Features of preoperative examination of dogs prone to cardiac pathologies. Clinical case of heart transplantation in a dog with idiopathic dilated cardiomyopathy

Illarionova V.K.

Cardiomyopathies are a group of myocardial diseases that were described relatively recently - in the late fifties of the twentieth century in the medical literature and in the seventies in veterinary publications. Since then, this group of pathologies of the heart muscle has aroused continued interest among clinicians, morphologists and geneticists. Over the past 20 years, significant progress has been made in the study of cardiomyopathies in animals and humans, for example, such a separate form of pathology as arrhythmogenic dysplasia of the right ventricle in humans and Boxer dogs has been described, a rare form of restrictive cardiomyopathy has been identified in humans and cats, and genetic factors have been identified. factors of occurrence various forms pathologies in humans and individual breeds dogs and cats. Over the past twenty years, there has been a real breakthrough in the ability to diagnose and treat cardiomyopathies in pets, but despite obvious progress, many clinical issues are far from being resolved.

The term "cardiomyopathy" was proposed by W. Brigden in 1956. According to the WHO classification of 1980, cardiomyopathy is a myocardial disease of unknown etiology. Based on structural, hemodynamic and clinical features, three main forms of pathology are distinguished: dilated, hypertrophic and restrictive. Veterinary and medical classifications are the same.

Dilated cardiomyopathy (DCM) is one of the most commonly diagnosed myocardial diseases in dogs. Large and giant breed dogs are predisposed to this pathology. The exception is cocker spaniels, the only small breed known to have DCM. In some breeds, the genetic nature of the disease has been proven, so the pathology can be transmitted by an autosomal dominant type in Newfoundlands, Boxers and Doberman Pinschers, by an autosomal recessive type in Portuguese water dogs and by a recessive type associated with the X chromosome in Great Danes. Males get sick 2-3 times more often. One UK retrospective study analyzed a group of 369 dogs with DCM. Large breeds accounted for 95%. Males accounted for 73%. The most commonly encountered breeds were Doberman Pinschers and Boxers (Martin MW, Stafford Johnson MJ, Celona B; J Small Anim Pract. 2009 Jan).

The classic form of DCM is characterized by diffuse expansion of all chambers of the heart, impaired contractile function of the myocardium, rapid development heart failure and arrhythmias. On pathological examination, the heart is greatly enlarged due to the expansion of all chambers and has a rounded shape (bovine heart - cor bovinum). Eccentric myocardial hypertrophy is determined, but the heart muscle appears thinner as a result of pronounced dilatation of the cavities. The fibrous rings of the atrioventricular valves are stretched, the papillary muscles are thinned and weakened. At histological examination Degeneration, necrosis of cardiomyocytes, multiple zones of fibrosis and mononuclear infiltration are detected.

Clinical signs

As a rule, clinical signs appear in the later stages of the disease, when structural changes in the myocardium lead to functional failure of the heart and all the body’s adaptive mechanisms are disrupted. Most often, the first manifestations of the disease are signs of left ventricular failure: shortness of breath, cough (with this disease, a quiet, rare cough), congestive wheezing in the lungs. Typically, owners do not pay due attention to such symptoms, attributing them to a “common cold.” Signs of right ventricular failure appear later (after about two to three weeks) and include the appearance of ascites, less often pleural/pericardial effusion. With the appearance of signs of right ventricular failure, symptoms of general weakness and intolerance progress physical activity and cardiac cachexia. Sometimes the manifestation of the disease occurs very quickly, simulating acute heart failure. Such a sharp decompensation of chronic heart failure can manifest itself acute edema lungs with very severe shortness of breath, orthopnea and general weakness. Such a rapid course of the disease has a very poor prognosis. When the disease is complicated by rhythm disturbances, all symptoms are accompanied by episodes of loss of consciousness. Although in some cases, fainting may be the only symptom for quite a long time.

Physical examination

Physical examination findings in dogs in the early stages of the disease may be completely normal. Sometimes the only anomaly is a violation heart rate(most often this occurs in dogs of the Boxer and Doberman Pinscher breeds). At the stage of decompensation, signs of cardiomegaly are revealed: expansion and displacement of the apex beat of the heart downward and caudally. The pulse in the femoral artery is weakened. At atrial fibrillation, which is a common complication of DCM, determine pulse deficiency. Arterial pressure may be normal or reduced. Vascular insufficiency manifested by pale mucous membranes and an increase in the capillary refill rate (CRF) for more than 2 seconds. With pulmonary edema, the mucous membranes acquire a bluish tint (Fig. 1).

In the presence of such a symptom complex as cough, shortness of breath and orthopnea, it is necessary to exclude the presence of large pleural effusion or acute edema lungs. Hepatomegaly and ascites lead to abdominal enlargement. A large volume of ascites fluid is sometimes accompanied by edema subcutaneous tissue pelvic limbs.

During auscultation of the heart, muffled heart sounds are heard, sometimes a third sound; a weak systolic murmur at the apex of the heart can often be detected, which is a consequence of relative insufficiency mitral valve as a result of stretching of the mitral ring and dysfunction of the papillary muscles. With an irregular rhythm, such as frequent extrasystoles, ventricular tachycardia, or atrial fibrillation, such a murmur may be difficult to auscultate. When listening to the lungs, they determine hard breathing or congestive wheezing in the presence of interstitial or alveolar edema lungs.

Electrocardiographic study

In the early stages of the disease, the ECG may remain unchanged. In breeds prone to rhythm disturbances, rare ventricular extrasystoles are recorded at the onset of the disease. In our practice, there have been cases of detection of atrial fibrillation already in the early stages of the development of the pathology. With significant remodeling of the heart, signs of left ventricular enlargement are found: large amplitude of R waves in leads I, II, III, V4, V2. If intraventricular conduction is impaired, the R waves may become jagged. With pronounced fibrotic changes myocardium or the presence of pleural and/or pericardial effusion, the amplitude of the QRS complexes may be reduced. When the left atrium enlarges two or more times, P-mitral waves appear on the ECG, which are expanded for more than 0.05 seconds. With the development of significant pulmonary hypertension, the ECG records signs of enlargement/overload of the right atrium - high-amplitude (more than 0.4 mV) P-pulmonale waves (Fig. 2) and deep (more than 0.8 mV) S waves (especially in leads V4 and V2 ).

In the later stages of heart failure, most dogs develop arrhythmias. The most common arrhythmia is atrial fibrillation (atrial fibrillation). Most often it is constant and has a tachysystolic form (Fig. 3).

A separate group consists of dogs of the Doberman Pinscher and Boxer breeds, in which DCM occurs with a long latent phase, sometimes lasting 2-3 years. During this period, the only deviation from the norm is a heart rhythm disturbance. In Dobermans, left ventricular extrasystole and ventricular tachycardia are most often recorded (Fig. 5). In boxers, extrasystoles and tachycardia are of proaventricular origin (Fig. 4).

Echocardiographic examination

An echocardiographic (EchoCG) study reveals an increase in the left and right parts of the heart, a significant decrease in the global contractility of the left ventricular myocardium (decrease in the values ​​of the ejection fraction and shortening fraction) (Fig. 6.). Doppler cardiography can reveal the relative insufficiency of the mitral and tricuspid valves. In Doberman Pinschers, the normal size of the left ventricle is slightly lower than in dogs of other breeds with a body weight of 35-40 kg, therefore the end-diastolic size (EDD) of the left ventricle is more than 46 mm, and the end-systolic size (ESD) of the left ventricle is more than 39 mm are considered enlarged. With an advanced stage of the disease and significant expansion of the chambers of the heart, an echocardiographic study provides comprehensive diagnostic information, but if the pathology has not yet reached its full development, then additional echocardiographic studies using tissue Dopplerography are necessary.

Rice. 6. EchoCG of a dog with DCM (B- and M-modes). Significant increase in the cavity of the left ventricle and a decrease in global myocardial contractility.

X-ray examination

On radiographs in the lateral projection, generalized cardiomegaly is determined. At the same time, the shadow of the heart is large and round. Advanced left atrium manifested by enlargement and straightening of the caudodorsal part of the heart figure with the formation of a right angle pattern. An enlarged left ventricle results in straightening of the caudal edge of the heart (disappearance of the caudal cardiac waist) and closer contact with the diaphragm. The expansion of the right sections increases the cardiac shadow in the craniodorsal direction, which leads to the disappearance of the cranial cardiac waist and wider contact with the sternum. In this case, a dorsal displacement of the trachea is observed, which makes it parallel to the spine.

Cardiomegaly can be assessed by calculating the cardiovertebral score (VHS). VHS is the sum of the lengths of the short and long axes of the heart figure. The length of each segment is measured by the thoracic vertebrae, starting with T4. On average, the cardiovertebral indicator should not exceed 10.7 vertebrae (for boxers - 12.6 vertebrae). Disturbances in the pulmonary circulation that develop as a result of left ventricular failure manifest themselves diffuse increase density lung tissue. In the initial stage of pulmonary edema, fuzzy (cotton-wool) darkening occurs at the roots of the lungs. As the edema progresses, the darkening spreads caudally. Air bronchograms appear - X-ray negative linear formations, reflecting air-filled bronchi surrounded by edematous lung tissue. With pulmonary edema, the width of the pulmonary vein of the cranial lobes of the lungs exceeds the width of the artery of the same name (normally their width should be the same).

Differential diagnosis DCM with infiltrative myocardial diseases and myocarditis, which can also lead to cardiomegaly with a clinical picture identical to DCM, is difficult and may require a puncture biopsy of the myocardium. However differential diagnosis These diseases are of rather theoretical interest, since the approaches to treatment are the same. Valve defects hearts resulting in left-sided enlargement are easily identified with a careful physical examination and echocardiography. Pericardial effusions and peritoneal-pericardial diaphragmatic hernia are easily diagnosed by echocardiography and contrast-enhanced radiography of the gastrointestinal tract.

There are a number of myocardial diseases of non-inflammatory origin that manifest themselves in at a young age animals and are difficult to treat with medication.

Dilated cardiomyopathy (DCM) refers to these types of diseases and is characterized by increasing organ dysfunction, resulting in the death of the animal. This pathology is inherent in young animals and today is of an idiopathic nature and a hereditary factor.

Available methods surgical treatment of this disease are ineffective, and therefore, an intensive search is currently underway for alternative options for surgical treatment of DCM.

Purpose This study was to evaluate the possibility of orthotopic donor heart transplantation in clinical practice in dogs with dilated cardiomyopathy.

Materials and methods.

The material was an animal (dog) with DCM of the Doberman Pinscher breed at the age of two years, which underwent orthotopic donor heart transplantation.

The animal was subjected to special research methods, which included blood and urine tests, ECG, radiography, ECHO cardiography with assessment of stroke volume, cardiac output, end-diastolic pressure in the left ventricle and myocardial contractile function. A prerequisite was the exclusion of pulmonary hypertension.

At the stage of compensation of cardiac activity supported drug therapy, intramyocardial injection of autologous stem cells was performed in a volume of 2 million per 1 ml. The material was taken under local anesthesia using the humerus and ilium.

Stem cells were injected intramyocardially under minithoracotomy conditions. general anesthesia into the wall of the left ventricle.

Stem cell transplantation did not produce a functional result, which was assessed after 65 days.

The animal became refractory to therapy and developed NYHA IV (Human Functional Class Assessment) congestive heart failure. At the stage of development of decompensation, a decision was made to perform a donor heart transplantation (Fig. 1).

The donor was a dog approximately similar in weight and chest size with a concomitant injury (vertebral fracture and damage to the abdominal organs) incommensurable with the animal’s future life.

The donor's heart condition was instrumentally assessed and the donor-recipient blood group compatibility was immunologically determined by conducting cross-tests and a "cross-match" lymphocyte compatibility study was carried out.

The donor stage (removal of the heart) was carried out according to the generally accepted method and pharmaco-cold preservation was carried out in the cardioplegic solution “Consol” for 120 minutes.

The recipient stage of the operation was performed under artificial circulation (CPB) using a pediatric oxygenator.

The IR device was connected according to the femoral artery, vena cava (extrapericardial) scheme. The adequacy of perfusion was assessed by indicators of the oxygen transport function of the blood, the acid-base state (ABS) of venous and arterial blood.

Donor heart was excised according to the following scheme: aorta, vena cava, pulmonary artery, left atrium (LA) with preservation of the pulmonary veins on single platform. During excision, excess of the recipient's own tissues of the above structures was left. Preparation of the donor heart for transplantation included excision of a portion of the left atrium comparable to the size of the recipient site. Excess aorta and pulmonary artery were excised, preserving their walls at a distance of at least 1 cm from the valves (Fig. 2a, b).

The final adjustment of the length of the aorta, PA and vena cava of the donor heart and similar structures of the recipient was carried out at the time of implantation.

The first to perform an anastomosis with the LA was with a 2-row continuous suture using Prolene 4-0 thread. Next, anastomoses with the inferior and superior vena cava using Prolene 4-0 thread, aorta and PA (Fig. 3a, b, c).

Removal of air from the cavity of the left ventricle using LV drainage and through an aspiration needle in the suture area of ​​the ascending aorta; after restoration of blood flow, spontaneous restoration of sinus rhythm was noted. Myocardial ischemia was 38 minutes (main stage) (Fig. 4a, b).

At the stage and after completion of the operation, satisfactory pumping function of the graft was noted according to flowmetry and invasive assessment of blood pressure in the cardiac cavities.

We did not note any signs of encephalopathy or manifestations of multiple organ failure in the dog.

In the post-transplantation period, the animal received two-component immunosuppressive therapy with cyclosporine A (Sandimmune NEORAL) at a dose of 800-1000 ng/ml per day and prednisolone 0.5 mg/kg.

Intensive therapy and inotropic support with dopamine were provided for five days.

Treatment of acute renal failure was required against the background of bilirubin tubular necrosis - as a result of hemolysis of erythrocytes using an IR field.

Despite the preservation of satisfactory hemodynamic parameters and graft function, on the 23rd day after surgery the animal died due to the development of complex rhythm disturbances and progression of renal failure resistant to intensive therapy.

Conclusion.

Dilated cardiomyopathy in dogs a complex problem characterized by a rapid, uncontrollable course of the disease, which results in the inevitable death of the animal.

Orthotopic heart transplantation in dogs with idiopathic DCM is feasible in clinical practice.

Optimization of approaches to carrying out cardiopulmonary bypass, the early postoperative period and the widespread introduction of the operation into clinical practice will save the lives of animals with end-stage cardiovascular failure.

Publications on the topic.

1. Vorontsov A.A., Belyanko I.E. et al. Clinical case of orthotopic heart transplantation in a dog with idiopathic dilated cardiomyopathy. Ekaterinburg “Veterinary Clinic”, 2005, No. 4, pp. 25-28.

2. Vorontsov A.A., Belyanko I.E. et al. Clinical case of heart transplantation in a dog with idiopathic dilated cardiomyopathy. M., XIII International Veterinary Congress, 2005, pp. 77-78.

List of abbreviations: CHD – congenital heart defect, PDA – patent ductus arteriosus, LA - left atrium, LV – left ventricle, RV – wall of the right ventricle, PA – pulmonary artery, ACEI – angiotensin-converting enzyme inhibitors, ADSD – Amplatzer duct occluder devices.

A patent ductus arteriosus is the presence of an abnormal vascular connection between the aorta and the pulmonary artery. The name “patent ductus botalli,” previously used, was associated with the name of the Italian physician Leonardo Botalli (1530–1600), but the first anatomical descriptions of the PDA probably belong to Galen (130–200), and the explanation of the functional significance of the duct for pre- and postnatal blood circulation - Harvey.

Incidence

Pathophysiology

Clinical signs

Physical examination

Diagnostics

X-ray:

• Dilatation of the pulmonary trunk on the dorsoventral projection (for 1–2 hours);
• Dilatation of the ascending aorta (12–1 hour);
• Dilatation of the left atrial appendage (2–3 hours in DW projection). All of the above changes on the DW projection occur in 25% of cases;
• Dilatation of the left ventricle;
• Hyperemia of the lungs leading to pulmonary edema.

Echocardiography(2D and M mode):

• Often dilatation of the left atrium;
• The left ventricle is spherical and dilated (eccentric hypertrophy, increased EPSS as one of the criteria);
• Dilatation of the main pulmonary trunk;
• Normal left ventricular function in the initial stage and decreased contractility fraction in severe stages;
• The duct can be visualized between the main pulmonary artery and the ascending aorta (preferably a left parasternal cranial short-axis view with the pulmonary valve);

Echocardiography (Doppler):

• Constant retrograde systolic and diastolic flow in the main pulmonary artery from the patent duct;
• The patent duct can be visualized with color Doppler;
• Secondary mitral regurgitation (common).

Treatment

Death during ligation of a PDA occurs in 6% of cases, of which 1% are anesthetic risks and 5% are due to bleeding due to rupture of the duct wall during ligation and other complications (the authors note that the risks of bleeding due to rupture of the duct wall decrease with increasing surgeon experience). One of the complications is duct recanalization (out of 173 dogs operated on, four animals required repeat surgery).
It is noteworthy that in the case of closure using the percutaneous method using Amplatzer duct occluder devices, no reoperation was required in any animal. It is also worth noting that intraoperative mortality occurred in four animals with ligation, and 0 with ADSD.
Postoperative treatment should be aimed at restoring the myocardium after prolonged volume overload and, in some cases, at relieving pulmonary hypertension. As a rule, pimobendan (Vetmedin) is used - 0.125–0.5 mg/kg 2 times a day; sildenafil – 0.5–2 mg/kg 2–3 times a day (for pulmonary hypertension). ACE inhibitors and diuretics are used, as a rule, for severe heart failure.

Bibliography:

1. Virginia Luis Fuentes, Lynelle R. Johnson and Simon Dennis. BSAVA Manual of Canine and Feline Cardiorespiratory Medicine, 2nd Edition. 2010.
2. Manual of Canine and Feline Cardiology, 4th Edition. 2008.
3. Small Animal Surgery (Fossum), 4th Edition. 2012.
4. Cardiovascular Disease in Small Animal Medicine. 2011.
5. E. Christopher Orton in Veterinary Surgery - Small Animal 2 Volume Set. 2012.
6. Long-term outcome in dogs with patent ductus arteriosus: 520 cases (1994–2009).
7. Lectures on cardiac surgery edited by L. A. Bockeria. Moscow. 1999.

Abbreviations: HM – Holter monitoring, DCM – dilated cardiomyopathy, OAP – patent aortic duct, LA – pulmonary artery, LV – left ventricle, LP – left atrium, MK – mitral valve, TK – tricuspid valve, ZSN – congestive heart failure, PVC – ventricular extrasystole, CHF – chronic heart failure, EOS – electric axle hearts, SNK – capillary refill rate.

Introduction

Tasks:
– ABOUTdesignate rocks with increased risk cardiac diseases;
– INreveal visible and hidden symptoms diseases;
– WITHformulate clinical predictors of increased perioperative cardiovascular risk (CHF, life-threatening arrhythmias, death);
– ABOUTidentify diagnostic methods that allow a qualitative assessment of the condition of cardio-vascular system and hemodynamics, which means more accurately determining the degree of anesthetic risk.

Materials and methods

2. Giant breed dogs ( Great Danes, Irish wolfhounds, Newfoundlands and cocker spaniels) are predisposed to DCM and, unlike other dogs, even at the initial stage of the disease can have severe rhythm disturbances (atrial fibrillation and PVCs).
Standard examination: the same as for Dobermans. Particular attention should be paid to auscultation, since atrial fibrillation has a characteristic pronounced sound.
Echocardiography shows chamber dilatation and decreased contractility; a normal variant is also often possible.
ECG – normal, PVCs or atrial fibrillation.
HM ECG - the presence of 50-100 PVCs, paired PVCs or at least one episode of atrial fibrillation may indicate latent DCM.
Chest X-ray - with the development of CHF, an increase in the shadow of the heart, signs of venous stagnation, in other cases - the norm.
The anesthetic risk in the presence of DCM increases to grade 3-5. Treatment is appropriate in patients with changes on echocardiography at least 2 weeks before surgery.

3. Ventricular arrhythmias in German shepherds. Research is not completed, it is observed genetic predisposition, but histological changes in the myocardium and conduction system have not yet been found.

HM ECG – the only way determine the risk of sudden death and the presence of pathology.
Dobermans, giant breeds, cocker spaniels. !!!The table needs to be corrected

4. German Boxer dogs have a genetically inherited predisposition to arrhythmogenic right ventricular dysplasia (ARVC). They, like Dobermans, have three stages. Only, unlike classical DCM, remodeling of the heart chambers is often absent. Males are more predisposed to the disease. Clinical symptoms may be absent, fainting is possible, and in severe cases, right-sided heart failure is likely to develop.
Routine examination: Cardiac auscultation should be performed simultaneously with pulse assessment to identify the presence of PVCs. Sometimes there may be noise on the TV. Much attention must be paid to family history.
Additional diagnostics. Echocardiography of the heart: normal or signs of remodeling of the right and sometimes left chambers.
ECG: isolated rhythm disturbances are possible, the absence of changes in the clinic does not exclude the presence of arrhythmias, the presence of one or more PVCs is an indication for chemotherapy.
HM ECG: gold standard, recommended for all boxers from 3 years of age. The presence of more than 50-100 PVCs or group PVCs is a sign of the disease; With age, the number of disorders increases.
Chest X-ray: Almost always non-diagnostic, direct X-ray may be more helpful.
Troponin-I test: not very sensitive, but better than NP-proBNP. Genetic tests are available. When ARVC is diagnosed, the anesthetic risk increases to grade 3-5, with long-term use Omega-3 fatty acids the risk of bleeding during surgery increases. Antiarrhythmic therapy from 1000 PVCs.

5. Dogs of toy breeds (toy terrier, chihuahua, miniature poodle, dachshund, Yorkshire terrier, Cavalier King Charles spaniel, etc.) are predisposed to the development of myxomatous changes in the mitral valve, as a result of which the valve becomes denser and deformed. These changes develop more often after 5 years.
Standard examination: auscultation is highly informative; pronounced noise at the MV optimum point most likely indicates the presence of changes in the valve. The degree of noise does not correlate with the volume of the lesion!
Additional diagnostics. Cardiac echocardiography: the gold standard. Regurgitation on the MV, LA dilatation, LV dilatation, signs depend on the duration of the disease.
ECG: usually normal, with dilatation of the chambers there is a levogram, there may be a P-pulmonale.
HM ECG: rare disorders even with pronounced remodeling of the chambers. Indicated in the presence of syncope.
Chest X-ray: signs of an increase in the shadow of the heart due to the LA and other chambers, in severe cases - signs of venous stagnation.
The degree of anesthetic risk increases depending on the degree of CHF. It is always advisable to prescribe treatment if there are no acute indications for surgery.

A separate group includes congenital heart defects. A defect is a violation of the normal structure of the heart. On average, 1% of all dogs are born with birth defects hearts (Buchanan, 1999). Most defects reveal themselves to auscultation, but experience and attention are important here. More often detected in puppies; old dogs either die or have clear signs of CHF.

6. Newfoundlands, retrievers and Rottweilers have a breed predisposition to aortic stenosis. Subaortic stenosis is the most common of the defects; the degree of manifestation of symptoms depends on the severity of stenosis: with slight narrowing of the lumen external changes there may not be any at all, and with severe obstruction, fainting, shortness of breath and fatigue are common.
Auscultation: noise at the optimum point of AC.
EchoCG: gold standard, regurgitation on the AC, velocity above 1.9 m/s.
X-ray is not very informative.
ECG and HM ECG: changes are more often observed with the development of CHF. There may be a levogram (shift of the EOS to the left).
The degree of risk depends on the degree of stenosis and the development of CHF.

7. Wire-haired terriers, beagles, Scotch terriers, and miniature schnauzers are predisposed to pulmonary artery stenosis. Clinical signs also depend on the degree of stenosis.
Auscultation can detect a murmur on the PA and often on the TC. If the noise is pronounced, it can be confused with MK.
EchoCG: gold standard, rate above 1.9 – stenosis. Pancreatic hypertrophy. With a pressure gradient above 40-60 mm Hg. surgical treatment should be considered. If the operation is planned, then it makes sense to carry it out after eliminating the defect, most often using balloon valvuloplasty. Without correction, the anesthetic risk increases to grade 4-5.

8. Patent ductus arteriosus (Botallov) is normal; this vessel ceases to function after birth, but in some animals (Chihuahua, Pomeranian, collie, Newfoundland, etc. + cats) it may persist. It has been noted that males are more often affected.
Standard inspection. This defect is characterized as “blue” because it is accompanied by severe cyanosis of the mucous membranes. On auscultation, a constant murmur is heard during systole and diastole.
Cardiac ECHO: the gold standard, there may be an error with a common aortopulmonary trunk.
Surgical treatment is indicated, both direct access and endovascular.

9. Less common than others are defects of the interventricular and interatrial septa, tetralogy of Fallot (a hereditary predisposition has been proven in Keeshonds).

10. Tricuspid valve dysplasia is inherited in retrievers.
On auscultation there is a noise in the TC area. The ECG shows signs of a right gram. X-ray: increase in the shadow of the heart due to the right parts. Echo is the gold standard, signs of right chamber dilatation and regurgitation on the TC. In severe cases, right-sided HF and ascites. The disease progresses rapidly. Recommended surgical plastic surgery TK.

11. MK dysplasia. More often susceptible large breeds. The disease can remain without clinical manifestations for a long time. On auscultation there is a murmur on the heart valve. EchoCG: regurgitation on the MV, other changes depend on the duration of the disease. ECG and X-ray are usually unchanged; there may be a levogram and venous stagnation. Surgical plasty of the MV is recommended, and, if necessary, plasty of the left atrium.

Conclusion

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VORONTSOV A.A., Vet clinic Mi V. ZUEVA N.M.
veterinary clinic CENTER

As a rule, primary heart tumors, depending on their location, are divided into three groups: tumors developing at the base of the large vessels of the heart, tumors of the heart wall and pericardial tumors. The problems of early diagnosis, as well as the choice of treatment method for primary tumors of the heart and large vessels, remain relevant.

CLINICAL EXAMINATION

A 9-year-old collie dog was brought to the clinic for consultation regarding worsening general condition, shortness of breath and cough. At the moment clinical examination ataxia, enlarged chest contours, tachypnea, anemic mucous membranes, low capillary refill rate (3 seconds), and exaggerated tracheal reflex were noted. The temperature was within the physiological norm. When auscultating the heart at the apex, the cardiac impulse is diffuse, a dull first sound and a soft systolic murmur are heard. In projection pulmonary artery and aortic sounds are sonorous, the systolic murmur is amplified and transmitted to the jugular vein, the pulse in the femoral artery is rhythmic, weak filling with a frequency of 150 beats per minute. The initial physical examination required additional methods clinical and laboratory studies.

ADDITIONAL RESEARCH METHODS

X-ray examination of the chest was performed in the lateral (lateral-lateral) and direct (dorso-ventral) projections. A lateral radiograph revealed a significant increase in the silhouette of the heart with displacement of the trachea and lobes of the lungs in the dorsal and caudodorsal directions, respectively (photo 1).

A decrease in the voltage of the Q, R, and T waves was recorded on the graphical curve of the electrocardiogram, and with repeated studies it became more pronounced.

An echographic examination of the chest cavity organs indicated the accumulation of fluid in the pericardial cavity (hydropericarditis), as well as thickening of the walls in the right atrium with myocardial heterogeneity due to hyperechoic diffusely localized areas. At the base of the aorta, heterogeneous echogenic masses with uneven and poorly defined boundaries are visualized (the diameter of the aorta is within normal limits).

During pericardiocentesis in the 5-7 intercostal space, about 800 milliliters of serous-hemorrhagic exudate mixed with fibrin were aspirated. The obtained material was sent to the laboratory for cytological examination.

Further echographic examination of the heart and blood vessels after pericardiocentesis showed that the ejection fraction was 62%, contractility 34% and stroke volume 61%.

Laboratory blood tests indicated anemia, moderate leukocytosis, increased biochemical parameters of blood serum: albumin 48 g/l, ALT 123 -IU/l, AST - 62 IU/l, alkaline phosphatase - 164 IU/l.

A microscopic examination of the centrifugate revealed the presence of a polymorphic cellular infiltrate with characteristic elements of inflammation without signs of atypia.

After pericardiocentesis and intensive symptomatic therapy (use of inotropic drugs, ACE inhibitors, antibiotics, cardioprotectors), the animal felt better, appetite appeared and symptoms of shortness of breath disappeared. Clinical signs of the disease recurred again ten days later.

Based on observations of the course of the disease, recurrence of clinical signs and the results of the studies, after obtaining the consent of the owners, the animal underwent surgical intervention in the scope of a diagnostic thoracotomy.

A sternotomy and wide pericardiotomy were performed under general anesthesia. During inspection of the chest cavity, the following were discovered: pericardial effusion, a tumor at the base of the pulmonary artery and aorta with a characteristic

Fogo 1. X-ray of the chest in the laterolateral projection.

zophytic growth and spread to the right atrium (photo 2). Palliative removal of the tumor in the area of ​​the aorta and pulmonary artery was performed, followed by step-by-step suturing surgical wound subject to the conditions of postoperative drainage of the pericardial and thoracic cavities (photo 3,4).

Histomorphological examination of the obtained surgical material indicated a neoplasm in the area of ​​the paraganglionic structures of the aorta, which was identified as non-chromaffin paraganglioma (chemodectoma) (photo 6).

The rehabilitation period after surgery was 12 days.

After 9 months, the animal was again taken to the clinic with signs of increasing weakness and shortness of breath. When carrying out additional methods of radiographic and echographic studies, metastases of the neoplasm into the cavity of the right atrium with obstruction of the latter and hepatomegaly were identified. The animal was euthanized.

Pathological examination confirmed the presence of a tumor in the right atrium (Figure 5). Repeated histomorphological examination revealed the presence of partial necrosis of the atrium wall and metastases of the chemodectoma into the cavity of the right atrium.

Photo 2. Neoplasms at the base of the aorta and inaccurate artery.

Photo 3. Appearance aorta after tumor removal.

Photo 4. The final stage of the operation.

Photo 5. Macroscopic specimen of a heart with metastasis in the right atrium.

DISCUSSION

Various literature sources indicate the rarity of primary cardiac tumors in small domestic animals. Clinical picture The persistence of primary tumors in the heart region has not been sufficiently studied; it largely depends on both the nature (type, degree of differentiation, growth rate, nature) and the location of their localization. The general clinical signs of most neoplasms are: worsening of the disease with rapidly progressing heart failure, poorly effective etiotropic and symptomatic therapy. Early diagnosis in the preclinical period of the disease is accompanied by certain difficulties.

In the in-depth diagnosis of primary tumors of the heart and large vessels, differentiation of benign and malignant neoplasms, as well as obtaining additional information about the localization of the affected area and metastasis, computed tomography (CT) and nuclear magnetic resonance (MRI) play a leading role. Due to the impossibility of conducting this type of research, diagnostic surgery in our conditions is the method of choice. Waiting tactics for primary cardiac tumors are justified in the absence of disturbances in intracardiac and general hemodynamics.

In our case, changes in the radiographic picture (increased silhouette of the heart with displacement of the trachea and lobes of the lungs) and ECG data (hypovoltage of the Q, R, T waves) caused the assumption of the presence of hydropericarditis of an oncological nature, which was confirmed by echographic examination. Aspiration of the contents of the pericardial cavity made it possible to temporarily restore hemodynamics and cardiac function, but conservative treatment was not effective and, as a result, resolved with a rapid relapse.

Despite the echographic picture indicating the presence of a neoplasm, cytological examination aspirate did not make it possible to identify elements indicating the development of a neoplastic process. Diagnostic sternotomy resulted in removal of the tumor and prevention of recurrence of fluid accumulation in the pericardial cavity through drainage.

During the anatomy - morphological research The presence of a malignant non-chromaffin paroganglioma (chemodectoma)* of the aortic paroganglioma with metastasis to the right atrium was established. The malignancy or benignity of a tumor is determined not on the basis of morphological characteristics, but by the presence or absence of metastases. In dogs, cases of metastases of nonchromafin paragangliomas (chemodectomas) spreading to distant organs, for example, the lungs, have been reported [1]. In our situation, the target of chemodectoma metastasis was the wall of the right atrium with subsequent spread into its cavity, which, in fact, provoked hemodynamic disturbances and a sharp deterioration in the functional activity of the heart.

*Paraganglioma paragangiomaj. Syn. parasympathoma. / chromaffin parasympathoma or chromaffinnoma (pheochromocytoma). Fechromocytoma (gr. phaitos, brown or brown; Shospa, color; kutos. cell) (English pheochromocyloma]. A tumor highly enriched with adrenaline and norepinephrine, developing in the depot of chromaffin cells of the adrenal medulla (medullosurrenaloma, hypertensive surrenaloma, medullary hyperneforma) or , which happens extremely rarely (10-20% of cases), in a depot of aberrant (deviating from the norm) formations of the tissue itself, localized in the sympathetic plexuses of the adrenal glands or pelvis (chromafin paroganglioma).Classically (in humans) it manifests itself as paroxysmal hypertensive crises with hyperglycemia , sometimes glucosuria and the release of catecholamines into the urine, leading to cardiorenal disorders and disorders of the blood supply to the brain of an arterial nature. Most often (60% of cases), it provokes permanent and severe arterial hypertension. - 2 parasympathomas non-chromafin chemoreceptoma (also known as chemodectoma). Chemodectoma ( gr. khemeia. chemistry; dektes, which collects; ota. tumor) [English] chemodectoma]. This is a rare, mostly benign tumor that develops in the chemoreceptor part of the organs, in particular in the carotid glomeruli. Its structure is similar to that of parogangliomas, but it does not contain chromaffin cells. Neurogenic tumor. Neurogenic tumors in the chest cavity most often arise in the mediastinum from the parovertebral nerve trunks, less often from the membrane elements of the chest wall, and only sometimes affect the paroganglia of large vessels.

Photo 6. Chemodectoma (hemotoxylin - eosin, x 200).

CONCLUSION

Due to the impossibility of using more in-depth additional advanced methods clinical trial(CT and MRI), diagnostic sternotomy was the method of choice.

Cytological examination of the aspirate, despite the echographic picture indicating the presence of a neoplasm, did not make it possible to identify elements indicating the development of a neoplastic process. Waiting for primary cardiac tumors is justified in the absence of disturbances in intracardiac hemodynamics and general hemocirculation.

The tactics of surgical intervention depend on the size of the tumor, its location, mobility, as well as the degree of involvement of the valve apparatus and myocardium in the pathological process.

Literature

1. Makey A, Appleby E. Bulletin of the international classification of pathology and morphology of small domestic animals. 1975, Ar. 34.

2. Richard A.S. White. Oncological diseases small domestic animals, 1993, art. 50-52.

3. J. Delamare. Dictionere des termes de medicine. 25th edition, Maloine, 1998, pp. 1-973.

4. Sutter PF: Thoraccic Radiography: A Text Atlas of Thoraccic Deseasis of the Dog und Cat. Wettswil, Switzerland 1984, pp. 210-216.

5. Reif JS, Rhodes WH: The lungs of aged dogs: A radiographic-morphologic correlation. JAmVetRad Soc, 1966, 7, pp. 5-11.

magazine "Veterinarian" 2/2004