rate at rest. If the disease has been identified, such an extremely simple study will determine the moment of deterioration of the pet's condition, after which it will be necessary to pay a visit to the veterinarian.

If your dog is already undergoing treatment, you need to be extremely careful about the recommendations of the veterinarian-cardiologist. In general, the cooperation between the patient and the doctor plays a vital role and is a guarantee of effective treatment. You should not be afraid to ask if something is unclear. If for any reason the veterinarian is not credible, you should not self-medicate, it is better to look for another veterinarian. But it should be borne in mind that the frequent change of doctors impairs the effectiveness of treatment.

Many owners ask themselves: can the owner of the dog himself provoke the development of this disease? The answer here is no, since endocardiosis is a genetically determined disease, it does not depend in any way on the conditions in which the dog is kept. But such a factor as the obesity of the dog can lead to an aggravation of the course of the disease. Therefore, maintaining the correct weight of the pet is an important responsibility of the owner.

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

Predisposition

The Cavalier King Charles Spaniel breed has the highest predisposition to this disease and the earliest onset of it. Presumably, polygenic inheritance is carried out, 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, whipet, miniature pinscher. Of the larger breeds, endocarditis occurs in German Shepherds, Dalmatians and Ridgebacks.

Pathophysiology

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

Valvular degeneration consists in 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, activating fibroblast growth and causing subendothelial deposition of glycosaminoglycans with subsequent fibrosis. Over time, all these processes lead to a violation of the valve structure, as well as to an increase in regurgitation, at the same time, high pressure as a result of prolapse and changes in the structure of the leaflets cause rupture of tendon strings (chords), which aggravates regurgitation. At the final stage of the development of the disease, the heart valve becomes a fibrous narrowed leaflet, most often with rupture of tendon strings.

The progression of valve damage leads to insufficiently tight closure of the leaflets and regurgitation, the development and severity of which are 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 increased strength and heart rate, as well as activation of neurohormonal systems. Dilation of the ventricles at the same time increases regurgitation and leads to secondary valvular insufficiency.

As the disease progresses, compensation for regurgitation becomes impossible, this leads to a decrease in cardiac output and an increase in venous pressure, as well as to subsequent pulmonary edema or ascites. Pulmonary hypertension can result from left-sided heart disease.

Canine endocardiosis symptoms

The most common symptoms of endocarditis in dogs are coughing (sometimes 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 while lying down. with physical activity or excitement, with coughing (so-called cough fainting) or associated with supraventricular tachyarrhythmia.

An increase in coughing fits is noted after drinking and physical exertion. Persistent diffuse pulmonary edema develops, leading to moist wheezing. Over time, damage develops not only to the left, but also to the right part of the heart, this entails expansion of peripheral veins, ascites, and enlargement of the liver. Due to myocardial degeneration and atrial stretching, premature atrial contraction often appears - paroxysmal tachycardia.

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

A holosystolic murmur when listening to the heart is more pronounced in the upper left part of it (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 heard exclusively in early systole (in this case, there is a protosystolic murmur).

Physical activity or emotional arousal often leads to an increase in the intensity of soft murmurs during mitral regurgitation. In the later 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 mild or completely inaudible. In some cases, it resembles a musical tone.

Some animals with chronic mitral valve disease have a mid-late clicking systolic sound, with or without murmur. The sound of a gallop 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 more clearly heard in the upper left part of the heart.

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

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

In some dogs with mitral regurgitation, abnormal pulmonary sounds are observed, which are caused to a greater extent 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 arrhythmias at a normal heart rate. Due to pleural effusion, pulmonary sounds are weakened.

Clinical examination

During auscultation, a dog that is not currently showing any clinical signs reveals:

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

A complete examination of the dog reveals:

• severe 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 infrequent pulse observed in the femoral artery;
• pallor of the mucous membranes;
• tachypnea, orthopnea, respiratory distress;
• wheezing in breathing, 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 cervical veins (in the presence of right-sided heart failure).

Complicating factors

Canine endocardiosis is a slowly progressive disease, but several factors can lead to acute symptoms in dogs with a compensated form of the disease. In particular, the severity of tachyarrhythmias may be severe enough to cause decompensation of congestive heart failure. Paroxysmal atrial tachycardia, frequent atrial extrasystoles and atrial fibrillation can reduce the filling time of the heart ventricles, increase the oxygen demand of the heart muscle, and aggravate pulmonary edema. There are also ventricular tachyarrhythmias, but they are less common.

Due to the sudden rupture of the tendon chords that have undergone pathological changes, the volume of regurgitation rapidly increases, which can lead to the rapid development of pulmonary edema - in a few hours in a completely symptomless or compensated dog. In addition, there are symptoms of heart failure. In some cases, a torn tendon notochord is found by chance (on an echocardiogram), especially when it is a chord of the 2nd or 3rd order.

Due to a significant increase in the left atrium, compression of the main left bronchus sometimes occurs and persistent cough is stimulated. This can happen 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 commonly seen 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 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 volume of regurgitation due to a decrease in blood pressure.

The progression of the disease leads to the need for regular assessment of the condition of the dog, as well as periodic correction of treatment. In many dogs with severe mitral regurgitation, compensation is maintained for several years with proper treatment. Heart failure in a significant proportion of affected dogs develops slowly, 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 eliminated. When treating, it is necessary to take into account the clinical status of the animal and the factors that complicate the course of the disease in a particular case. Surgical interventions such as plastic surgery of the fibrous mitral annulus, as well as other methods of mitral valve replacement and valve function restoration, can be used in some cases, but they are not widely available.

About the author: Anna Alexandrovna Maksimenkova

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