Myocarditis

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

[1], [2], [3], [4], [5], [6]

Epidemiology

The true prevalence of myocarditis is difficult to estimate, because in a number of cases the disease is latent or subclinical, without bright manifestations of the disease, resulting in complete recovery.

According to pathological and anatomical studies, the prevalence of myocarditis among the deceased is 1-4%, reaching 9.5% when examining a larger than normal section of myocardial tissue. In people who died from sudden cardiac death at a young age, the signs of myocardial inflammation range from 8.6 to 12%. The frequency of intravital diagnosis of myocarditis is quite wide (0.02-40%). It is worth noting that people with young age become sick with myocarditis (the average age is from 30 to 40 years). The incidence of women is slightly higher than that of men, but men tend to have more severe forms.

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

[7], [8], [9], [10], [11]

Pathogenesis

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

• The direct cytopathic effect of infectious agents that are able to penetrate inside the cardiomyocyte (viruses, trypanosomes, rickettsia) or localize in the interstitial tissue, forming small abscesses (bacteria). It was shown that with active myocarditis and dilated cardiomyopathy in cardiomyocytes, fragments of the genome of the virus can be detected.
• Damage to cardiomyonites by toxins released by the pathogen into the blood in case of systemic infection or directly into the heart. This mechanism of damage is most typical for diphtheria myocarditis, but it can develop with an infectious-toxic shock.
• Development of coronary arteries and endothelial dysfunction of the heart vessels followed by coroparogenic damage to the heart muscle (rickettsia).
• Nonspecific 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 during the introduction of pathogens or are reactivated as a result of a persistently persistent primary infection.

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

The risk factors for myocarditis include:

• pregnancy;
• hereditary predisposition;
• immunodeficiency states.

[12], [13], [14], [15], [16], [17]

Symptoms of the myocarditis

Symptoms of myocarditis do not have specific features, but in most cases, one can trace the chronological association of heart disease with infection or other etiologic factors that can lead to the development of toxic or allergic myocardial damage. The disease most often develops in a few days (less often - weeks) after a viral infection and in some cases it is asymptomatic.

Pains in the heart are often (60% of cases), they are usually located in the region of the apex of the heart, they can spread to the entire precordial region of the heart, they are piercing or pressing, usually prolonged, they are not associated with physical activity and are not stopped by the intake of nitrates. This type of pain can be associated with the involvement of the pericardium (myopericarditis) in the pathological process, but rare cases of angina pectoris are possible, for example, with the current viral coronary artery disease and vasospasm.

Dyspnea is the second most frequent symptom (47.3%) of the current myocarditis. It is associated with developing left ventricular failure, can occur only with intense physical exertion (with mild myocarditis) or even at rest (with moderate to severe and severe forms). Dyspnoea may increase in the horizontal position of the body due to an increase in preload to the heart. A serious sign of myocarditis is the sudden appearance of symptoms of congestive heart failure in a young patient without clinical signs of IHD.

Palpitation (47.3%) is associated with a decrease in cardiac output and a reflex increase in 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 disorders of rhythm and conduction (atrioventricular blockades of the 2nd degree, 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 blockade are characteristic of severe diffuse myocarditis and can lead to a sudden arrest of the circulation.

Edema on the legs, pain in the right hypochondrium and other manifestations of circulatory insufficiency over a large range often develop in chronic myocarditis.

We present the clinical observation of myocarditis of Coxsackie group B (according to the materials of Professor Yu.L. Novikov).

Patient A., 36 years old, was taken to the clinic with diagnosis of postgripposis myocarditis, left-sided pleurisy, extrasystolic arrhythmia. A month before hospitalization, he noted signs of a mild ORL with symptoms of rhinitis, pharyngitis, bronchitis. Continued to work. On the 6th day, sudden acute paroxysmal pains appeared in the precardial region and behind the breastbone, in connection with which the suspicion of myocardial infarction initially arose. Then the pains were localized mainly in the left hypochondrium, intensified with movements, breathing, coughing.

At admission, body temperature is 37.9 ° C. Breathing is superficial, sparing the left half of the chest during inspiration, the number of breaths is 28 per minute. Heart tones are moderately muffled, arrhythmic, I tone is preserved, no noise. Pulse - 84 per minute, extrasystolic arrhythmia. Blood pressure 130/80 mm Hg On the left in the fifth intercostal space, pleuropericardial noise is heard. With an X-ray study, there was an increase in the size of the heart. Changes in the lungs and restriction of the mobility of the diaphragm were not detected. On the ECG in dynamics - group ventricular extrasystoles, flattening of the T wave in the leads I, II, III, V5-V6. Blood test: Hb - 130 g / l, leukocytes - 9,6х10 ⁹ / l, ESR - 11 mm / h, C reactive protein - 15 mg / L antistreptolysin-O - negative, the reaction of direct hemagglutination to influenza A, B and parainfluenza - negative. A high titer of Coxsacki B2 antibodies (1: 2048) with a double increase for 12 days.

Treatment was prescribed: bed rest for 2 weeks, non-steroidal anti-inflammatory drugs inside. With the subsequent radiographic examination, the size of the heart decreased, a restriction of the left dome of the diaphragm was found to form a pleuropericardial adhesion. The body temperature returned to normal within the first day of treatment, and the pain in the heart completely disappeared after 2 weeks. The ECG retained ventricular extrasystoles with a frequency of 10-12 per minute.

The preceding ARI, serological data, characteristic pain syndrome caused by simultaneous involvement of the pleura, pericardium, and myocardium in the process made it possible to diagnose: "Bornholm disease (epidemic myalgia caused by the Coxsackie B virus.) Fibrinous pleurisy., Acute Coxsacki. In viral myopicarditis of severe degree. II A, II FC.

[18]

Forms

Classification of myocarditis according to the pathogenetic (etiologic) variant

Infectious and infectious-toxic:

• viral (adenoviruses, Coxsackie viruses B, influenza, infectious hepatitis, human immunodeficiency-1, parainfluenza, ECHO, measles, infectious mononucleosis, cytomegalovirus, etc.);
• bacterial (diphtheria, mycobacteria, mycoplasmas, streptococci, meningococci, staphylococci, gonococci, legionella, clostridia, etc.);
• fungal (aspergillosis, actinomycosis, candidiasis, coccidomycosis, cryptococcosis, histoplasmosis);
• rickettsia (typhus fever, fever Q, etc.);
• spirochetosis [lentospiroz, syphilis, borreliosis (Lyme carditis)];
• protozoal [trypanosomiasis (Chagas disease), toxoplasmosis, amoebiasis];
• parasitic (schistosomiasis caused by the larva of the helminth, syndrome of the "wandering larva", echinococcosis).

Allergic (immunological):

• medicinal preparations (sulfonamides, cephalosporins, detoxin, dobutamine, tricyclic antidepressants, etc.), serum sickness;
• systemic connective tissue disease;
• transplantation of organs and tissues.

Toxic:

• drugs, especially cocaine;
• uremic conditions;
• thyrotoxicosis;
• alcohol and others. 

Others:

• giant cell myocarditis;
• Kawasaki's disease;
• radiation treatment. 

[19], [20], [21], [22]

Classification of myocarditis downstream

• Acute myocarditis. It is characterized by acute onset, increased body temperature, marked clinical manifestations, changes in laboratory data, indicative of the ongoing inflammatory process, an increase in the level of cardiospecific markers of damage. Viral myocarditis is characteristic of viremia. The histological picture indicates necrosis of cardiomyocytes.
• Subacute myocarditis. Characterized by a less vivid clinical picture, moderate deviations in laboratory data. There is an increase in specific antibodies in the diagnostic titer. Activation of T- and B-lymphocytes occurs. The histological picture indicates the infiltration of the myocardium by mononuclear cells.
• Chronic myocarditis. Characterized by long-term course with periods of exacerbation and remission. Establish a high titer of anticardial antibodies and other disorders of cellular and humoral immunity. The histological picture is fibrosis and inflammatory infiltration. At the end, post-inflammatory dilated cardiomyopathy develops.

[23], [24], [25], [26], [27]

Classification of myocarditis in the prevalence of the inflammatory process

Focal myocarditis. The focus of damage to cardiomyocytes and inflammatory cell infiltration is located mainly r of one of the walls of the left ventricle. Depending on its location and size, different 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, which can be detected in echocardiography, may appear.

Diffuse myocarditis. In the pathological process, the entire myocardium of the left ventricle is involved, which leads to a substantial violation of its contractility, a decrease in the PV, cardiac index, and an increase in CDF and BWW, and, consequently, the development of heart failure.

[28], [29], [30], [31], [32]

Classification of myocarditis in terms of severity

Classification by severity - to light, moderate (moderate) and severe forms - is based on two main criteria; changes in the size of the heart and the degree of manifestation of heart failure.

• An easy 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 (after 2-3 weeks) after the infection; general weakness, minor dyspnea that occurs when performing physical exertion, various pain sensations in the heart, palpitations and irregularities.
• The medium-heavy form. It flows with cardiomegaly, but without signs of heart failure at rest. This form includes diffuse myocarditis and myopericarditis, terminating more often with complete recovery with normalization of the heart, but in the acute period it is characterized by more pronounced objective and subjective manifestations.
• Heavy form. It is characterized by cardiomegaly and marked signs of heart failure (acute or chronic). In rare cases, severe myocarditis may manifest as cardiogenic shock or severe rhythm and conduction disorders with Morgagni-Adams-Stokes syndrome.

[33], [34], [35], [36], [37], [38]

Diagnostics of the myocarditis

In the process of collecting anamnesis, it is necessary to clarify and clarify the following points in the patient:

• Whether the present condition was preceded by a cold disease, whether the patient had a fever, fever, weakness, joint or muscle pain, a rash on the skin. The period between the transferred infection of the upper respiratory tract or gastrointestinal tract is about 2-3 weeks.
• Does the patient worry about pain in the heart or in the chest of a constant stitching or pressing character that intensify during physical exertion that does not pass after taking nitroglycerin.
• Are there any complaints indicating a different or developing cardiovascular insufficiency (fatigue, shortness of breath, nocturnal attacks of suffocation) of varying severity, palpitations, syncopal conditions.

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

Physical examination

With myocarditis, tachycardia, hypotension and fever are noted. If myocarditis occurs in medium-severe or severe form with the formation of heart failure, then acrocyanosis, swelling of the veins of the neck at rest or with insignificant physical exertion, peripheral edema, wheezing and crepitation in the lungs are possible.

It should also be remembered that with a more detailed physical examination, one can find clinical signs of an infectious or systemic disease (fever, skin rash, lymphadenopathy, etc.) that caused myocarditis.

When palpation of the heart, you can find a weakening of the apical impulse, as well as its displacement outside the left mid-clavicular line in cardiomegaly.

With percussion in patients with medium-severe and severe forms of myocarditis, the left border of relative dullness of the heart shifts to the left. In severe cases, when the dilatation of not only the left ventricle cavity but also the left atrial cavity occurs, the upper limit of relative dullness shifts upward.

With auscultation, a decrease in the volume of the I tone, an emphasis on tone II on the pulmonary artery, III and IV tones, as well as gallop rhythm, a predictor of severe myocarditis, in particular a progressive decrease in myocardial contractility and systolic dysfunction. Usually, its appearance precedes the development of clinical signs of heart failure.

When the focus is located in the area of the papillary muscles or as a result of the enlargement of the fibrous ring of the left atrioventricular orifice, the noise of mitral regurgitation is listened.

With the development of myopericarditis, pericardial friction noise is heard.

Myocarditis usually develops a tachycardia that does not correspond to the degree of increase in body temperature ("toxic scissors"), and does not disappear in sleep, which serves as a significant differential diagnostic feature. Tachycardia can occur both with physical activity and at rest. Rare bradycardia and a decrease in pulse pressure are rare.

Laboratory diagnostics of myocarditis

In the clinical analysis of blood there may be a slight leukocytosis with a shift to the left and an increase in ESR. The diagnostic value of this reaction may decrease with the development of congestive heart failure and hepatitis. The increase in the level of eosinophils is characteristic of parasitic diseases and can increase with recovery from myocarditis.

In a number of patients, the level of myocardial enzymes (CK, CF fraction of creatine phosphokinase (CPC-MB), lactate dehydrogenal-1 (LDG-1)) was elevated. Which reflects the severity of cytolysis. A specific and sensitive marker of myocyte damage is cardiac troponin-I (cTnI). Possible increase in the level of fibrinogen, C-reactive protein, seromucoid, a2- and y-globulin, 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 antibody titer to cardiotropic viruses, a fourfold increase in which is of diagnostic significance.

Electrocardiogram or daily monitoring of the ECG according to Holter in myocarditis

Myocarditis can cause the following changes on the ECG (one or more):

• various disorders of the heart rhythm, such as sinus tachycardia or bradycardia, atrial fibrillation, paroxysmal supraventricular or ventricular tachycardia, ectopic rhythms. Nadzheludochkovaya tachycardia especially occurs with congestive heart failure or pericarditis;
• disturbances in the conductivity of an electrical impulse along the conduction system of the heart, which can manifest themselves as an atrioventricular block of degree I-III, blockade of the left or, more rarely, the right leg of the bundle. There is a definite correlation between the degree of conduction disturbance and the severity of myocarditis flow. Often there is a complete atrioventricular blockade, often found after the first episode of loss of consciousness. It may be necessary to install a temporary pacemaker;
• changes in the final part of the ventricular complex with the form of depression of the ST segment and the appearance of a low-amplitude, smoothed or negative tooth generally defined in the thoracic leads, but are also possible in standard ones;
• pseudo-infarct changes, including a negative coronary T, rise of the ST segment and the formation of a pathological tooth that reflects the defeat of the heart muscle and a decrease in its electrical activity.

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

[39], [40], [41], [42], [43], [44], [45]

Echocardiography with myocarditis

When performing echocardiogram in patients with low-symptom or asymptomatic myocarditis, there may be no changes or a slight increase in CSR and left ventricular BVD can be determined. In severe cases of myocarditis, accompanied by a decrease in the contractility of the myocardium, there is a decrease in PV and cardiac index. There is an expansion of the left ventricular cavity, local breach of contractility in the form of separate areas of hypokinesia (sometimes - global hypokinesia) or akinesia. For the acute stage, the most common increase in the thickness of the walls of the heart, caused by interstitial edema. The insufficiency of mitral and tricuspid valves is possible. With myopericarditis, the separation of pericardial sheets and a small amount of fluid are noted. In 15% of cases, parietal thrombi are diagnosed.

[46], [47], [48], [49], [50], [51], [52], [53]

X-ray diagnosis of myocarditis

In a significant part of patients, there are no changes in chest radiography, and in the other part of the patients, cardiomegaly (cardiothoracic index increase of up to 50% or more) and signs of venous stasis in the small circulation range are determined in varying degrees: strengthening of the lung pattern, expansion 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 an active inflammatory process in the myocardium. To determine the damage of cardiomyocytes in patients with an unexplained clinical picture of heart failure, scintigraphy with monoclonal antibodies to myosin labeled with ¹¹¹ In can be used .

Myocardial biopsy

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

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

Despite the fact that usually from 4 to 6 samples are taken with endomyocardial biopsy, with careful postmortem analysis of proven cases of myocarditis it was established that more than 17 samples (biopsy samples) are necessary for correct diagnosis of myocarditis in more than 80% of cases. In clinical practice this is unrealistic, and therefore the lack of sensitivity of endomyocardial biopsy is evident. Another significant limitation in histopathological diagnosis is the inconstancy of the microscopic picture of myocarditis.

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

A promising method of diagnosis can be the isolation of genetic viral material from the myocardium using the recombinant DNA technique, using PCR and in situ hybridization.

Clinical diagnostic criteria of myocarditis

In 1973, the New York Heart Association (NUNA) developed diagnostic criteria for non-rheumatic myocarditis. In accordance with the degree, diagnostic significance, the criteria for myocarditis were divided into two groups, "large" and "small."

Clinical diagnostic criteria for myocardium are as follows:

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

Plus the presence of signs of myocardial damage.

"Big" criteria:

• increased activity of cardiospecific enzymes and isoenzymes in the patient's blood serum (CK, MB-CK, LDH, LDG-1) and the content of troponins;
• pathological changes in the electrocardiogram (disorders of the heart rhythm and conductivity);
• cardiomegaly, established by roentgenological data;
• presence of heart failure or cardiogenic shock;
• Morgagni-Adams-Stokes syndrome.

"Small" criteria:

• proto-diastolic rhythm of the canter;
• weakened I tone;
• tachycardia.

To diagnose a mild form of myocarditis, it is sufficient to combine the signs of a transmitted infection (or another effect on the body) and the first two "big" criteria or one of them with two "small" ones. If the patient, in addition to the first two "big" criteria, has at least one of the following "big" criteria, then it makes it possible to diagnose a moderate and severe form of myocarditis.

Dallas morphological criteria of myocarditis (USA, 1986)

Diagnosis of myocarditis	Histological signs
Reliable	Inflammatory infiltration of the myocardium with necrosis and / or degeneration of adjacent cardiomyocytes, uncharacteristic for changes in MBS
Doubtful (probable)	Inflammatory infiltrates are quite rare, or cardiomyocytes are infiltrated by leukocytes. There are no areas of necrosis of cardiomyocytes. Myocarditis can not be diagnosed because of the absence of inflammation
Not verified	Normal histological picture of the myocardium, or there are pathological changes in non-inflammatory tissue

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

• Prior infection, as evidenced by clinical and laboratory data (including excretion, neutralization response, DSC, HSCA, increased ESR, increased CRP) or other underlying disease (drug allergy, etc.).

Plus signs of myocardial damage.

"Big":

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

"Small":

• tachycardia;
• weakened I tone;
• the rhythm of the canter.

The diagnosis of "myocarditis" is valid when combining a previous infection with one "large" and two "small" signs.

[54], [55], [56], [57], [58], [59], [60]

Structure of the diagnosis of myocarditis

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

After that, complications (if any) are indicated, the stage of circulatory failure according to ND. Strazhesko and V.Kh. Vasilenko and the functional class (FK) according to the New York classification (NYHA),

Examples.

• Acute focal postgripposic myocarditis, mild form. Nadzheludochkovaya extrasystole, NK0. I FC.
• Acute diffuse myocarditis, unspecified etiology. Ventricular extrasystole. Paroxysm of ventricular tachycardia from _____ NK IIA stage, III FC.

Differential diagnosis

For the diagnosis of "myocarditis" it is necessary to exclude diseases that occur with secondary myocardial damage, as well as primary heart lesions of unknown ethnology, not related to diseases of other organs and systems (cardiomyopathies). In the differential diagnosis of non-rheumatic myocarditis, endocrine, metabolic, and general systemic diseases should be excluded as the cause of cardiac muscle damage.

The most practical value is the differential diagnosis of myocarditis with:

• myocardial infarction;
• dilated cardiomyopathy,
• rheumatic and non-rheumatic heart valve lesions;
• heart damage with long-term arterial hypertension;
• chronic exudative and constructive pericarditis.

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

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

Differential diagnosis of myocarditis and acute coronary syndrome

The similarity:

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

Differences:

• Presence of predisposing risk factors for IHD (smoking, dyslipidemia, arterial hypertension, violation of carbohydrate metabolism, hyperhomocysteinemia, etc.);
• effect of nitroglycerin for relief of pain;
• typical for acute myocardial infarction of ECG dynamics;
• presence of large-focal disturbances of regional contractility of the left ventricular myocardium in acute myocardial infarction, established with the help of echocardiography

[61], [62], [63], [64], [65], [66]

Differential diagnosis of myocarditis and dilated cardiomyopathy

The similarity:

• clinical manifestations of heart failure (dyspnea, dry cough, orthopnea, edema, etc.);
• expansion of the chambers of the heart and reduction of hemodynamic parameters (decrease in cardiac index, FV, increase in BWW and KDD, etc.) submitted by EchoCG;
• changing the RS-T segment;
• disturbance of the rhythm of the heart (with severe forms of myocarditis).

Differences:

• patients with myocarditis usually indicate a transferred infectious disease in the preceding 2-3 weeks;
• in most cases of myocarditis, the signs of congestive heart failure are much less pronounced than in DCM, nor does the troboembolic syndrome;
• in patients with myocarditis, laboratory signs of an inflammatory syndrome, an increased level of cardiospecific enzymes, which is not typical for DCMP;
• most patients with myocarditis have no persistent myocardial defects at the end, spontaneous recovery is possible, the degree of ventricular dysfunction can be stabilized. Only with 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 DCMP disease is characterized by steady progression, refractory course of congestive heart failure.

In a number of cases, endomiocardial biopsy may be required for differential diagnosis of severe (diffuse) myocarditis and DCMD.

[67], [68], [69], [70], [71], [72], [73]

Treatment of the myocarditis

The main goals of treatment of patients with myocarditis, for the achievement of which it should be directed:

• preventing the formation of irreversible dilatation and heart chambers;
• preventing the development of chronic heart failure;
• prevention of life-threatening patient conditions (severe rhythm and conduction disorders).

All patients with suspected myocarditis are hospitalized. Patients who have been found to have ECG changes that are characteristic of myocarditis or resemble myocardial infarction, who have elevated cardiospecific markers in their blood, and / or signs of heart failure, must be hospitalized in a compulsory emergency order.

Non-drug treatment of myocarditis

Essential non-pharmacological methods of treatment of myocarditis are bed rest, observance of which reduces the frequency of complications and the duration of the recovery period, as well as oxygen therapy. The duration of bed rest is determined by the severity of myocarditis. With a mild form of myocarditis, it is 3-4 weeks before the normalization or stabilization of the ECG at rest. At the moderate form - for 2 weeks appoint a strict bed rest with its expansion in the next 4 weeks. In cases where the patient develops a severe form of myocarditis, strict bed rest is shown in the intensive care unit before compensating for circulatory failure, with subsequent expansion within 4 weeks. Treatment of severe forms of myocarditis in an acute period in the intensive care unit is due to the possibility of developing a patient with acute heart failure, cardiogenic shock, threatening rhythm disturbances or sudden cardiac death.

Restriction of physical exertion to persons who underwent myocarditis is indicated until the ECG is fully returned to the initial parameters.

Depending on the severity of the clinical picture of heart failure patients are prescribed a diet with restriction of table salt and liquid, all patients are recommended to quit smoking and alcohol.

Medical treatment of myocarditis

Medical treatment of myocarditis should be aimed at eliminating the etiologic factor, affecting the underlying disease, correcting hemodynamic disorders and immune status, preventing and treating cardiac rhythm and conduction disorders, and thromboembolic complications.

Etiological treatment of myocarditis

Due to the fact that in the overwhelming majority of cases the main etiologic factor in the development of non-rheumatic myocarditis is a viral infection, it is suggested that antiviral drugs (polyclonal immunoglobulins, interferon-alpha, ribavirin, etc.) should be used in the acute period of viral myocarditis, but this approach requires further study .

With the development of myocarditis against a background of bacterial infections, patients are shown antibacterial agents (antibiotics). Antibiotic prescribe 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 grams orally 4 times a day for 7-10 days
	Tetracyclines	Doxycycline 0.1 g inside 1-2 times a day
Bacterial	Penicillins	Benzylpenicillin 1 million units every 4 hours intramuscularly; Oxacillin 0.5 grams orally 4 times a day, 10-14 days

A favorable outcome of myocarditis is also facilitated by the sanation 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 repair process in the damaged myocardium, thereby worsening the patient's condition.

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

• severe myocarditis (with marked immunological disorders);
• myocarditis of moderate severity in the absence of the effect of the treatment;
• development of myopericarditis;
• gigantocellular myocarditis;
• myocarditis, developing in people with immunodeficiency, rheumatic diseases.

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

The appointment of immunosuppressors (cyclosporine, azathioprine) in 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 expedient to administer heparins. The purposes of their appointment in such cases - the prevention of thromboembolic complications, as well as immunodepressive, anti-inflammatory (by reducing the activity of lysosomal enzymes) action. Heparins are prescribed in a dose of 5000-10 000 units 4 times a day subcutaneously 0 for 7-10 days, then the dosage is gradually reduced in the course of 10-14 days under the control of the coagulogram, followed by patient transfer to warfarin (under the control of INR). With concomitant pericardial anticoagulant effects - can be contraindicated. Prolonged use of warfarin is indicated in patients with systemic or pulmonary embolisms or with parietal thrombi diagnosed by echocardiography or ventriculography.

With the development of congestive heart failure apply:

• ACE inhibitors (enalapril 5-20 mg orally 2 times a day, captopril 12.5-50 mg 3 times a day, lisinopril 5-40 mg once a 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 inside 1-2 times a day, bumetanide 1-4 mg orally 1-2 times a day) and spironolactone (12.5-20 mg orally once a day).

When fulminapnom flow, manifested by cardiogenic shock, requires active treatment: intravenous vasodilators and inotropic drugs, inside aortic balloon counterpulsation or the use of an artificial left ventricle. The early onset of such an active effect with mechanical support of blood circulation can allow you to gain time before heart transplantation, and also to be a "bridge to recovery".

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

Patients with persistent conduction abnormalities that do not respond to conservative treatment may be implanted with a cardioverter-defibrillator. Patients with clinically significant bradyarrhythmias or high-grade blockades are shown to be implanted with a temporary pacemaker.

[74], [75], [76], [77], [78]

Prevention

Myocarditis can develop as a manifestation or complication of any infectious disease, primarily of a viral disease, so the prevention of non-rheumatic myocarditis is mainly reduced to the prevention of these diseases. It consists in carrying out preventive vaccinations and vaccinations in threatened collectives or population groups against those cardiotropic infectious agents to which vaccines already exist (measles, rubella, influenza, parainfluenza, poliomyelitis, diphtheria, etc.). Nevertheless, since seroprophylaxis is absent or insufficiently effective in many viral infections, the restriction of occupational exercise or sports and a thorough electrocardiographic examination serve as the most important measures to prevent the development of myocarditis for a short time after a respiratory infection. Identifying people with asymptomatic forms of myocarditis and timely monitoring of their physical activity can prevent the transition to a more severe form.

All persons who have a family history with a history of sudden death or development of heart failure at a young age among relatives need medical examination and electrocardiographic examination at least once a year. In addition, they must avoid overloading associated with work or professional sports.

[79], [80], [81], [82], [83], [84], [85], [86], [87], [88]

Forecast

With respect to the prognosis of myocarditis, the rule of "three-thirds" is really: one-third of patients recover, one-third develops stable left ventricular dysfunction and another one-third rapidly deteriorates (transition to DCMP).

[89], [90], [91], [92]

Background

The term "myocarditis" was first proposed in 1837.

S. Sobernheim, who described the relationship of myocardial inflammation and acute vascular disorders with the transmitted infection. The diagnosis of "myocarditis" for a long time was collective, and it was put 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) the main form of the disease, and degenerative changes, the so-called myocardoses, - only the first stage of myocarditis. Myocarditis was often included in the rubric of cardiomyopathies and was considered among others as inflammatory cardiomyopathies. 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, which leads to death in a few days or 2-3 weeks) belongs to Fidler (CL Fiedler). He first introduced interfibrillar circular cell infiltrates as the main symptom of the disease and put forward an assumption of its infectious nature with the presence of a "sui generic infection localized directly in the cardiac muscle and causing inflammation." This Fiedler, as it were, predicted the viral etiology of the "idiopathic" myocarditis, which was established for the majority of such myocarditis in numerous subsequent studies (Silber, Stacmmler, Smith, Grist, Kitaura et al.). A great contribution to the study of non-rheumatic myocarditis and the development of criteria for diagnosing, popular in our country to this day, was made by Professor Yu.I. Novikov. In recent decades, new clinical laboratory and instrumental methods have made it possible to specify the concept of "myocarditis" to a considerable extent and give it a detailed morphological, immunological and histochemical characterization.

[93], [94], [95], [96], [97], [98], [99], [100], [101]