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2.Acute severe myocarditis.

3.Recurrent myocarditis with recurrent exacerbations.

4.Myocarditis with increasing dilatation of the heart cavities and, to a lesser extent, hyper myocardial trophy (usually diffuse form).

5.Chronic myocarditis.

clinical picture. The symptomatology of myocarditis is determined by the type and virulence of the pathogen, the resistance of the macroorganism, the severity of inflammatory and fibrotic changes in the myocardium, as well as its initial state. Acute myocarditis developing against the background of an infectious disease (viral infection, diphtheria, typhoid fever

etc.), is manifested by symptoms of the disease that led to the development of myocarditis, and by objective signs of damage to the heart muscle. If, in acute infectious and toxic myocarditis, complaints of a cardiac nature appear in the first days and even hours after

the influence of an etiological factor, then with chronic myocarditis, there is usually no direct connection between the onset of heart disease and infection - complaints and

clinical symptoms suggesting the development of myocarditis appear later

2 - 3 weeks from pathogenic effects.

The main symptoms of myocarditis are pain in the heart area, general weakness, fatigue, shortness of breath, palpitations, heart failure, fever, sweating. Some patients have a tendency to bradycardia and arterial hypotension. Physical examination reveals tachycardia, arrhythmia, expansion of the boundaries and weakening of the heart sounds. Often a systolic murmur is heard

at the apex of the heart and at the Botkin point, due to mitral regurgitation due to dysfunction of the papillary muscles. Patients with severe myocardial injury develop a proto-diastolic gallop rhythm and symptoms of congestive heart failure.

There are some features of the manifestations of acute myocarditis, depending on

type of pathogen. For example, with viral myocarditis, along with inflammation of the myocardium, often pericarditis develops, and with diphtheria myocarditis - conduction disturbances.

Laboratory and instrumental diagnostics. The study of the blood of patients myocarditis reveals changes characteristic of the current inflammatory process: neutrophilic leukocytosis, an increase in ESR, an increase in the level of C-reactive protein, fibrinogen, á- and ã- globulins. In favor of myocardial localization of inflammation may

indicate an increase in the concentration of creatine phosphokinase (MB-fraction), lactate dehydrogenase (cardiac fractions with a predominance of 1 over 2), aspartic aminotransferase, cardiac troponins T and I. More sensitive to detect inflammation in

myocardium are immunological techniques. With myocarditis in 40% of patients in serum blood, cardiac antigens are detected, and in 70% of patients antimyocardial antibodies to various proteins of the cardiomyocyte cytoskeleton are detected. An increase is registered concentrations of pro-inflammatory cytokines - interleukins-1â, -8, -10, necrosis factor tumor-á, interferon-á and adhesion molecules. 75% of patients with myocarditis have hypersensitivity of lymphocytes to myocardial tissue and a positive degranulation test basophils, confirming the fact of the antigen-antibody reaction that occurs on the surface of these cells. In patients with viral myocarditis after 2-3 weeks. after suffering

acute respiratory disease, specific antibodies are detected in the blood (more often

only to influenza viruses, Coxsackie A and B, enteroviruses with the highest cardiotropism). The viral genome is found in myocardial biopsies in 40–70% of patients with acute

myocarditis.

The most common electrocardiographic sign of myocarditis, which occurs in 50–70% of patients, is a change in the T wave (flattening, inversion, biphasic). AT

30 - 50% of cases are recorded depression or elevation of the ST segment. In 25 - 45% of patients

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supraventricular and ventricular extrasystoles are detected, in 25 - 30% - blockade of the legs

bundle of His, in 5-15% - sinoatrial and AV blockade. With myocarditis, the formation of

pathological Q waves and regression of R waves is possible, which is explained by the development of non-co

myocardial necrosis.

Echocardiographic examination in 20 - 50% of cases reveals dilatation of the chambers heart, decreased systolic and diastolic dysfunction of the left ventricle.

In some patients with myocarditis, ultrasound examination of the heart revealed

there is mitral and tricuspid regurgitation, a slight divergence of the sheets of the peri

card, indicating concomitant pericarditis.

All changes detected in laboratory, immunological, electrocardiographic and echocardiographic studies are not specific for myocarditis, therefore, in doubtful cases, it is advisable to confirm the diagnosis by morphometric methods, which allow obtaining a more reliable diagnostic

information. This group of methods includes: endomyocardial biopsy followed by

histological examination of myocardial tissue; tomoscintigraphy of the heart with radiopharmaceuticals that selectively accumulate in the area of inflammation and in intact cardiac tissue

muscles; magnetic resonance imaging of the heart with contrast.

Diagnosis. Due to the absence of any single symptom pathognomonic for

inflammatory myocardial damage, the diagnosis of myocarditis is established on the basis of an analysis of the totality of diagnostic criteria identified in the process of a comprehensive examination of the patient. Diagnostic criteria for myocarditis were proposed by the experts of the New York Heart Association. There is a chronological relationship of the transferred infection

(or allergic reaction, or toxic effect) with the appearance of the following car

dial symptoms:

"Big" criteria:

1.Cardiomegaly.

2.Heart failure.

3.Cardiogenic shock.

4.Morgagni-Adams-Stokes syndrome.

5.Pathological ECG changes, including cardiac arrhythmias and distance.

6.Increased activity of cardiospecific enzymes (CPK, MB-CPK, LDH, LDH1 and LDH2) and troponin content.

"Small" criteria:

1.Laboratory confirmation of past infection (for example, high titers of antiviral antibodies).

2.Weakening of the I tone.

3.Protodiastolic gallop rhythm.

Combination of signs of past infection and two major criteria or one large and two small is considered sufficient for the diagnosis of "myocarditis".

Examples of diagnoses:

1. Acute diphtheria myocarditis. Atrioventricular block II stage. with Samoilov-Wenckebach periods.

2.Acute viral myocarditis (Coxsackie B). Paroxysmal ventricular tachycardia 20.12.09, acute heart failure (interstitial pulmonary edema 20.12.09).

3.Acute myocarditis of unspecified etiology. Chronic tonsillitis in Art. exacerbations. Ventricular extrasystole.

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differential diagnosis. In differential diagnosis, first of all, it is necessary to exclude coronary artery disease. Clinical symptoms and ECG changes in acute

myocarditis in some cases are similar to those in acute coronary syndrome. For both

diseases are characterized by an increase in the concentration of biomarkers of myocardial necrosis in the blood.

Clinical and electrocardiographic manifestations of chronic myocarditis in a number of patients reminiscent of angina pectoris. The correct diagnosis allows you to establish a detailed questioning

the patient (the relationship between the appearance of complaints and past infection, history and risk factors for coronary artery disease),

analysis of the nature of the pain syndrome (localization, intensity, connection with physical activity, reaction to taking nitroglycerin), the results of physical examination (in patients myocarditis, cardiomegaly and heart murmurs are more often detected), monitoring of ECG dynamics, as well as a number of additional studies: ECG Holter monitoring, stress tests, coronary angiography, magnetic resonance imaging

contrast-enhanced hearts.

The main non-coronary heart diseases that should be treated

differential diagnosis of myocarditis are: rheumatic fever, infective endocarditis

subacute course, cardiomyopathy, as well as heart damage in amyloidosis, sarcoidosis,

hemosiderosis. Symptoms similar to myocarditis are often observed in patients with thyroid diseases and autonomic dystonia.

When making a differential diagnosis with rheumatic myocarditis, it should be remembered that that rheumatic fever occurs after an acute inflammatory disease of the nasopharynx caused

by group A ÿ- hemolytic streptococcus. Rheumatism is characterized by a multiorganism of clinical manifestations. Heart disease in rheumatic fever

infectious-immune myocarditis includes specific endocarditis with the form

heart disease and pericarditis.

Difficult is the differential diagnosis of chronic severe myocarditis

course (traditionally, this form is called Abramov-Fiedler myocarditis) and dilated cardiomyopathy. Both diseases are characterized by severe cardiomegaly, HF, and thromboembolic complications. Histological changes in the myocardium in these diseases are not have specific characteristics. In favor of myocarditis may indicate the relationship of onset diseases with infection, vaccination or medication, manifestations of systemic allergy, inflammatory changes in the blood test and a positive clinical reaction to

anti-inflammatory therapy. At the same time, it should be taken into account that the viral and

immune components of the pathogenesis of myocarditis and dilated cardiomyopathy completely coincide. A Dilated cardiomyopathy is based on numerous genetic disorders that cause changes in the

properties of myocardial proteins, membranes, and mitochondria of cardiomyocytes. As a result of these changes, there is a decrease in energy production in cells.

heart muscle, myocardial systolic function decreases, heart failure and disorders develop heart rhythm. Viral infection and subsequent autoimmune reactions can serve as a trigger for genetically determined disorders in the structure and function of the myocardium. Thus, in patients with a hereditary predisposition, it is possible to transform acute myocarditis into chronic, and later into dilated cardiomyopathy.

Endomyocardial biopsy data play an important role in the differential diagnosis of myocarditis with other heart diseases. Endomyocardial biopsy is considered appropriate in patients with a fulminant course of the disease, accompanied by the onset and exacerbation of heart failure within 2 weeks, progressive

cardiomegaly, severe arrhythmias and conduction disturbances, as well as with the ineffectiveness of standard therapy.

Flow. In most cases, myocarditis is characterized by a benign course. However, in some patients, the disease is complicated by severe heart failure,

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AV blockade, ventricular arrhythmias, thromboembolism. The occurrence of complications significantly worsens the prognosis.

Forecast and outcomes. The most common outcome of myocarditis is recovery. AT

At the same time, in many patients, in the absence of any clinical symptoms, ECG changes remain, indicating the development of focal or diffuse myocardial cardiosclerosis. The development of fibrous tissue in the myocardium is the pathophysiological basis for rhythm and conduction disturbances, which are often recorded in

patients with myocarditis. One of the adverse outcomes of myocarditis is sudden death, the main causes of which are ventricular arrhythmias

heart and complete AV block. Often in patients with myocarditis cardiosclerosis, systolic dysfunction is noted, which intensifies over time and begins to manifest symptoms of chronic HF. For AbramovFiedler myocarditis, as well as acute

diffuse myocarditis of various etiologies is characterized by the development of severe cardiomegaly and severe heart failure, progressing to the terminal stage. In patients with a genetic predisposition, the outcome of viral myocarditis may be a dilated cardiomyopathy.

Treatment. Treatment of patients with myocarditis is carried out in a hospital.

General measures are to limit physical activity to half bed

(in the most severe patients with bed rest) and the appointment of a hypoallergenic diet with the predominance of dairy products, vegetables, fruits and cereals.

Etiotropic therapy is indicated for patients with bacterial myocarditis. For elementary

stage of antibacterial treatment, cephalosporins are preferred. Persistent viral infection in patients with myocarditis complicated by heart failure is theoretically the basis for the use of exogenous interferons á and â. preliminary

clinical observations have shown that antiviral therapy leads to the disappearance

viral genome from the myocardium, but its effectiveness has not yet been confirmed in large clinical research.

The main means of treating patients with myocarditis are drugs with anti-inflammatory and desensitizing properties. From the group of non-steroidal anti-inflammatory drugs, indomethacin (up to 200 mg / day), diclofenac

(up to 150 mg / day), ibuprofen (up to 1.5 g / day). In parallel, antihistamines are prescribed: suprastin (75 - 100 mg / day), tavegil (2 - 4 mg / day). The duration of therapy is 4 - 5 weeks. In the future, it is advisable to use compounds of the quinoline series - delagil (0.25 -

0.5 mg/day) or plaquenil (0.4 g/day) for 4-6 months.

Infectious myocarditis is a contraindication to the use of steroids. anti-inflammatory agents. The appointment of glucocorticoids is advisable only in those cases where a pronounced autoimmune component of inflammation has been proven, i.e.

cardiac antigen, antibodies to the myocardium, significantly increased concentration of the factor tumor necrosis-ÿ and interferon-á. Clinically, immune myocarditis manifests itself quickly increasing cardiomegaly and progressive heart failure. Prednisone should be used

a short course in the form of pulse therapy (3-5 mg per 1 kg of the patient'sbody weight intravenously through

day 5 injections). Perhaps the appointment of prednisolone inside (at a dose of 0.5 mg per 1 kg of body weight

within 7-10 days) with subsequent cancellation within a month. In order to enhance the immunocorrective effect, along with drug treatment, it is possible to use plasmapheresis (to remove cardiac antigens, antibodies to the myocardium, tumor necrosis factor choli-á and adhesion molecules).

Patients who develop HF require standard therapy,

recommended to prevent the progression of this complication and includes (with no contraindications) ACE inhibitors or angiotensin II receptor blockers,

ÿ- blockers, in the presence of stagnation - diuretics and veroshpiron. Cardiac gly-

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cosides are not indicated for patients with myocarditis even with a pronounced decrease in contractility heart muscle due to the high risk of ventricular arrhythmias. The complex therapy of patients

with cardiac arrhythmias includes antiarrhythmic drugs (cordarone, sotalol). In cases of development of clinically significant disorders of AV conduction, a temporary, and if necessary, permanent pacemaker is used.

Prevention. Patients who have undergone acute myocarditis need rehabilitation of foci chronic infection and long-term use of anti-inflammatory drugs, multivitamins, preparations containing potassium and magnesium salts. If necessary, antiarrhythmic drugs and drugs for the treatment of chronic heart failure are prescribed. control examination with

using laboratory and instrumental methods, it is advisable to carry out after 12

months from the start of therapy. Taking into account its results, the nature of the flow is specified, the the outcome of the disease and the expediency of continuing drug treatment is determined.

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1.7. PERICARDITIS

Definition. Pericarditis is an inflammation of the connective tissue lining of the heart.

(pericardium).

Prevalence. Polyetiology and clinical diversity of pericarditis

make it difficult to estimate the true prevalence of this disease. Pathological anatomical examination shows signs of pericarditis in 3-6% of cases. Women get sick

pericarditis 3 times more often than men.

Etiology. The causes of inflammation of the pericardium are varied. Most often, pericarditis is caused by infectious agents (viruses, Mycobacterium tuberculosis, other bacterial agents, protozoa, fungi). The etiological factors of aseptic pericarditis are systemic diseases of the connective tissue, metastases of malignant tumors, autoimmune and allergic diseases, chest trauma, radiation

heart disease, blood diseases, medicinal effects. Quite often, pericarditis develops as a complication of myocardial infarction, cardiac surgery, pneumonia, chronic

kidney failure, gout. In a significant proportion of cases, the cause of pericardial inflammation cannot be identified. In such patients, the term “idiopathic pericarditis” is used in formulating the diagnosis. Most pericarditis of unknown etiology

are of viral origin.

Pathogenesis. Inflammation of the pericardium with the accumulation of exudate in its cavity in most cases is a direct consequence of the influence of an etiological factor. both infectious and non-infectious. In some pathological conditions, the accumulation of fluid in the pericardial cavity is not directly related to inflammation. Non-inflammatory fluid may accumulate in the pericardium in chronic HF, hypoproteinemia, and myxedema. Injuries, wounds and ruptures of the heart can serve

cause of hemopericardium.

Morphology. The pericardium consists of two sheets - the visceral serous layer (epicardium) and the parietal fibrous layer (the pericardium itself). Between them

the slit-like space (pericardial cavity) normally contains about 25 ml of serous fluid. In acute exudative pericarditis, the amount of fluid in the pericardial cavity can

increase to 1000 ml or more.

The nature and severity of the cellular reaction in pericarditis depends on the cause

of the inflammatory process. Distinguish between fibrinous and effusion (exudative) form of acute

pericarditis. The fibrinous form is characterized by the deposition of fibrin on the sheets of the

pericardium, which makes it difficult for them to slide, the effusion form is characterized by the accumulation of fluid in pericardium. In most cases, fibrinous pericarditis precedes exudative.

Viral and most aseptic pericarditis is characterized by the formation of serous or serous hemorrhagic effusion. With bacterial pericarditis, effusion in the cavity

the pericardium becomes purulent. In some cases (usually after trauma, hemopericardium, bacterial infections, and most often due to tuberculous lesions

pericardium) acute fibrinous or fibrinous-exudative pericarditis ends

the formation of fibrous tissue, sometimes with calcium deposition, which causes adhesion of the visceral and parietal layers of the pericardium with partial or complete obliteration

of its cavity. This form of the disease is called chronic constrictive pericarditis.

Classification. In well-known classifications, pericarditis is divided according to the nature course, features of changes in the pericardium and etiology.

Clinical classification of pericarditis (Braunwald E., 2001): A. Acute pericarditis (less than 6 weeks):

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- fibrinous; -

exudative (exudative). B.

Subacute pericarditis (from 6 weeks to 6 months): - constrictive; - constrictive-effusion. B. Chronic pericarditis (more than 6 months): - constrictive; - effusion; - adhesive (adhesive) without constriction. Etiological classification of acute pericarditis (Spondick DN, 2001, abbr.): II. Idiopathic pericarditis.

II. Infectious pericarditis: 1)

bacterial (mycobacterium tuberculosis, staphylococcus, pneumococcus, borrelia, chlamydia, etc.);

2) viral (Coxsackie, influenza, hepatitis, Epstein-Barr virus, cytomegalovirus, adenovirus, HIV, etc.); 3) fungal (candidiasis, histoplasmosis, coccidiosis, aspergillosis);

4) parasitic (amebic, with echinococcosis, toxoplasmosis, etc.); 5) others.

III. Pericarditis in vasculitis and connective tissue diseases: 1) rheumatoid arthritis; 2) rheumatic fever; 3) systemic lupus erythematosus; 4) scleroderma; 5) nodular periarteritis; 6) Reiter's syndrome; 7) others.

IV. Pericarditis in diseases of the heart and surrounding (adjacent) organs:

1)myocardial infarction (epistenocarditis pericarditis, Dressler'ssyndrome);

2)dissection of the aortic aneurysm; 3) diseases of the pleura and lungs; 4) diseases of the esophagus.

V. Pericarditis in metabolic disorders: 1) renal failure; 2) myxedema; 3) cholesterol pericarditis; 4) gout; 5) scurvy.

VI. Neoplastic (tumor) pericarditis: 1) secondary (metastatic, hematogenously spread, associated with

swelling of the

tumor); 2) primary (mesothelioma, sarcoma, lipoma, fibroma). VII. Traumatic pericarditis: 1)

direct damage to the pericardium (penetrating wound of the chest, perforation of the pericardium, trauma to the heart due to surgery, catheterization, catheter ablation of the pathways, implantation of a pacemaker, coronary angioplasty);

2) indirect damage to the pericardium (non-penetrating wound or trauma to the chest, radiation exposure).

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VIII. Pericarditis of unclear pathogenesis and associated with various syndromes:

1)postmyocardial and pericardial syndromes (immune diseases);

2)necrosis of pericardial fat;

3)inflammatory bowel disease;

4)Leffler'ssyndrome;

5)thalassemia and other hereditary anemias;

6)reactions to drugs;

7)sarcoidosis;

8)Takayasu'ssyndrome;

9)acute pancreatitis;

10)others.

clinical picture. The clinical manifestations of pericarditis are mainly composed of symptoms due to inflammatory lesions of the pericardium, accumulation

exudate in the pericardial cavity and (in the late period of the disease) fibrous deformity

sheets of the pericardium.

The main symptoms of acute pericarditis are chest pain and fever.

The intensity of the pain syndrome in pericarditis varies from moderate to very strong.

The pain has a pressing or burning character, localized behind the sternum and in the precordial region, sometimes radiating to the left arm and neck. Distinctive features of pain in pericarditis are permanent, many hours long, associated with swallowing. For

pericarditis typically increases pain on inhalation and coughing. Pain is relieved by sitting or lying on your stomach. Some patients take a characteristic posture: sitting, bending over forward, with knees pressed to the chest. Body temperature in most patients

does not exceed the subfebrile level. Severe fever is noted in cases of bacterial pericarditis with purulent exudate.

A pericardial friction rub is a pathognomonic symptom of acute pericarditis.

coarse noise of a scraping or scratching character, which occupies the presystole, systole and diastole. Best of all, the pericardial friction rub is heard at the left edge of the lower third of the sternum during breath holding. Pericardial friction noise increases on inhalation and on bending over torso forward. On the first day of the disease, this auscultatory phenomenon is recorded

in 60 - 80% of patients. Subsequently, when an effusion appears, which pushes the rubbing

sheets of the pericardium, the intensity and duration of the noise decrease up to its floor

disappearance, which is sometimes accompanied by a weakening of the sonority of heart sounds. The accumulation of fluid in the pericardial cavity leads to disruption of ventricular relaxation

and obstruction of blood flow to the heart. Slow expansion of the pericardial effusion is often asymptomatic. At the same time, the rapid accumulation of even

a small amount of fluid is accompanied by severe hemodynamic disorders and can lead to pericardial tamponade. Signs of massive pericardial effusion are the expansion of the boundaries of relative and absolute cardiac dullness,

displacement of the apex beat medially from the left border of the heart, swelling of the jugular veins, puffy face. Pericardial tamponade is a decompensated phase of cardiac compression. Due to a pronounced increase in intrapericardial pressure, there is a significant restriction of venous inflow and diastolic relaxation of the heart, which

leads to a violation of the filling of its cavities and a decrease in cardiac output. With the gradual

development of tamponade, there is an increase in shortness of breath and the development of orthopnea, an incre

weakness, cough, dysphagia, pallor of the skin, swelling of the neck veins, acrocyanosis, weakening of heart sounds, hepatomegaly. The most important symptom of cardiac tamponade is "paradoxical" pulse: weakening and even disappearance of pulse waves on inspiration due to

with a decrease in systolic blood pressure by more than 10 mm Hg. Art. With the rapid development of tampo-

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nada (for example, due to myocardial rupture or bleeding into the pericardial cavity of another genesis) dysfunction of the heart as a pump progresses rapidly and often ends in the

death of the patient. Most often, pericardial tamponade develops in acute purulent, tuberculous and tumor pericarditis.

Chronic adhesive (adhesive) pericarditis is usually the outcome of an acute fibrinous or fibrinous-exudative pericarditis. As a result of gluing the pericardial sheets, the diastolic relaxation of the heart is disturbed, therefore, the main features

adhesive pericarditis is an increase in venous pressure and a decrease in heart

ejection with corresponding clinical symptoms. Chronic constrictive

pericarditis develops when, as a result of healing of an acute effusion pericarditis

carditis occurs complete or partial obliteration of the pericardial cavity with scar tissue,

sometimes with calcium deposition, as a result of which the filling of the ventricle is significantly disturbed

cov. In most patients, chronic constrictive pericarditis has tuberculous

etiology. In some cases, it develops as a result of acute purulent pericarditis, cardiac surgery, mediastinal irradiation, chest trauma, acute

viral pericarditis. Compression of the heart by a thickened, inelastic pericardium prevents diastolic filling of the ventricles and causes persistent impairment of central hemodynamics. The main manifestations of chronic constrictive pericarditis

are weakness, fatigue, weight loss, shortness of breath, cyanosis of the lips, swelling of the feet, shins and anterior abdominal wall, abdominal enlargement, oliguria. Examination of

patients reveals swollen and pulsating jugular veins, hepatomegaly, ascites, tachycardia, small heart size. Noises are usually not audible. A common sign of chronic constrictive pericarditis is an early third tone (pericardial beat or

click). The occurrence of this auscultatory phenomenon is associated with a sudden cessation of the filling of the ventricles, which are in a dense "shell" of fibrous-changed

pericardium.

Laboratory and instrumental diagnostics. Blood analysis of patients with acute infectious pericarditis reveals typical inflammatory changes: leukocytosis, an increase in ESR, an increase in the content of C-reactive protein, fibrinogen. For

clarification of the etiology of pericarditis depending on the clinical manifestations of the disease virological and serological studies, tuberculin skin test,

blood cultures, determination of antinuclear antibodies, rheumatoid factor, anti- streptolysin-0 titer, thyroid hormone levels in the blood, and other studies.

In the normal course of acute pericarditis, a slight increase in the activity of aspartic and alanine amiotransferases, lactate dehydrogenase is possible. Level Up

total creatine phosphokinase and its MB fraction for pericarditis is uncharacteristic. Definition in serum cardiospecific enzymes and cardiac troponins are considered

as a sign of myocardial damage.

ECG changes in acute pericarditis are observed in more than 80% of cases. Early electrocardiographic signs of the disease are generalized (concordant) elevation of the ST segment, positive T wave, and depression of the PQ segment. These changes are

associated with damage to the subepicardial layer of the ventricular and atrial myocardium. Subsequently, the ST segment returns to the isoelectric line. Then a negative T wave is formed. For pericarditis, the formation of a pathological Q wave is not typical. In many patients, heart rhythm disturbances, mainly supraventricular ones, are recorded. With a large volume of effusion, due to the changing position of the heart in the pericardial

cavity, electrical alternation is noted - a change in the amplitude of the ECG waves in

various ventricular complexes.

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X-ray examination with a moderate amount of fluid in the pericardial cavity, fibrinous and adhesive pericarditis does not reveal changes in the size and configuration of the heart shadow. With a significant amount of effusion, cardiomegaly, smoothing

waist of the heart, the formation of an obtuse angle between the right contour of the heart and the shadow of the diaphragm.

Further accumulation of effusion in the chronic course of the process leads to the formation of a trapezoid configuration of the heart. In patients with constrictive pericarditis,

against the background of the shadow of the heart calcium deposits are found.

Echocardiographic examination reveals a free space between

sheets of the pericardium. The accumulation of fluid at its minimum amount is found in region of the posterior atrioventricular sulcus. The effusion is considered small if the width

echo-negative space does not exceed 1 cm. The divergence of the sheets of the pericardium by 1 - 2 cm is regarded as a sign of moderate, and 2 cm or more - as a sign of severe effusion

in the pericardial cavity. With a large volume of effusion, free movement of the heart is noted in the pericardial cavity (“floating heart”), which is combined with signs simulating

mitral valve prolapse ("pseudoprolapse"), and paradoxical movement of the interventricular septum. A sign of the development of tamponade is the collapse of the chambers of the heart - a decrease in the diastolic size of the right ventricle, right atrium and less often the left atrium and left ventricle, expansion (lack of collapse on inspiration) of the inferior vena cava. At patients with fibrinous pericarditis revealed an uneven thickening of the pericardial

card, with constrictive pericarditis, this symptom is combined with calcium deposition.

Computed tomography and magnetic resonance imaging can also detect the presence of effusion in the pericardial cavity and thickening of the sheets of the pericardium. Compared to echocardiography, these methods are more sensitive for detecting encysted effusions and

expansion of the hollow veins.

Pericardiocentesis and pericardial fluid analysis are indicated for significant effusion, suspected purulent or tuberculous pericarditis, and high likelihood

oncological process. Biopsy of the pericardium has a rather low diagnostic value and is rarely used in the examination of patients with pericarditis.

Diagnosis. At the first stage of the diagnostic process, physical, electrocardiographic, radiological, echocardiographic studies and a clinical blood test are performed. Depending on the results obtained, additional

laboratory and instrumental studies to determine the etiology of pericarditis.

At the second stage, if there are indications in a limited number of patients, pericardiocentesis is performed, followed by biochemical, cytological, bacteriological, and immunological analysis of the fluid. At the third stage, with repeated accumulation of significant

volume of exudate after a recent puncture in isolated patients with an unknown etiology of pericarditis, pericardioscopy and pericardial biopsy are performed.

When formulating a diagnosis, it is necessary to indicate the clinical form, the nature of the course

and, where possible, the etiology of pericarditis.

Examples of diagnoses:

1.Acute effusion idiopathic pericarditis.

2.Gastric cancer with metastases to the pericardium. Acute effusion hemorrhagic pericarditis.

3.Chronic constrictive pericarditis of tuberculous etiology.

Chronic heart failure III stage, IV f. to.

differential diagnosis. Specific tests for diagnosing pericarditis does not exist, so the differential diagnosis is made by exclusion.

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