Myocarditis

Myocarditis is a focal or diffuse inflammation of the heart muscle as a result of various infections, exposure to toxins, drugs or immunological reactions leading to damage to cardiomyocytes and the development of cardiac dysfunction.

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Epidemiology

The true prevalence of myocarditis is difficult to assess, since in some cases the disease is latent or subclinical, without obvious manifestations of the disease, ending in complete recovery.

According to pathological studies, the prevalence of myocarditis among the deceased is 1-4%, reaching 9.5% when examining a larger than usual area of myocardial tissue. In people who died from sudden cardiac death at a young age, signs of myocardial inflammation range from 8.6 to 12%. The frequency of myocarditis diagnosis during life is quite wide (0.02-40%). It is worth noting that myocarditis most often affects young people (the average age of those affected is from 30 to 40 years). The incidence in women is slightly higher than in men, but men often have more severe forms.

According to histological studies of myocardial biopsies, the following forms are common: lymphocytic (55%), mixed (22%), granulomatous (10%), giant cell (6%), eosinophilic (6%), etc. (1%).

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Pathogenesis

There are several mechanisms that cause the development of inflammation and damage to the heart muscle in myocarditis, which depend on the etiological factor:

• Direct cytopathic action of infectious agents capable of penetrating into cardiomyocytes (viruses, trypanosomes, rickettsia) or localizing in interstitial tissue, forming small abscesses (bacteria). It has been shown that in active myocarditis and dilated cardiomyopathy, fragments of the virus genome can be detected in cardiomyocytes.
• Damage to cardiomyocytes by toxins released by the pathogen into the blood during a systemic infection or directly into the heart. This mechanism of damage is most typical for diphtheria myocarditis, but can develop with infectious toxic shock.
• Development of coronary artery disease and endothelial dysfunction of the heart vessels with subsequent coroparogenic damage to the heart muscle (rickettsia).
• Non-specific damage to myocardial cells as a result of autoimmune diseases (systemic lupus erythematosus, systemic scleroderma, rheumatoid arthritis, serum sickness), in which the heart is one of the target organs of the generalized process.
• Specific damage to cardiomyocytes by factors of humoral and cellular immunity, which are activated upon introduction of the pathogen or reactivated as a result of a long-term persistent primary infection.

The most widespread hypothesis is that of autoimmune damage, according to which a viral infection at the stage of active viral replication triggers immunopathological reactions involving cells (CD8+ lymphocytes): autoantibodies to various components of cardiomyocytes (myosin), filaments and pro-inflammatory proteins (IL-1, 2, 6, TNF-a), which leads to damage to cardiomyocytes. In addition, local release of cytokines, nitric oxide can affect the activity of T cells and support the autoimmune process. It has been shown that cytokines can reversibly reduce myocardial contractility without causing cell death. It is also believed that viral RNA found in cardiomyocytes can serve as an antigen that supports immune reactions.

Risk factors for myocarditis include:

• pregnancy;
• hereditary predisposition;
• immunodeficiency states.

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Symptoms myocarditis

The symptoms of myocarditis do not have specific features, but in most cases it is possible to trace the chronological connection of the heart disease with an infection or other etiological factors that can lead to the development of toxic or allergic damage to the myocardium. The disease most often develops several days (less often - weeks) after a viral infection and in some cases is asymptomatic.

Pain in the heart area is common (60% of cases), it is usually localized in the area of the apex of the heart, can spread to the entire precordial region of the heart, is of a stabbing or pressing nature, usually long-lasting, is not associated with physical exertion and is not relieved by taking nitrates. This type of pain may be associated with the involvement of the pericardium in the pathological process (myopericarditis), but rare cases of angina are also possible, for example, with ongoing viral coronaryitis and vasospasm.

Dyspnea is the second most common (47.3%) symptom of current myocarditis. It is associated with developing left ventricular failure and may occur only during intense physical activity (with mild myocarditis) or even at rest (with moderate and severe forms). Dyspnea may increase in a horizontal position due to increased preload on the heart. A serious sign of myocarditis is the sudden onset of symptoms of congestive heart failure in a young patient without clinical signs of coronary heart disease.

Palpitations (47.3%) are associated with a decrease in cardiac output and a reflex increase in the activity of the sympathoadrenal system.

Interruptions in the work of the heart, dizziness and fainting occur in 38% of patients and are caused by various disturbances of rhythm and conduction (second-degree atrioventricular blocks, extrasystole, atrial fibrillation, etc.), determined by the localization of the focus of necrosis, inflammation and the degree of its prevalence. Life-threatening ventricular arrhythmia and iodine atrioventricular block are characteristic of severe diffuse myocarditis and can lead to sudden cessation of blood circulation.

Swelling of the legs, pain in the right hypochondrium and other manifestations of circulatory failure in the systemic circulation often develop with chronic myocarditis.

We present a clinical observation of Coxsackie myocarditis group B (based on materials from Prof. Yu. L. Novikov).

Patient A., 36 years old, was admitted to the clinic with a diagnosis of post-influenza myocarditis, left-sided pleurisy, and extrasystolic arrhythmia. A month before hospitalization, he noted signs of mild acute respiratory disease with symptoms of rhinitis, pharyngitis, and bronchitis. He continued to work. On the 6th day, acute paroxysmal pains in the precordial region and behind the sternum suddenly appeared, which initially led to a suspicion of myocardial infarction. Then the pains were localized mainly in the left hypochondrium, and intensified with movement, breathing, and coughing.

On admission, body temperature was 37.9 °C. Breathing was shallow, sparing the left half of the chest when inhaling, the respiratory rate was 28 per minute. Heart sounds were moderately muffled, arrhythmic, the first heart sound was preserved, there were no murmurs. Pulse was 84 per minute, extrasystolic arrhythmia. Blood pressure was 130/80 mm Hg. A pleuropericardial murmur was heard in the fifth intercostal space on the left. X-ray examination revealed an increase in the size of the heart. No changes in the lungs or limitation of diaphragm mobility were detected. Dynamic ECG showed group ventricular extrasystoles, flattening of the T wave in leads I, II, III, V5-V6. Blood test: Hb - 130 g/l, leukocytes - 9.6x10 ⁹ /l, ESR - 11 mm/h, C-reactive protein - 15 mg/l, antistreptolysin-O - negative, direct hemagglutination reaction for influenza A, B and parainfluenza - negative. High titer of Coxsackie B2 antibodies (1:2048) with a two-fold increase over 12 days.

The treatment prescribed was bed rest for 2 weeks, nonsteroidal anti-inflammatory drugs orally. During subsequent X-ray examination, the heart size decreased, limited mobility of the left dome of the diaphragm with the formation of pleuropericardial adhesion was detected. Body temperature returned to normal within 1 day of treatment, heart pain completely disappeared after 2 weeks. Ventricular extrasystoles with a frequency of 10-12 per minute persisted on the ECG.

Previous acute respiratory disease, serological data, characteristic pain syndrome caused by simultaneous involvement of the pleura, pericardium, myocardium in the process, allowed us to make a diagnosis: "Bornholm disease (epidemic myalgia caused by the Coxsackie B virus). Fibrinous pleurisy. Acute Coxsackie B viral myopericarditis of severe degree. NK II A, II FC.

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Forms

Classification of myocarditis by pathogenetic (etiological) variant

Infectious and infectious-toxic:

• viral (adenoviruses, Coxsackie B viruses, influenza, infectious hepatitis, human immunodeficiency virus-1, parainfluenza, ECHO, measles, infectious mononucleosis, cytomegaloviruses, etc.);
• bacterial (diphtheria, mycobacteria, mycoplasma, streptococci, meningococci, staphylococci, gonococci, legionella, clostridia, etc.);
• fungal (aspergillosis, actinomycosis, candidiasis, coccidiomycosis, cryptococcosis, histoplasmosis);
• rickettsia (typhus, Q fever, etc.);
• spirochetosis [lentospirosis, syphilis, borreliosis (Lyme carditis)];
• protozoan [trypanosomiasis (Chagas disease), toxoplasmosis, amebiasis];
• parasitic (schistosomiasis caused by helminth larvae, wandering larva syndrome, echinococcosis).

Allergic (immunological):

• medications (sulfonamides, cephalosporins, ditoxin, dobutamine, tricyclic antidepressants, etc.), serum sickness;
• systemic connective tissue diseases;
• transplantation of organs and tissues.

Toxic:

• drugs, especially cocaine;
• uremic conditions;
• thyrotoxicosis;
• alcohol, etc.

Other:

• giant cell myocarditis;
• Kawasaki disease;
• radiation therapy.

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Classification of myocarditis by course

• Acute myocarditis. Characterized by acute onset, increased body temperature, pronounced clinical manifestations, changes in laboratory data indicating an ongoing inflammatory process, increased levels of cardiac-specific markers of damage. Viral myocarditis is characterized by viremia. The histological picture indicates cardiomyocyte necrosis.
• Subacute myocarditis. Characterized by a less vivid clinical picture, moderate deviations in laboratory data. An increase in specific antibodies in the diagnostic titer is observed. Activation of T- and B-lymphocytes occurs. The histological picture indicates myocardial infiltration by mononuclear cells.
• Chronic myocarditis. Characterized by a long course with periods of exacerbation and remission. A high titer of anticardiac antibodies and other disorders of cellular and humoral immunity are established. The histological picture is fibrosis and inflammatory infiltration. Post-inflammatory dilated cardiomyopathy develops as a result.

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Classification of myocarditis by the prevalence of the inflammatory process

Focal myocarditis. The focus of damage to cardiomyocytes and inflammatory cell infiltration is located predominantly in one of the walls of the left ventricle. Depending on its location and size, various clinical manifestations may occur: rhythm and conduction disturbances, changes in the ST segment on the ECG in several leads, areas of hypokinesia, akinesia and dyskinesia may appear, revealed by echocardiography.

Diffuse myocarditis. The entire myocardium of the left ventricle is involved in the pathological process, which leads to a significant impairment of its contractility, a decrease in EF, cardiac index, and an increase in EDP and EDV, and, as a consequence, to the development of heart failure.

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Classification of myocarditis by severity

The classification by severity - into mild, moderate and severe forms - is based on two main criteria: changes in the size of the heart and the degree of severity of heart failure.

• Mild form of myocarditis. There is no change in the size and contractility of the heart, mainly the left ventricle. This form of myocarditis occurs with the formation of subjective symptoms that appear soon (2-3 weeks) after the infection; general weakness, slight shortness of breath that occurs during physical exertion, various painful sensations in the heart area, palpitations and interruptions.
• Moderately severe form. Occurs with cardiomegaly, but without signs of heart failure at rest. This form includes diffuse myocarditis and myopericarditis, which often end in complete recovery with normalization of heart size, but in the acute period it is characterized by more pronounced objective and subjective manifestations.
• Severe form. Characterized by cardiomegaly and pronounced signs of heart failure (acute or chronic). In rare cases, severe myocarditis may manifest as cardiogenic shock or severe rhythm and conduction disturbances with Morgagni-Adams-Stokes syndrome.

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Diagnostics myocarditis

During the process of collecting anamnesis, it is necessary to find out and clarify the following points with the patient:

• Was the current condition preceded by a cold, were the patient's body temperature elevated, fever, weakness, joint or muscle pain, skin rash noted? The period between the previous upper respiratory tract or gastrointestinal tract infection is about 2-3 weeks.
• Does the patient suffer from pain in the heart area or in the chest of a constant stabbing or pressing nature, which intensifies with physical exertion and does not go away after taking nitroglycerin?
• Are there any complaints indicating varying or developing cardiovascular insufficiency (fatigue, shortness of breath, nocturnal attacks of suffocation) of varying severity, palpitations, syncopal states?

It is necessary to clarify the chronological connection of the above symptoms with the previous infection, as well as the burden of the family history of cases of sudden cardiac death or the development of heart failure in relatives at a young age,

Physical examination

Myocarditis is characterized by tachycardia, hypotension, and fever. If myocarditis is moderate or severe with heart failure, acrocyanosis, swelling of the neck veins at rest or with minor physical exertion, peripheral edema, wheezing, and crepitations in the lungs are possible.

It should also be remembered that a more detailed physical examination may reveal clinical signs of an infectious or systemic disease (fever, skin rash, lymphadenopathy, etc.) that caused the development of myocarditis.

When palpating the heart area, one can detect a weakening of the apical impulse, as well as its displacement outward from the left midclavicular line in case of cardiomegaly.

Percussion of patients with moderate to severe myocarditis reveals a shift of the left border of relative cardiac dullness to the left. In severe cases, when dilation of not only the left ventricular cavity but also the left atrium cavity occurs, the upper border of relative dullness shifts upward.

Auscultation may reveal a decrease in the volume of the first heart sound, an accentuation of the second heart sound on the pulmonary artery, the third and fourth heart sounds, as well as a gallop rhythm, a predictor of severe myocarditis, in particular a progressive decrease in myocardial contractility and systolic dysfunction. Its appearance usually precedes the development of clinical signs of heart failure.

When the lesion is located in the area of the papillary muscles or as a result of expansion of the fibrous ring of the left atrioventricular orifice, mitral regurgitation noise is heard.

When myopericarditis develops, pericardial friction rub is heard.

Myocarditis usually causes tachycardia, which does not correspond to the degree of increase in body temperature ("toxic scissors"), and does not disappear during sleep, which is a significant differential diagnostic sign. Tachycardia can occur both during physical exertion and at rest. Bradycardia and decreased pulse pressure are rare.

Laboratory diagnostics of myocarditis

In the clinical blood test, slight leukocytosis with a left shift and an increase in ESR may be noted. The diagnostic value of this reaction may decrease with the development of congestive heart failure and hepatitis. An increase in the level of eosinophils is characteristic of parasitic diseases and may increase as recovery from myocarditis occurs.

In some patients, the level of myocardial enzymes (CPK, MB-fraction of creatine phosphokinase (CPK-MB), lactate dehydrogenase-1 (LDH-1)), is increased, which reflects the severity of cytolysis. Cardiac troponin-I (cTnI) is a specific and sensitive marker of myocyte damage. It is possible to increase the level of fibrinogen, C-reactive protein, seromucoid, a2- and y-globulins, which is not considered a specific confirmation of myocarditis, but may indicate the presence of an inflammatory focus in the body.

Of great importance is the study of the titer of antibodies to cardiotropic viruses, a fourfold increase of which has diagnostic value.

Electrocardiogram or 24-hour Holter ECG monitoring for myocarditis

Myocarditis may cause one or more of the following ECG changes:

• various cardiac rhythm disorders such as sinus tachycardia or bradycardia, atrial fibrillation, paroxysmal supraventricular or ventricular tachycardia, ectopic rhythms. Supraventricular tachycardia is especially common in congestive heart failure or pericarditis;
• conduction disturbances of the electrical impulse along the cardiac conduction system, which may manifest as atrioventricular block of grades I-III, block of the left or, less commonly, right leg of the bundle of His. There is a certain correlation between the degree of conduction disturbance and the severity of myocarditis. Complete atrioventricular block often occurs, most often detected after the first episode of loss of consciousness. Installation of a temporary pacemaker may be necessary;
• changes in the terminal part of the ventricular complex in the form of depression of the ST segment and the appearance of a low-amplitude, smoothed or negative wave, usually determined in the chest leads, but are also possible in the standard ones;
• pseudo-infarction changes, including a negative coronary T wave, ST segment elevation and the formation of a pathological wave, which reflects damage to the heart muscle and a decrease in its electrical activity.

Changes in the ECG may be short-term and persistent. The absence of pathological changes in the ECG does not exclude the diagnosis of myocarditis.

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Echocardiography for myocarditis

When performing echocardiography in patients with low-symptom or asymptomatic myocarditis, changes may be absent or a slight increase in the ESV and EDV of the left ventricle may be detected. In severe cases of myocarditis, accompanied by a decrease in the contractility of the myocardium, there is a decrease in EF and cardiac index. Expansion of the left ventricular cavity, local contractility disorders in the form of individual areas of hypokinesia (sometimes - global hypokinesia) or akinesia are detected. For the acute stage, an increase in the thickness of the heart walls caused by interstitial edema is most characteristic. Mitral and tricuspid valve insufficiency is possible. In myopericarditis, separation of the pericardial leaflets and a small amount of fluid are noted. In 15% of cases, parietal thrombi are diagnosed.

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X-ray diagnostics of myocarditis

In a significant proportion of patients, there are no changes in chest X-ray, while in another part of patients, cardiomegaly of varying degrees is determined (an increase in the cardiothoracic index up to 50% or more) and signs of venous congestion in the pulmonary circulation: increased pulmonary pattern, dilation of the roots of the lungs, the presence of effusion in the pleural sinuses. With the development of exudative pericarditis, the heart acquires a spherical shape.

Scintigraphy

Myocardial scintigraphy with [ ^{67 Ga] is a sensitive method for diagnosing active inflammatory processes in the myocardium. Scintigraphy with monoclonal antibodies to myosin labeled with111} In can be used to determine damage to cardiomyocytes in patients with unexplained clinical presentation of heart failure.

Myocardial biopsy

According to modern concepts, a final diagnosis can only be established after an endomyocardial biopsy, which is currently considered the "gold standard" of diagnostics. Indications for endomyocardial biopsy:

• development of severe or life-threatening rhythm disturbances, especially progressive ventricular tachycardia or complete block;
• significant decrease in EF and the presence of clinical signs of congestive heart failure, despite adequate treatment;
• exclusion of other myocardial lesions requiring specific treatment (giant cell myocarditis, systemic lupus erythematosus and other rheumatic diseases; newly diagnosed cardiomyopathy with suspected amyloidosis, sarcoidosis, hemochromatosis).

Although endomyocardial biopsy typically involves taking 4 to 6 samples, careful postmortem analysis of proven myocarditis cases has shown that more than 17 samples (biopsies) are needed to correctly diagnose myocarditis in more than 80% of cases. This is unrealistic in clinical practice, and therefore the lack of sensitivity of endomyocardial biopsy is evident. Another significant limitation in histopathological diagnosis is the inconsistency of the microscopic picture of myocarditis.

It should be remembered that histological examination can confirm the diagnosis of myocarditis, but never exclude it.

A promising diagnostic method may be the isolation of genetic viral material from the myocardium using recombinant DNA techniques, PCR and in situ hybridization.

Clinical diagnostic criteria for myocarditis

In 1973, the New York Heart Association (NYHA) developed diagnostic criteria for non-rheumatic myocarditis. According to the degree and diagnostic significance, the myocarditis criteria were divided into two groups, “major” and “minor”.

The clinical diagnostic criteria for myocardial infarction are as follows:

• The presence of a previous infection confirmed by clinical and laboratory data (direct isolation of the pathogen, increased ESR, increased blood leukocytes, fibrinogenemia, the appearance of C-reactive protein and other signs of inflammatory syndrome) or another underlying disease (allergic reactions, toxic effects, etc.).

Plus the presence of signs of myocardial damage.

"Big" criteria:

• increased activity of cardiac-specific enzymes and isoenzymes in the patient's blood serum (CPK, MB-CPK, LDH, LDH-1) and troponin content;
• pathological changes in ECG (heart rhythm and conduction disturbances);
• cardiomegaly established by radiological data;
• presence of heart failure or cardiogenic shock;
• Morgagni-Adams-Stokes syndrome.

"Small" criteria:

• protodiastolic gallop rhythm;
• weakened first tone;
• tachycardia.

To diagnose a mild form of myocarditis, it is enough to combine the signs of a previous infection (or other impact on the body) and the first two "major" criteria or one of them with two "minor" criteria. If the patient, in addition to the first two "major" criteria, has at least one of the subsequent "major" criteria, then this allows us to diagnose moderate and severe forms of myocarditis.

Dallas morphological criteria for myocarditis (USA, 1986)

Diagnosis of myocarditis	Histological features
Reliable	Inflammatory infiltration of the myocardium with necrosis and/or degeneration of adjacent cardiomyocytes, which are not typical for changes in MBS
Doubtful (probable)	Inflammatory infiltrates are rare, or cardiomyocytes are infiltrated by leukocytes. There are no areas of cardiomyocyte necrosis. Myocarditis cannot be diagnosed due to the absence of inflammation.
Not confirmed	Normal histological picture of the myocardium, or there are pathological changes in the tissue of a non-inflammatory nature

In 1981, Russian criteria for the clinical diagnosis of myocarditis were proposed by Yu. I. Novikov.

• Previous infection proven by clinical and laboratory data (including isolation of the pathogen, results of the neutralization reaction, RBC, RTGA, increased ESR, increased CRP) or another underlying disease (drug allergy, etc.).

Plus signs of myocardial damage.

"Big":

• pathological changes in ECG (rhythm disturbances, conduction, ST-T, etc.);
• increased activity of sarcoplasmic enzymes and isoenzymes in serum [CPK, CPK-MB, LDH and the ratio of 1 and 2 LDH isoenzymes (LDH1/LDH2)];
• cardiomegaly according to radiological data;
• congestive heart failure or cardiogenic shock,

"Small":

• tachycardia;
• weakened first tone;
• gallop rhythm.

The diagnosis of myocarditis is valid when a previous infection is combined with one “major” and two “minor” signs.

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Structure of the diagnosis of myocarditis

The course of myocarditis	Prevalence of the inflammatory process	Etiological factor	Severity
Acute Subacute Chronic	Focal Diffuse	Viral Bacterial Fungal Parasitic Allergic Toxic Unspecified	Mild form Moderate form Severe form

After this, complications (if any) are indicated, the stage of circulatory failure according to N.D. Strazhesko and V.Kh. Vasilenko and the functional class (FC) according to the New York Classification (NYHA),

Examples.

• Acute focal post-influenza myocarditis, mild form. Supraventricular extrasystole, NC0. I FC.
• Acute diffuse myocarditis of unspecified etiology. Ventricular extrasystole. Paroxysm of ventricular tachycardia from _____ NC stage IIA, III FC.

Differential diagnosis

To diagnose myocarditis, it is necessary to exclude diseases that occur with secondary myocardial damage, as well as primary heart lesions of unknown etiology that are not associated with diseases of other organs and systems (cardiomyopathy). In the differential diagnosis of non-rheumatic myocarditis, endocrine, metabolic, and general systemic diseases should be excluded as the cause of damage to the heart muscle.

Of greatest practical importance is the differential diagnosis of myocarditis with:

• myocardial infarction;
• dilated cardiomyopathy,
• rheumatic and non-rheumatic lesions of the heart valves;
• heart damage due to long-term arterial hypertension;
• chronic exudative and constructive pericarditis.

In young children, one must keep in mind the possibility of developing congenital neuromuscular diseases, endocardial fibroelastosis, glycogenosis, congenital anomalies of the coronary arteries of the heart, and Kawasaki disease.

Since in medical practice the differential diagnosis of myocarditis is most often carried out with the first two diseases, we will dwell on them in more detail.

Differential diagnosis of myocarditis and acute coronary syndrome

Similarities:

• prolonged intense chest pain;
• Rs-T segment displacement and T wave changes, as well as other infarction-like changes (pathological Q wave or QS complex);
• increased activity of cardiac-specific enzymes and troponin levels.

Differences:

• the presence of predisposing risk factors for coronary heart disease (smoking, dyslipidemia, arterial hypertension, carbohydrate metabolism disorders, hyperhomocysteinemia, etc.);
• the effect of nitroglycerin on pain relief;
• ECG dynamics typical for acute myocardial infarction;
• the presence of large-focal disturbances of regional contractility of the left ventricular myocardium in acute myocardial infarction, established using echocardiography

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Differential diagnosis of myocarditis and dilated cardiomyopathy

Similarities:

• clinical manifestations of heart failure (shortness of breath, dry cough, orthopnea, edema, etc.);
• dilation of the heart chambers and a decrease in hemodynamic parameters (decrease in cardiac index, EF, increase in end-diastolic volume and end-diastolic pressure, etc.) as determined by echocardiography;
• change of RS-T segment;
• heart rhythm disturbances (in severe forms of myocarditis).

Differences:

• patients with myocarditis usually indicate a history of an infectious disease in the previous 2-3 weeks;
• in most cases of myocarditis, signs of congestive heart failure are much less pronounced than in DCM, and thromboembolic syndrome is also not characteristic;
• in patients with myocarditis, laboratory signs of inflammatory syndrome and elevated levels of cardiac-specific enzymes may be detected, which is not typical for DCM;
• Most patients with myocarditis do not have persistent myocardial defects in the outcome, spontaneous recovery is possible, the degree of ventricular dysfunction can stabilize. Only in giant cell myocarditis (a rare form of myocarditis associated with autoimmune diseases, Crohn's disease, myasthenia), myocarditis in AIDS, fulminant course, chronic course with transformation into DCM, the disease is characterized by steady progression, refractory course of congestive heart failure.

In some cases, endomyocardial biopsy may be required for differential diagnosis of severe (diffuse) myocarditis and DCM.

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Treatment myocarditis

The main goals of treatment of patients with myocarditis, towards which it should be aimed:

• prevention of the formation of irreversible dilation of the heart chambers;
• prevention of development of chronic heart failure;
• prevention of the occurrence of life-threatening conditions for the patient (severe rhythm and conduction disturbances).

All patients with suspected myocarditis are subject to hospitalization. Patients whose ECG reveals changes characteristic of myocarditis or resembling myocardial infarction, whose blood levels of cardiac-specific markers are elevated, or who develop signs of heart failure, must be hospitalized urgently.

Non-drug treatment of myocarditis

Essential non-drug methods of treating myocarditis are bed rest, the observance of which reduces the frequency of complications and the duration of the recovery period, and oxygen therapy. The duration of bed rest is determined by the severity of myocarditis. In mild myocarditis, it is 3-4 weeks, until the ECG at rest is normalized or stabilized. In moderate myocarditis, strict bed rest is prescribed for 2 weeks with its expansion in the following 4 weeks. In cases where the patient develops a severe form of myocarditis, strict bed rest in the intensive care unit is indicated until circulatory failure is compensated, with its subsequent expansion over 4 weeks. Treatment of severe forms of myocarditis in the acute period in the intensive care unit is due to the possibility of developing acute heart failure, cardiogenic shock, threatening rhythm disturbances or sudden cardiac death.

Limiting physical activity in individuals who have had myocarditis is indicated until the ECG has completely returned to baseline values.

Depending on the severity of the clinical picture of heart failure, patients are prescribed a diet with limited table salt and liquids; all patients are advised to quit smoking and drinking alcohol.

Drug treatment of myocarditis

Drug treatment of myocarditis should be aimed at eliminating the etiological factor, influencing the underlying disease, correcting hemodynamic disorders and immune status, preventing and treating cardiac rhythm and conduction disorders, as well as thromboembolic complications.

Etiological treatment of myocarditis

Due to the fact that in the overwhelming majority of cases the main etiological factor in the development of non-rheumatic myocarditis is a viral infection, there is an assumption to use antiviral drugs (polyclonal immunoglobulins, interferon-alpha, ribavirin, etc.) in the acute period of viral myocarditis, however, this approach requires further study.

When myocarditis develops against the background of bacterial infections, patients are prescribed antibacterial agents (antibiotics). The antibiotic is prescribed taking into account the underlying disease.

Antibacterial drugs for the treatment of bacterial myocarditis

Etiological variant of myocarditis	Groups of antibiotics	Examples
Mycoplasma	Macrolides	Erythromycin 0.5 g orally 4 times a day for 7-10 days
	Tetracyclines	Doxycycline 0.1 g orally 1-2 times a day
Bacterial	Penicillins	Benzylpenicillin 1 million units every 4 hours intramuscularly; oxacillin 0.5 g orally 4 times a day, 10-14 days

A favorable outcome of myocarditis is also facilitated by the treatment of foci of chronic infection.

The use of NSAIDs in the treatment of non-rheumatic myocarditis is not recommended, since there is no convincing evidence of their positive effect on the outcome of the disease; NSAIDs slow down the reparation processes in the damaged myocardium, thereby worsening the patient's condition.

Glucocorticoids are not recommended for the treatment of viral myocarditis in the early stages of the disease, as this leads to viral replication and viremia, but they are indicated in the following cases:

• severe myocarditis (with pronounced immunological disorders);
• myocarditis of moderate severity with no effect from the treatment;
• development of myopericarditis;
• giant cell myocarditis;
• myocarditis developing in individuals with immunodeficiency and rheumatic diseases.

As a rule, prednisolone is used at a dose of 15-30 mg/day (for moderate myocarditis) or 60-80 mg/day (for severe forms) for 5 weeks to 2 months with a gradual reduction in the daily dose of the drug and its complete withdrawal.

The use of immunosuppressants (cyclosporine, azathioprine) for myocarditis is currently not recommended, except in cases of giant cell myocarditis or other autoimmune diseases (eg, SLE).

In severe forms of myocarditis with high laboratory and clinical activity, it is advisable to prescribe heparins. The purposes of their administration in such cases are prevention of thromboembolic complications, as well as immunosuppressive, anti-inflammatory (due to a decrease in the activity of lysosomal enzymes) action. Heparins are prescribed in a dose of 5000-10,000 IU 4 times a day subcutaneously for 7-10 days, then the dosage is gradually reduced over 10-14 days under the control of a coagulogram, with subsequent transfer of the patient to warfarin (under the control of INR). In case of concomitant pericarditis, anticoagulant effect may be contraindicated. Long-term use of warfarin is indicated for patients with repeated systemic or pulmonary embolism or with mural thrombi diagnosed using echocardiography or ventriculography.

In the development of congestive heart failure, the following are used:

• ACE inhibitors (enalapril 5-20 mg orally 2 times a day, captopril 12.5-50 mg 3 times a day, lisinopril 5-40 mg 1 time per day);
• beta-blockers (metoprolol 12.5-25 mg/day, bisoprolol 1.25-10 mg/day once, carvedilol 3.125-25 mg 2 times a day);
• loop diuretics (furosemide 10-160 mm orally 1-2 times a day, bumetanide 1-4 mg orally 1-2 times a day) and spironolactone (12.5-20 mg orally 1 time per day).

In the case of a fulminant course, manifested by cardiogenic shock, active treatment is required: intravenous administration of vasodilators and inotropic drugs, intra-aortic balloon counterpulsation or the use of an artificial left ventricle. Early initiation of such active intervention with mechanical support of blood circulation can help to gain time until heart transplantation and also prove to be a "bridge to recovery".

Antiarrhythmic drugs are used in patients with tachyarrhythmias or ventricular rhythm disturbances (drugs with a pronounced negative inotropic effect should be avoided).

For patients with persistent conduction disorders that do not respond to conservative treatment, implantation of a cardioverter-defibrillator is possible. For patients with clinically significant bradyarrhythmias or high-grade conduction blocks, implantation of a temporary pacemaker is indicated.

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Prevention

Myocarditis may develop as a manifestation or complication of any infectious disease, primarily viral, therefore prevention of non-rheumatic myocarditis is reduced mainly to prevention of these diseases. It consists of prophylactic vaccinations and immunizations in threatened groups or populations against those cardiotropic infectious agents for which vaccines already exist (measles, rubella, influenza, parainfluenza, poliomyelitis, diphtheria, etc.). Nevertheless, since seroprophylaxis is absent or insufficiently effective for many viral infections, the most important measures for preventing the development of myocarditis are, for a short period after a respiratory infection, limitation of professional physical activity or sports and a thorough electrocardiographic examination. Identification of individuals with asymptomatic forms of myocarditis and timely control of their physical activity can prevent the transition to a more severe form.

All individuals with a family history of sudden death or heart failure at a young age in their relatives should have a medical examination and an electrocardiogram at least once a year. In addition, they should avoid overexertion associated with work or professional sports.

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Forecast

In terms of prognosis of myocarditis, the “three-thirds rule” is true: one third of patients recover, one third develop stable left ventricular dysfunction, and another third rapidly deteriorate (transition to DCM).

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History of the issue

The term "myocarditis" was first proposed in 1837.

S. Sobernheim, who described the relationship between myocardial inflammation and acute vascular disorders with previous infection. The diagnosis of "myocarditis" was a collective one for a long time, and it was made for all myocardial diseases. In 1965, TW Mattingly described myocarditis as an idiopathic inflammatory lesion of the heart muscle, not associated with damage to the heart valves. G. Gabler considered inflammation of the heart muscle (myocarditis) to be the main form of the disease, and degenerative changes, the so-called myocardoses, to be only the first stage of myocarditis. Myocarditis was often included in the rubric of cardiomyopathy and was considered, among others, as inflammatory cardiomyopathy. The merit of the Russian cardiologist G.F. Lang was the introduction of the term "myocardial dystrophy" and the isolation of this pathology from the group of myocarditis.

One of the first detailed descriptions of myocarditis (acute interstitial inflammation of the myocardium, leading to a fatal outcome in a few days or 2-3 weeks) belongs to Fiedler (CL Fiedler). He was the first to present interfibrillary round-cell infiltrates as the main symptom of the disease and suggested its infectious nature with the presence of "sui generic infection, localized directly in the heart muscle and causing inflammation." In this way, Fiedler predicted the viral etiology of "idiopathic" myocarditis, which was established for most such myocarditis in numerous subsequent studies (Silber, Stacmmler, Smith, Grist, Kitaura et al.). Professor Yu. I. Novikov made a great contribution to the study of non-rheumatic myocarditis and the development of diagnostic criteria, popular in our country to this day. In recent decades, new clinical, laboratory and instrumental methods have made it possible to significantly concretize the concept of “myocarditis” and give it a detailed morphological, immunological and histochemical characterization.

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