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4)hematuria, glomerulonephritis and kidney infarcts;

5)fever plus:

-the presence of artificial materials in the heart;

-the presence of other factors predisposing to IE;

-the appearance of new ventricular arrhythmias or conduction disturbances;

-for the first time manifesting heart failure;

– positive blood culture results (if the isolated microorganism is typical for IE);

-skin (Osler'snodules, Janeway spots) and eye (Roth'sspots) symptoms;

-multifocal pulmonary infiltrates with rapid dynamics (with IE of the right parts hearts);

-peripheral abscesses (kidneys, spleen, spine) of an unclear nature; Predisposing to IE, recent diagnostic or therapeutic

interventions accompanied by significant bacteremia.

Low chance of IE: fever in the absence of all of the above.

Laboratory and instrumental diagnostics. Of decisive importance for confirming the diagnosis of infective endocarditis and the choice of antibiotic therapy are

results of bacteriological examination of blood. For acute infective endocarditis

taking blood samples in the amount of 10 ml is carried out every 15 minutes for 1 hour.

in the subacute course of the disease, it is recommended to take at least 3 blood samples during the day.

Blood for bacteriological analysis is recommended to be obtained by vein puncture

or arteries directly, and not through a catheter, after twice treating the skin with 2% iodine solution and 70% alcohol solution, preferably before starting antibiotic therapy and necessarily at the height of the fever. Repeated isolation of the same microorganism is considered as evidence that it is the causative agent of infective endocarditis. Subject to the rules for taking and cultivating blood, the frequency of detection of the pathogen in bacterial infective endocarditis reaches 95%. Absence

Growth of microorganisms in blood cultures does not rule out infective endocarditis. The causes of infective endocarditis with negative blood culture are the previous

antibiotic therapy, as well as viral or fungal etiology of inflammatory pro

process.

A general blood test in most patients with infective endocarditis reveals normochromic anemia, a normal or moderately elevated white blood cell count.

(pronounced leukocytosis indicates the addition of purulent-septic complications),

shift of the leukocyte formula to the left, thrombocytopenia, increased ESR. Some patients with subacute infective endocarditis caused by a low-virulence pathogen have leukopenia. A biochemical blood test reveals inflammatory changes (the presence of C-reactive protein, an increase in the content of fibrinogen, ã- and

á2globulins, positive sedimentary tests - sublimate, formol). In 50% of patients rheumatoid factor is detected, an increase in the number of circulating immune complexes, a decrease in complement titer, in some patients a false positive reaction

Wasserman. Urinalysis in more than half of patients with infective endocarditis proteinuria is found, in 30% of patients - microhematuria.

The main method of instrumental diagnosis of infective endocarditis is echocardiography, which makes it possible to identify its direct signs - vegetations on the heart valves. Transthoracic echocardiography should be performed in all patients with suspected infective endocarditis. If transthoracic echocardiography does not reveal changes characteristic of infective endocarditis, but the patient has convincing clinical signs of this disease, it is recommended to perform a highly sensitive

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transesophageal echocardiography, which allows visualization of vegetations smaller than 5 mm. When transesophageal echocardiography does not confirm the diagnosis infective endocarditis, the study must be repeated in a week.

If the result is again negative, the diagnosis of infective endocarditis becomes improbable. The main echocardiographic criteria for infectious

endocarditis are: the presence of mobile dense masses attached to the valves, with

to the wall endocardium or to the material of the intracardiac implant, abscesses of the fibrous rings, perforations of valve leaflets or fistulas, avulsion of a prosthetic valve, especially if it

occurred long after implantation.

The diagnosis of infective endocarditis should be based on other findings. methods of instrumental diagnostics. Chest X-ray reveals

cardiomegaly, signs of pulmonary congestion and pulmonary infarction. Electrocardiography gives the ability to detect rhythm and conduction disturbances, signs of myocardial infarction and other changes due to complications of infective endocarditis. Ultrasound examination

and computed tomography of the abdominal organs can reveal

abscesses and infarcts of internal organs, and computed tomography and magnetic resonance imaging of the skull - abscesses and infarcts of the brain.

Diagnosis. For the diagnosis of infective endocarditis, the criteria developed in 1994 by the staff of Duke University Medical Center are used.

Main criteria:

Hemoculture characteristic of IE:

a)a microorganism typical for IE, isolated from two vials: Str. viridians, Str. bovis, NASEC, community-acquired S. aureus, or enterococci

the absence of a primary focus; single isolation of Coxiella burnetti or IgG antibody level

(1st phase) to Coxiella burnetti > 1: 800;

b)re-isolation of blood cultures characteristic of IE: in blood samples taken from more than 12 hours apart; in all three, three out of four, or most of the other number

of blood samples taken for culture with more than an hour gap between the first and last samples.

Echocardiographic signs of IE:

a) the presence of characteristic echocardiographic signs: vegetations on the valves of the heart or other structures; abscesses; dysfunction of prosthetic valves;

b) the appearance of new signs of regurgitation through the valves.

Additional criteria:

1. Predisposition to IE, which includes certain pathology of the heart and

intravenous drug use.

2.Fever > 38°C.

3.Vascular phenomena (arterial embolism, pulmonary infarctions, mycotic anesthetics vrysma, intracranial hemorrhage, Lukin-Libman symptom, Janeway spots).

4.Immunological phenomena (glomerulonephritis, Osler'snodules, Roth'sspots, put test for rheumatoid factor).

5.Microbiological findings (positive microbiological results not meeting the

major criterion, or serological evidence of active infection with a microorganism capable of causing IE).

The diagnosis of IE is considered certain if 2 main criteria are present, or 1 main and 3 additional criteria, or 5 additional criteria. The diagnosis of infective endocarditis is considered possible if: 1 main criterion and 1 additional criterion or 3 additional criteria are present.

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The diagnosis must reflect the clinical and morphological features of the disease.

(primary, secondary), with an identified pathogen - etiology, nature of the pathology that preceded the development of infective endocarditis, localization of local changes, complications.

Examples of diagnoses:

1. Primary infective endocarditis caused by green streptococcus, aortic insufficiency. Embolic infarction of the right kidneys. Chronic heart failure I st., II f. to.

2.Secondary infective endocarditis of the mitral valve. Combined mitral defect of rheumatic etiology.

Embolic myocardial infarction 12.11.09. Chronic cardiac insufficiency IIA Art., III f. to.

3.Secondary infective endocarditis of the artificial aortic valve valve caused by enterococcus, paraprosthetic fistula. Atherosclerosis aorta, aortic stenosis, aortic valve replacement in 2002.

Atrial fibrillation (permanent form). Embolic stroke in basin of the left internal carotid artery 24.11.09, right-sided hemiparesis. Chronic heart failure IIB Art., III f. to.

differential diagnosis. Due to the variety of clinical manifestations

of infective endocarditis, many diseases can be considered as competing diagnostic hypotheses: systemic vasculitis, acute infections (influenza, abdominal

typhoid, malaria, brucellosis), lymphogranulomatosis, lymphoma and other oncological diseases, thrombocytopenic purpura, rheumatism, aortic insufficiency of non-rheumatic etiology, etc. Fever of unknown etiology should serve as a basis for

a thorough examination of the patient in order to identify a possible infectious endocardium dita.

Flow. The nature of the course of infective endocarditis is determined by virulence pathogenic microbes, the reactivity of the macroorganism, the initial state of the heart and internal organs of the patient.

Acute infective endocarditis is sepsis with primary localization of the infection to the valvular apparatus of the heart, which proceeds with vivid clinical symptoms. The causative agents of acute infective endocarditis are highly virulent microorganisms.

- staphylococcus, enterococcus, gram-negative bacteria. For this form of the disease characterized by high fever and severe intoxication. Already on the 5th - 7th day of the disease, gross destructive changes in one or more heart valves are detected. Patients who in

heart valve replacement is not urgently performed, as a rule, die in

over the next 2 months. from progressive heart failure. In some patients, signs of damage to other organs come to the fore, and the main cause of death is damage to

kidney or cerebral vascular occlusion.

Subacute infective endocarditis is septicemia with damage to the heart valves.

and parietal endocardium. This form of the disease is caused by relatively low-virulent pathogens (streptococci, NASEK group microorganisms, fungi). Temperature reaction and intoxication are less pronounced, signs of damage to the valvular apparatus

heart and other clinical symptoms appear after 2 weeks. after an episode of bacteremia, at a later date, HF develops.

Staphylococci affect both intact valves and valves changed by previous diseases, as well as artificial heart valves. Staphylococcal infective endocarditis is characterized by rapid destruction of valves, rapid metastasis of infectious

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tions, peripheral vascular embolism with the formation of abscesses. Gram negative microorganisms are also very aggressive, often causing infective endocarditis in patients with prosthetic valves and in drug addicts. Group microorganisms

NASEC usually cause subacute infective endocarditis with the formation

large vegetations. Fungal infective endocarditis is common in patients with prosthetic valves and drug addicts. Fungal vegetations are fragile, therefore

This type of disease is characterized by a high incidence of embolic complications. A typical feature of infective endocarditis in injection drug users

is the defeat of the tricuspid valve and the acute course of the disease. In patients with with artificial heart valves, infection of the aortic valve predominates. At

In hemodialysis infective endocarditis, the mitral valve is affected more frequently than the aortic and tricuspid valves. In elderly patients, the secondary form of infective endocarditis predominates against the background of heart defects of atherosclerotic and

rheumatic origin, a fever-free course and a blurred clinical picture are common. diseases.

Forecast and outcomes. Infective endocarditis is one of the most serious diseases cardiovascular system with high mortality. The acute form of infective endocarditis without treatment, as a rule, ends in death within 4 to 6 weeks.

subacute - within 4 - 6 months. With adequate antibiotic therapy, mortality averages 30%. However, complete recovery from microbiological

eradication of the microbe-causative agent within 1 year and the absence of pronounced structural changes in the valvular apparatus of the heart is a rare outcome of infective endocarditis.

In most cases of successful antibiotic therapy, insufficiency of the affected valve develops, requiring subsequent surgical correction. One of the outcomes

of infective endocarditis is remission, i.e. clinical improvement without microbiological eradication. Treatment is considered ineffective if it does not

clinical improvement and persistence of the microbe-causative agent is noted. Some patients due to insufficiently effective therapy, there are relapses of infectious endocarditis, i.e., relapses of the disease caused by the same pathogen. If return disease is caused by another microorganism, it is called recurrent infective endocarditis.

The most unfavorable is the prognosis of patients with acute infective endocarditis, the causative agents of which are S. aureus and gram-negative bacteria. Patients with infected prosthetic heart valves generally have a worse prognosis than others.

forms of infective endocarditis. The main causes of death in patients with infectious diseases endocarditis are thromboembolism and hemorrhage, progressive heart failure, septic

shock.

Treatment. The appearance of symptoms suggestive of infective endocarditis is the basis for hospitalization of the patient. Antibacterial therapy is started immediately after blood sampling for bacteriological examination. In acute infective endocarditis, due to the high risk of developing septic shock, the formation

metastatic foci of infection and rapid destruction of the valves, treatment is started immediately. Until the results of blood cultures are obtained, the treatment is selected

empirically, assessing the possible entrance gates of the infection, the nature of the onset of the disease, valves, developed complications. After receiving information about the causative agent of the disease

and its sensitivity to antimicrobial drugs, therapy is being adjusted.

Given the predominance of staphylococcal etiology of acute infective endocarditis, it is advisable to start treatment with antistaphylococcal drugs: oxacillin and cephalosporins. If the causative agent is suspected to be methicillin-resistant

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staphylococcus aureus, vancomycin or lineloside should be used for initial therapy. In urogenital sepsis, infective endocarditis is most often caused by gram-negative bacteria or enterococci. Treatment of this category of patients is advisable to start

with fluoroquinolones III, IV generations and cefepime. Second-line drugs are vancomycin and imipenem. In patients with prior pneumonia (especially those with alcoholism), infective endocarditis is usually caused by pneumococcus, so

treatment is recommended to begin with third-generation cephalosporins and respiratory fluoroquinolones. The second-line drug is lineloside. Imipenem and cefepime are used as initial therapy for patients with an unidentified primary lesion. Selection Guide

initial empirical antibiotic therapy for infective endocarditis are presented in Table. 1.26.

After identification of the causative agent, a patient with infective endocarditis is prescribed targeted etiotropic antibiotic therapy, taking into account sensitivity.

isolated microorganism to antimicrobial drugs (Table 1.27). In the treatment of patients with For fungal infective endocarditis, antifungal drugs are used: amphotericin B (0.5 mg/kg/ day IV) and 5-flucytosine (100–200 mg/kg/day IV).

With properly selected antibiotic therapy, improvement in well-being and

a decrease in body temperature is observed 3 to 7 days after the start of treatment. The

duration of therapy is determined by the disappearance of clinical and laboratory signs of inflammation and averages 4-6 weeks.

Glucocorticoids are used in the treatment of patients with infective endocarditis only if there are absolute indications, which include bacterial shock,

immune complications (severe vasculitis, rapidly progressive immune complex nephritis), allergic reaction to antibacterial drugs. In order to prevent thromboembolic complications in the treatment of patients with infective endocarditis

antiplatelet agents are used (acetylsalicylic acid, clopidogrel), and if they occur, heparin. Plasmapheresis can be used as an auxiliary treatment for patients with immunocomplex complications.

Table 1.26

Choice of initial empiric antibiotic therapy for acute infection endocarditis (Tyurin V.P., 2003)

Table 1.27

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Etiotropic antibiotic therapy for acute infective endocarditis (Tyurin V.P., 2003)

The main indications for surgical treatment of patients with infective endocardium child are:

1) pronounced destructive changes in the aortic and mitral valves with progressive heart failure;

2)failure of adequate antimicrobial therapy - persistent fever and manifestations of bacteremia lasting more than 1 week;

3)abscesses of the fibrous ring and myocardium;

4)identification of microorganisms that are difficult to treat with antimicrobial agents (for example, Brucella and Coxiella fungi), or microorganisms that can quickly cause destruction of heart tissue (for example, S. lugdunensis);

5)the formation of mobile vegetations larger than 10 mm on the mitral valve and

their increase against the background of adequate antimicrobial therapy;

6)early infective endocarditis of the artificial valve;

7)late infective endocarditis of an artificial valve, complicated by prosthesis dysfunction.

The duration of surgical intervention and the duration of antimicrobial therapy before surgery are determined individually, taking into account the totality of circumstances. best forecast

noted in patients operated on at an early stage of the disease with preserved reserves

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myocardium and minimal manifestations of heart failure. In the postoperative period, antimicrobial therapy continues for 1 to 2 weeks.

Prevention. According to modern concepts, the prevention of infectious

endocarditis should be performed in individuals at high and moderate risk of developing it. To The high-risk group for developing infective endocarditis includes patients with artificial heart valves, congenital heart defects of the "blue" type, patients who have undergone implantation of vascular and pulmonary conduits, and patients who previously had diagnosed with infective endocarditis. Patients at moderate risk are

with acquired heart defects, mitral valve prolapse with regurgitation, congenital heart defects without cyanosis, hypertrophic cardiomyopathy. Active prevention

infective endocarditis is not considered mandatory for patients with mitral valve prolapse without valvular regurgitation, with a history of rheumatism without valvular disease

heart, with an artificial pacemaker, implanted cardioverter-defibrillator, as well as for patients who underwent coronary bypass surgery, surgical

correction of defects of the interatrial and interventricular septa.

Among the diagnostic and therapeutic interventions and manipulations, accompanied by bacteremia and requiring prophylactic use of antibacterial drugs,

include extraction (implantation) of the tooth, periodontal dental interventions

with the risk of gum damage, tonsillectomy and adenoidectomy, bronchoscopy (hard

instrument), bougienage of narrowing of the esophagus, bougienage of the urethra, prostate biopsy,

lithotripsy, gynecological procedures.

Before interventions in the oral cavity, upper respiratory tract and esophagus

in the absence of penicillin allergy, oral amoxicillin should be used in adults

2 g, children 50 mg per 1 kg of body weight for 1 procedure. Used for penicillin allergy

clindamycin inside adults 600 mg, children 20 mg per 1 kg of body weight. Before the gastrointestinal urogenital interventions in the absence of allergy to penicillin, it is recommended to use

amoxicillin in combination with gentamicin at a dose of 1.5 mg per 1 kg of body weight intravenously 1 hour before the procedure, and 6 hours after the intervention, ampicillin or amoxicillin orally for adults 1 g, children 25 mg per 1 kg of body weight. Patients allergic to

penicillin are recommended vancomycin: adults 1 g, children 20 mg per 1 kg of body weight intravenously fo 1 - 2 hours before the procedure. At high risk of developing infective endocarditis, vancomycin

combined with gentamicin (1.5 mg per 1 kg of body weight intravenously or intramuscularly).

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1.6. MYOCARDITIS

Definition. Myocarditis is a disease that is based on acute or chronic nic inflammatory process in the myocardium due to various reasons.

Prevalence. Due to the variety of clinical manifestations of myocarditis, ambiguous interpretation of the results of instrumental and laboratory studies, as well as objective diagnostic difficulties, the true prevalence of this disease is

unknown. In standard pathoanatomical studies, signs of myocardial inflammation are detected in 1–9% of the dead. According to various researchers,

sudden death of young people in 3-12% of cases is associated with myocarditis.

However, pathological studies cannot give a complete picture of the frequency of myocarditis, since how the vast majority of patients with acute myocarditis recover. In cardiological

departments of hospitals outside epidemic outbreaks of infectious diseases

patients with a diagnosis of "myocarditis" make up 0.2 - 0.7%. Most common myocarditis diagnosed in the age group of 30-40 years. Women get sick more often than men. However, myocarditis is a more common cause of death in the male population.

Etiology. The concept of "myocarditis" combines inflammatory diseases of the myocardium, different in etiology and pathogenesis. Directly or indirectly through immune mechanisms myocarditis is caused by various infectious agents (viruses, bacteria,

fungi), occurs as a result of parasitic and protozoal invasion, exposure to chemical (including medicinal) substances and physical factors. In addition, myocarditis often develops as a component of a generalized allergic reaction and complicates

course of autoimmune diseases (systemic lupus erythematosus, scleroderma, arteritis

Takayasu, Wegener'sgranulomatosis, etc.).

Pathogenesis. Myocarditis of infectious etiology begins with direct penetration into the myocardium of cardiotropic viruses or other pathogens. As a result, there is primary damage to myocardial cells, a local inflammatory reaction develops and

immune mechanisms are activated. Increase in clones of cytotoxic T- and B-lymphocytes causes activation of stepwise apoptosis and increased myocytolysis. Affected

cardiomyocytes acquire autoantigenic properties, which leads to the formation of antimyocardial antibodies. As a result of an autoimmune reaction, the integrity of cardiomyocyte

membranes is disrupted, a state of intracellular energy deficiency develops, and myocardial contractile dysfunction progresses. During inflammatory and immune

reactions, biologically active substances are released in the myocardium (bradykinin, serotonin, hista etc.), which contribute to an increase in vascular permeability, the occurrence of

hemorrhages and cause interstitial edema. Involved in the local inflammatory process

vessels of the microvasculature, as a result of which the process of intravascular

thrombosis. The development of ischemia becomes an additional factor that increases the likelihood of foci of necrosis in the myocardium. As the inflammation subsides process in the heart muscle, areas of replacement fibrosis are formed.

A viral infection can induce autoimmune reactions in the myocardium, which, without being accompanied by severe clinical symptoms, end in damage.

the cytoskeleton of cardiomyocytes, as a result of which a progressive dysfunction of the heart muscle develops and a dilated cardiomyopathy is formed. When exposed to

certain infectious agents (for example, pathogens of diphtheria and typhoid fever), as well as chemica medicinal compounds, direct toxic damage to cardiomyocytes comes to the fore.

Inflammatory changes in the myocardium in these variants of the disease are secondary character.

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Morphology. Histological examination of the cardiac muscle in the acute phase myocarditis, as a rule, nonspecific changes are detected in the form of an inflammatory cellular infiltration, signs of necrosis or damage to cardiomyocytes, uncharacteristic of ischemia, exudative-proliferative changes in the interstitium. The infiltrate may

consist of various types of cells: lymphocytes, polymorphonuclear cells, macrophages, eosinophils, plasma and giant cells. With a viral lesion, lymphocytes predominate,

with a bacterial one - polymorphonuclear cells, with allergic myocarditis - eosinophils. Diffuse myocarditis is characterized mainly by parenchymal changes, for focal - changes in interstitial tissue. After completion of acute phase, necrotic cardiomyocytes are replaced by fibrous tissue.

Specific changes in the heart muscle are found in cases where the development

of myocarditis is associated with rheumatism, tuberculosis, and syphilis. There are some relatively rare forms of myocarditis that are characterized by severe infiltration with a predominance of certain cellular elements or granulomatous damage - for example, necrotizing eosinophilic myocarditis, giant cell myocarditis, idiopathic granulomatous myocarditis.

Classification. There is no generally accepted classification of myocarditis. The best known is histopathological classification based on the results of endomyocardial myocardial biopsy using light microscopy (Dallas, USA,

1986). Dallas criteria for myocarditis are presented in Table. 1.28.

Microscopic analysis of a single biopsy specimen reveals histological signs of myocarditis in no more than 25% of cases. For an accurate diagnosis of myocarditis

according to the Dallas criteria, 15–20 biopsy specimens are required, which are obtained in real co clinical practice is difficult. The Dallas criteria do not provide for separation

patients depending on etiological factors, pathogenesis features, prevalence, clinical manifestations and course variants. In this regard, other classifications are used for the diagnosis of myocarditis, one of which is the clinical classification.

myocarditis (Gurevich M. A., Paleev N. R., 1997):

Table 1.28

Dallas criteria for myocarditis

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I. Etiological characteristics and pathogenetic variants: 1. Infectiousallergic and infectious: a) viral (influenza, Coxsackie viruses,

ECHO, AIDS, poliomyelitis, etc.); b) infectious (diphtheria, scarlet fever, tuberculosis, typhoid fever, etc.); c) with infective endocarditis; d) spirochetal (syphilis, leptospirosis, relapsing fever); e) rickettsial (typhus, Q fever); f) parasitic (toxoplasmosis, Chagas disease, trichinosis); g) fungal (actinomycosis, candidiasis, aspergillosis, etc.). 2. Allergic (immunological): a) medicinal; b) serum; c) nutritional; d) with systemic connective tissue diseases; e) with bronchial asthma; f) with Lyell'ssyndrome; g) with Goodpasture's syndrome; h) burns; i) transplantation. 3. Toxic-allergic: a) thyrotoxic; b) uremic; c) alcoholic.

III. Pathogenetic phase: 1. Infectious-toxic. 2. Immunoallergic. 3. Dystrophic. 4. Myocardiosclerotic.

III. Morphological characteristics: 1.

Alternative (dystrophic-necrobiotic). 2. Exudativeproliferative (interstitial): a) dystrophic; b) inflammatory-infiltrative; c) vascular; d) mixed.

IV. Prevalence: 1. Focal.

2. Diffuse.

IV. Clinical variants: 1. Pseudocoronary. 2. Decompensation. 3. Pseudovalve. 4. Arrhythmic. 5. Thromboembolic. 6. Mixed. 7. Asymptomatic.

VI. Course options: 1.

Benign myocarditis (usually focal form).

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