On the topic of: Non-rheumatic myocarditis

Performed by an intern

Ostankova A. Yu.

Semipalatinsk

Non-rheumatic myocarditis (NM) - inflammatory diseases myocardium caused by infectious, allergic, toxic effects with various pathogenetic mechanisms.

Classification

Myocarditis is an acute, subacute or chronic inflammatory lesion of the myocardium, predominantly of infectious and (or) immune etiology, which can manifest itself with general inflammatory, cardiac symptoms (cardialgia, ischemia, heart failure, arrhythmia, sudden death) or proceed latently.

Myocarditis is characterized by great variability clinical picture; it is often combined with pericarditis (the so-called myopericarditis); simultaneous involvement of the endocardium in the inflammatory process is also possible. For the convenience of distinguishing between rheumatic and other variants of myocarditis, the term “non-rheumatic myocarditis” is used.

Myocarditis, accompanied by dilation of the heart cavities and myocardial contractile dysfunction, is included in the American Classification of Primary Cardiomyopathies (2006) under the name “inflammatory cardiomyopathy.” This term was proposed to distinguish among patients with severe dilatation of the heart chambers (DCM), those whose disease is based on an inflammatory process that is subject to specific treatment (as opposed to patients with genetic DCM).

Myocarditis can be an independent condition or a component of another disease (for example, systemic scleroderma, SLE, IE, systemic vasculitis, etc.).

Epidemiology

The true prevalence of myocarditis is unknown due to difficulties in verifying the diagnosis. According to some data, the frequency of diagnosis of “myocarditis” in cardiology hospitals is about 1%, at autopsy in young people who died suddenly or as a result of injuries - 3-10%, in infectious diseases hospitals - 10-20%, in rheumatology departments - 30 -40%.

Classification

Classification of myocarditis, proposed in 2002 by N.R. Paleev, F.N. Paleev and M.A. Gurevich, built mainly on an etiological principle and presented in a slightly modified form.

Infectious and infectious-immune.

Autoimmune:

Rheumatic;

At diffuse diseases connective tissue (SLE, rheumatoid arthritis, dermatomyositis, etc.);

For vasculitis (periarteritis nodosa, Takayasu disease, Kawasaki disease, etc.);

For other autoimmune diseases (sarcoidosis, etc.);

Hypersensitive (allergic), including medicinal.

Toxic (uremic, thyrotoxic, alcoholic).

Radiation.

Burn.

Transplantation.

Of unknown etiology (giant cell, Abramov-Fiedler, etc.).

The etiological agent of infectious myocarditis can be bacteria (brucella, clostridia, corynebacteria, diphtheria, gonococci, Haemophilus influenzae, legionella, meningococci, mycobacteria, mycoplasmas, streptococci, staphylococci), rickettsia (Rocky Mountain fever, cool fever, tsutsugamushi fever, noah typhus), spirochetes (Borrelia, Leptospira, Treponema pallidum), protozoa (amoebas, Leishmania, Toxoplasma, trypanosomes that cause Chagas disease), fungi and helminths.

The most common causes of infectious myocarditis are adenoviruses, enteroviruses (Coxsackie group B, ECHO), herpetic viruses (cytomegalovirus, Epstein-Barr virus, herpes virus type 6, herpes zoster), HIV, influenza and parainfluenza viruses, parvovirus B19, and viruses of hepatitis B, C, mumps, polio, rabies, rubella, measles, etc. The development of a mixed infection (two viruses, a virus and a bacterium, etc.) is possible.

Myocarditis in infectious diseases may not have much clinical significance, develop as part of multiple organ damage (typhoid fever, brucellosis, borreliosis, syphilis, HIV infection, hepatitis C virus infection, cytomegalovirus) or come to the fore in the clinical picture and determine the prognosis (myocarditis with diphtheria, enterovirus infection, other viral myocarditis and Chagas disease).

In infectious (especially viral) myocarditis, the development of autoimmune reactions is typical, and therefore it can be difficult to distinguish between infectious and infectious-immune myocarditis.

According to the flow, there are three variants of myocarditis:

spicy- acute onset, pronounced clinical signs, increased body temperature, significant changes in laboratory (acute-phase) parameters;

subacute- gradual onset, prolonged course (from a month to six months), less severe acute-phase indicators;

chronic- long-term course (more than six months), alternating exacerbations and remissions.

According to the severity of the course, the following variants of myocarditis are distinguished:

easy- mild, occurs with minimal symptoms;

moderate severity - moderately expressed, symptoms are more distinct, slightly pronounced signs of heart failure are possible);

heavy- pronounced, with signs of severe heart failure;

fulminant (fulminant), in which extremely severe heart failure, requiring immediate hospitalization in the intensive care unit, develops within a matter of hours from the onset of the disease and often ends in death.

According to the prevalence of the lesion, the following variants of myocarditis are distinguished:

focal- usually does not lead to the development of heart failure, can only manifest as rhythm and conduction disturbances, and presents significant difficulties for diagnosis;

Non-rheumatic myocarditis (NM) is a disease characterized by the occurrence of an inflammatory process in the heart muscle. How to recognize the above disease? How to properly treat UI and how to prevent its occurrence? The answers to these questions can be found in this article.

Classification and causes

Children are more susceptible to the development of non-rheumatic myocarditis, but this disease occurs in all age categories population. The occurrence of the disease in question is facilitated by various factors. Most often the main reasons are:

In the vast majority of cases, the main cause of this disease is allergies and various viruses.

In some cases, nonrheumatic myocarditis may occur as a complication of lupus, scleroderma, or endocarditis infectious origin. Also, specialists have registered cases of UI without visible reasons.

Symptoms may vary depending on the location of the inflammatory process, but there are several common features:

• painful sensations of various nature in the chest area;
• significant increase in body temperature;
• feeling of heat;
• convulsions;
• malaise;
• drowsiness;
• various disorders heart rate(rapid heartbeat, irregular contractions, shortness of breath, increased volume of intercellular fluid);
• change in healthy shade of fingertips;
• swelling of the legs.

Complications and consequences

Often, non-rheumatic myocarditis in the lungs and average shape Provided timely contact with specialists, it responds well to treatment and does not cause complications or consequences. However, in the absence proper treatment or the presence of a severe form of the disease, the prognosis may not be very favorable. In the complicated form of UI, intoxication, impaired blood circulation, sclerosis and deformation of the valve apparatus are possible. Often the severe stage of the disease is accompanied by an inflammatory process serous membrane hearts.

Complications also include cardiosclerosis, which leads to persistent heart rhythm disturbances and a tendency to form blood clots.

The consequences include chronic heart failure, which, if left untreated, progresses and can lead to death. In some cases, when this disease There may be an arrhythmia, to eliminate which the patient is given a pacemaker.

Non-rheumatic myocarditis is also characterized by a recurrent latent form, which often progresses without severe symptoms, therefore, after treatment during the rehabilitation period, experts recommend observation by a cardiologist for 12 months after recovery, regular testing, as well as strengthening immune system.

Most often, children acquire the above ailment as a complication after suffering viral infections regardless of age. In some cases, non-rheumatic myocarditis can develop while still in the womb.

Symptoms are almost the same as in adults and depend on the severity of the disease. At mild form there may be a slight increase in heart rate, a decrease in the strength of myocardial contractions and a rhythm disturbance.

In the presence of moderate in severity Young patients experience fatigue and difficulty breathing, especially during physical activity. Also, upon examination, murmurs in the heart and wheezing in the lungs, disturbances in heart rhythm, a significant enlargement of the liver and a pronounced decrease in the strength of contractions of the heart muscle are detected.

At severe form respiratory distress is observed at rest, not only the work of the heart muscle is disrupted, but also blood circulation, an enlarged heart, hypotension and arrhythmia are observed, while the pulse is difficult to hear due to weak contractions. The liver is greatly enlarged and painful on palpation.

Cardiologists also treat non-rheumatic myocarditis in children. It is performed on the same principle as in adult patients; drugs and dosage for children are prescribed according to age.

In the vast majority of cases, with timely and correct treatment of UI, children recover completely without any complications or consequences. Full recovery occurs from 6 to 24 months after the start of treatment.

In some cases, such an illness can develop into chronic form Therefore, children need to be regularly monitored by a specialist, undergo timely examinations and be vaccinated against various diseases(provided there are no allergic reactions and only with the permission of the treating specialist).

Also, after an illness, young patients are recommended to attend therapeutic classes. physical culture recovery proper operation of cardio-vascular system. During rehabilitation, foods that can cause allergic reactions.

Diagnosis of the disease

Diagnosing this disease is quite difficult, therefore, if UI is suspected, the patient undergoes a fairly extensive series of studies and tests.

To make a diagnosis, you should contact family doctor who measures the heart rate, checks for abnormalities in the functioning of the heart muscle and the degree of swelling. Then he sends you for blood tests (general, biochemical, immunological, blood culture for sterility, PCR). The patient is also referred for echocardiography to study heart rhythm and changes in the functioning of the heart muscle.

Additionally, an X-ray of the lungs is prescribed to examine the condition of the heart, as well as possible congestive processes in the lungs. To obtain a more complete clinical picture, an endomyocardial biopsy may be required, which is used to diagnose and evaluate the development of inflammation. To make an accurate diagnosis, the patient is sent for scintigraphy and magnetic resonance imaging of the heart muscle (to identify the location of the inflammatory process).

Traditional treatment

The choice of therapy depends on the stage of development of the disease, of which there are several:

• acute;
• subacute;
• protracted;
• chronic.

At acute stage the patient is required to be referred to hospital treatment in hospital. Treatment is carried out by cardiologists in the appropriate department. The patient should limit as much as possible any physical activity on the body and observe bed rest on average 1-2 months until normal cardiac activity is restored.

Subacute stage characterized by a gradual deterioration of the patient’s condition and a longer recovery process. Depending on the severity of the disease, both inpatient treatment and at home are possible.

Protracted form, often occurs when contacting specialists is not done in a timely manner or improper treatment NM. May go to chronic, in which both periodic exacerbations of varying degrees and stages of relative remission are possible.

Regardless of the stage and form of the disease, it is necessary to observe dietary restrictions, namely, minimize the amount of salt in daily diet, do not drink a lot of water and stick to a protein diet to speed up the healing process.

Depending on the causative agent of the disease, appropriate drugs:

• antiviral (“Interferon”, “Viferon”);
• anti-inflammatory (Ibuprofen, Movalis, Indomethacin, Aspirin);
• to relieve swelling (Suprastin, Claritin);
• steroid medications (“Prednisolone”).

To improve the regeneration of the heart muscle, Panangin, Asparkam, Riboxin can be additionally prescribed, and for the prevention of various complications - Clexane, Fraxiparin, Plavix, Egitromb.

The duration of treatment and dosage of the above drugs depends on the stage and form of the disease and varies from 1 to 6 months.

All these drugs are provided for informational purposes only, before use. medicines it is necessary to obtain specialist advice.

Treatment with folk remedies

For the treatment of non-rheumatic myocarditis as additional funds use various folk recipes:

1. Infusion of arnica flowers. 2 small handfuls of flowers of this plant are poured into 400 ml of boiling water, covered with a lid and left for 60 minutes. You need to take 1 tablespoon, diluting with milk 1:1 after meals three times a day for 30 days in a row.

A vodka tincture is also prepared from the above plant. 2 handfuls of flowers are poured with 1 glass of vodka. Close tightly in a glass jar and keep for 1 week. After the expiration date, consume 35-40 drops of strained tincture 3 times a day after meals.

1. Medicinal collection herbs Ingredients:

• lily of the valley – 2 tablespoons;
• fennel (fruit) – 4 tablespoons;
• valerian – 8 tablespoons.

This mixture is poured with boiling water in an amount of 1.5 liters. After complete cooling, the infusion is carefully filtered and consumed half a glass three times a day after meals.

1. Alcohol tincture. Infuse 250 g of chopped lemon pulp, 120 g of chopped figs, half a glass of honey, 50 ml of vodka for a week, take 1 teaspoon in the morning and evening after meals.
2. Tincture for myocardial edema. To restore normal function of the heart muscle, people use the following recipe: add 1 tablespoon of honey and the juice of a medium-sized lemon to 1 glass of birch sap. This mixture is consumed once a day for 14 days.

Additionally in alternative medicine It is recommended to consume several tablespoons of honey daily, brew strawberry tea, and add it to your diet Walnut and raisins. Also, to normalize heart function, use a decoction of rose hips and hawthorn. But all the above means from traditional medicine should be used only after consultation with your doctor.

Prevention

Does not currently exist special means to prevent the development of non-rheumatic myocarditis. But experts have compiled a list of recommendations that help strengthen how cardiovascular system, and the body as a whole:

• fortified proper nutrition;
• cessation of use alcoholic drinks and cigarettes;
• regular exercise;
• timely contact with specialists for treatment various ailments;
• compliance with preventive measures during viral epidemics.

Since non-rheumatic myocarditis most often develops as a complication after various viral and bacterial ailments, good preventive measure There are various vaccines against influenza, rubella and other diseases.

Inflammation of the heart muscle is sufficient dangerous disease which, if not properly treated, can lead to the death of the patient. Therefore for complete cure and absence various consequences It is necessary to follow all the recommendations of specialists, and during the rehabilitation period undergo regular examinations and strengthen the immune system.

Classification non-rheumatic myocarditis(according to N. R. Paleev, 1982, in abbreviated form)

In pathogenesis are important:

• 1) direct introduction of an infectious factor into the myocardiocyte, its damage, release of lysosomal enzymes (Coxsackie viruses, sepsis);
• 2) immunological mechanisms - autoantigen - autoantibody reaction, formation of immune complexes, release of mediators and development of inflammation, activation of LPO.

Clinical, laboratory and instrumental data

Complaints: general weakness, moderate, pain in the region of the heart, constant, stabbing or aching character, interruptions in the heart area, possible palpitations, slight shortness of breath during physical activity.

Objective examination: general condition is satisfactory, no edema, cyanosis, or shortness of breath. The pulse is normal or somewhat rapid, sometimes arrhythmic, blood pressure is normal, the boundaries of the heart are not changed, the first tone is somewhat weakened, there is a quiet systolic murmur at the apex of the heart.

Laboratory data. OAK is not changed, sometimes there is a slight increase in ESR. BAC: moderate increase in blood levels of AST, LDH, LDH1_2, CPK, α2- and γ-globulins, sialic acids, seromucoid, haptoglobin. Antibody titers to Coxsackie viruses, influenza and other pathogens increase. A fourfold increase in antibody titers to pathogens during the first 3-4 weeks, high titers compared to the control, or a fourfold decrease subsequently are evidence of a cardiotropic infection. Counted permanently high level titers (1: 128), which is normally very rare.

ECG: a decrease in the T wave or ST segment in several leads and an increase in the duration of the P - Q interval are determined.

X-ray and echocardiographic examination does not reveal any pathology.

Complaints of patients: severe weakness, pain in the heart area of ​​a compressive nature, often stabbing, shortness of breath at rest and during exertion, palpitations and irregularities in the heart area, subfebrile body temperature.

Objective examination. The general condition is moderate. There is slight acrocyanosis, no edema or orthopnea, the pulse is frequent, satisfactory filling, often arrhythmic, blood pressure is normal. The left border of the heart is enlarged to the left, the first sound is weakened, a systolic murmur of a muscular nature is heard, and sometimes a pericardial friction murmur (myopericarditis).

Laboratory data. OAK: increased ESR, leukocytosis, shift leukocyte formula to the left, with viral myocarditis leukopenia is possible. BAC: increased content of sialic acids, seromucoid, haptoglobin, α2- and γ-globulins, LDH, LDH1_2, CPK, CPK-MB fraction, AST. AI: positive reaction inhibition of leukocyte migration in the presence of myocardial antigen, decrease in the number of T-lymphocytes and T-suppressors, increased levels of IgA and IgG in the blood; detection of CEC and antimyocardial antibodies in the blood; V in rare cases appearance of RF in the blood; detection of C-reactive protein in the blood, high titers of antibodies to Coxsackie viruses, ECHO, influenza or other infectious agents.

ECG: decreased S-T interval or T wave in one or more often several leads, possible appearance of a negative, asymmetrical T wave; monophasic ST elevation is possible due to pericarditis or subepicardial myocardial damage; varying degrees of atrioventricular block; extrasystolia, atrial fibrillation or flutter, decreased ECG voltage.

X-ray of the heart and echocardioscopy reveal an enlargement of the heart and its cavities.

Complaints: shortness of breath at rest and on exertion, palpitations, irregularities and pain in the heart area, pain in the right hypochondrium, swelling in the legs, cough on exertion.

Objective examination. The general condition is grave, forced position, orthopnea, severe acrocyanosis, cold sweat, swollen neck veins, swelling in the legs. The pulse is frequent, weak in filling, often thread-like, arrhythmic, blood pressure is reduced. The borders of the heart are enlarged more to the left, but often in all directions (due to concomitant pericarditis). Heart sounds are muffled, tachycardia, often gallop rhythm, extrasystole, often paroxysmal tachycardia, atrial fibrillation, systolic murmur at the apex and pericardial friction murmur (with concomitant pericarditis) are determined to be of muscular origin. When auscultating the lungs in lower parts You can listen to congestive fine rales and crepitus as manifestations of left ventricular failure. In the most severe cases There may be attacks of cardiac asthma and pulmonary edema. There is a significant enlargement of the liver, its pain, and ascites may appear. With significant enlargement of the heart, relative insufficiency may develop tricuspid valve, in the area of ​​the xiphoid process in this case a systolic murmur is heard, which intensifies with inspiration (Rivero-Corvalho symptom). Quite often thromboembolic complications develop (thromboembolism in the pulmonary, renal and cerebral arteries, etc.).

Laboratory data, including immunological indicators, undergo significant changes, the nature of which is similar to those in moderate myocarditis, but the degree of changes is more pronounced. With significant decompensation and enlargement of the liver, ESR may change little.

ECG: always changed, T wave significantly reduced and S-T interval in many leads, sometimes in all, a negative T wave is possible, atrioventricular blocks are often recorded various degrees, bundle branch block, extrasystoles, paroxysmal tachycardia, atrial fibrillation and flutter.

X-ray of the heart: cardiomegaly, decreased cardiac tone.

Echocardiography reveals cardiomegaly, dilatation of various chambers of the heart, decreased cardiac output, signs of total myocardial hypokinesia in contrast to local hypokinesia in ischemic heart disease.

Intravital myocardial biopsy: picture of inflammation.

Thus, mild myocarditis is characterized by focal damage to the myocardium, normal borders of the heart, absence of circulatory failure, low severity of clinical and laboratory data, and a favorable course. Moderate-severe myocarditis is manifested by cardiomegaly, the absence of congestive circulatory failure, the multifocal nature of the lesion, and the severity of clinical and laboratory data. Severe myocarditis is characterized by diffuse myocardial damage, severe course, cardiomegaly, severity of all clinical symptoms, congestive circulatory failure.

Diagnostic criteria (Yu. I. Novikov, 1981)

Previous infection, proven by clinical and laboratory data (including isolation of the pathogen, results of the neutralization reaction, RSK, RPHA, increased ESR, appearance of SRP), or another underlying disease ( drug allergy and etc.).

Signs of myocardial damage

• 1.Pathological ECG changes(disorders of rhythm, conduction, changes S-T interval and etc.)
• 2. Increased activity of sarcoplasmic enzymes and isoenzymes in blood serum (AST, LDH, CPK, LDH1-2)
• 3. Cardiomegaly, according to X-ray and ultrasound examinations
• 4. Congestive heart failure or cardiogenic shock

Combinations of a previous infection or other disease, according to etiology, with any two “minor” and one<большим» или с любыми двумя «большими» признаками достаточно для диагноза миокардита.

The clinical diagnosis of myocarditis is formulated taking into account the classification and main clinical features of the course: the etiological characteristics are indicated (if it is possible to accurately establish the etiology), the severity and nature of the course, the presence of complications (heart failure, thromboembolic syndrome, rhythm and conduction disorders, etc.).

Examples of diagnosis formulation

• 1. Viral (Coxsackie) myocarditis, moderate form, acute course, extrasystolic arrhythmia, stage I atrioventricular block. But.
• 2. Staphylococcal myocarditis, severe form, acute course, left ventricular failure with attacks of cardiac asthma.
• 3. Non-rheumatic myocarditis, mild form, acute course, H 0.

Therapist's Diagnostic Handbook. Chirkin A.A., Okorokov A.N., 1991

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Myocarditis: signs, causes, diagnosis, therapy

Myocarditis is a cardiac disease, namely, inflammation of the heart muscle (myocardium). The first studies on myocarditis were carried out in the 20-30s of the 19th century, therefore modern cardiology has a wealth of experience in the diagnosis and treatment of this disease.

Myocarditis is not “tied” to a certain age, it is diagnosed in both older people and children, and yet it is most often observed in 30-40 year olds: less often in men, more often in women.

Types, causes and symptoms of myocarditis

There are several classifications of myocarditis - based on the degree of damage to the heart muscle, the form of the disease, etiology, etc. Therefore, the symptoms of myocarditis also vary: from a latent, almost asymptomatic course to the development of severe complications and even sudden death of the patient. Pathognomonic symptoms of myocarditis, that is, those that unambiguously describe the disease, unfortunately, are absent.

The main, universal signs of myocarditis include a general loss of strength, low-grade fever, rapid fatigue during physical activity, accompanied by disturbances in the heart rhythm, shortness of breath and palpitations, and increased sweating. The patient may experience a certain discomfort in the chest on the left and in the precordial zone and even prolonged or constant painful sensations of a pressing or stabbing nature (cardialgia), the intensity of which does not depend on the size of the load or the time of day. Volatile pain in the muscles and joints (arthralgia) may also be observed.

Myocarditis in children is diagnosed as a congenital or acquired disease. The latter most often becomes a consequence of ARVI. In this case, the symptoms of myocarditis are similar to the symptoms of the disease in an adult: weakness and shortness of breath, lack of appetite, restless sleep, manifestations of cyanosis, nausea, vomiting. The acute course leads to an increase in the size of the heart and to the formation of the so-called cardiac hump, rapid breathing, fainting, etc.

Among the forms of the disease, acute myocarditis and chronic myocarditis are distinguished. Sometimes we are also talking about a subacute form of myocardial inflammation. Varying degrees of localization/prevalence of the inflammatory process in the heart muscle also make it possible to distinguish diffuse and focal myocarditis, and different etiologies serve as the basis for identifying the following groups and types of myocardial inflammation.

Infectious myocarditis

The second place is occupied by bacterial myocarditis. Thus, the cause of rheumatic myocarditis is rheumatic pathology, and the main causative agent of the disease is group A beta-hemolytic streptococcus. Among the main symptoms of this type of myocarditis are palpitations and shortness of breath, increasing chest pain, and in severe cases of the disease, also acute left ventricular failure in the form cardiac asthma or alveolar pulmonary edema, accompanied by moist rales in the lungs. Over time, chronic heart failure may develop with the appearance of edema, involvement of the liver, kidneys, and accumulation of fluid in the cavities.

The cause of myocarditis in parallel can be two or more infectious pathogens: one creates favorable conditions for this, the second directly “deals” with damage to the heart muscle. And all this is often accompanied by an absolutely asymptomatic course.

Myocarditis of non-rheumatic origin

Myocarditis of non-rheumatic origin manifests itself predominantly in the form of allergic or infectious-allergic myocarditis, which develops as a consequence of an immunoallergic reaction.

Allergic myocarditis is divided into infectious-allergic, drug, serum, post-vaccination, burn, transplantation, or nutritional. It is most often caused by a reaction of the human immune system to vaccines and serums that contain proteins from other organisms. Pharmacological drugs that can provoke allergic myocarditis include some antibiotics, sulfonamides, penicillins, catecholamines, as well as amphetamine, methyldopa, novocaine, spironolactone, etc.

Toxic myocarditis is a consequence of a toxic effect on the myocardium - with alcoholism, hyperfunction of the thyroid gland (hyperthyroidism), uremia, poisoning with toxic chemical elements, etc. Insect bites can also provoke inflammation of the myocardium.

Symptoms of allergic myocarditis include heart pain, general malaise, palpitations and shortness of breath, possible joint pain, and elevated (37-39°C) or normal temperature. Also sometimes there are disturbances in intracardiac conduction and heart rhythm: tachycardia, bradycardia (less often), ectopic arrhythmias.

The disease begins asymptomatically or with minor manifestations. The severity of the signs of the disease is largely determined by the localization and intensity of the development of the inflammatory process.

Abramov-Fiedler myocarditis

Abramov-Fiedler myocarditis (another name is idiopathic, which means it has an unclear etiology) is characterized by a more severe course, accompanied by cardiomegaly, that is, a significant increase in the size of the heart (the reason for which is pronounced cardiac dilatation), serious disturbances of cardiac conduction and rhythm, which ultimately results in heart failure.

This type of myocarditis is observed more often in middle age. Often it can even lead to death.

Diagnosis of myocarditis

Making a diagnosis such as “myocarditis” is usually complicated by the latent course of the disease and the ambiguity of its symptoms. It is carried out on the basis of a survey and anamnesis, physical examination, laboratory blood test and cardiographic studies:

Physical examination of myocarditis reveals an enlargement of the heart (from a slight displacement of its left border to a significant increase), as well as congestion in the lungs. The doctor notes that the patient has swelling of the neck veins and swelling of the legs; cyanosis is likely, that is, cyanosis of the mucous membranes, skin, lips and tip of the nose.

Upon auscultation, the doctor detects moderate tachycardia or bradycardia, symptoms of left and right ventricular failure, weakening of the first tone and gallop rhythm, and listens to a systolic murmur at the apex.

• A laboratory blood test is also informative in diagnosing myocardial inflammation. A general blood test may show leukocytosis (increased number of leukocytes), a shift to the left in the leukocyte formula, an increase in ESR, an increase in the number of eosinophils (eosinophilia).

A biochemical blood test demonstrates dysproteinemia (deviations in the quantitative ratio of blood protein fractions) with hypergammaglobulinemia (increased levels of immunoglobulins), the presence of C-reactive protein, increased content of seromucoid, sialic acids, fibrinogen.

Blood cultures can confirm the bacterial origin of the disease. During the analysis, the antibody titer indicator is also determined, informing about their activity.

• A chest x-ray shows expansion of the heart's borders and sometimes congestion in the lungs.
• Electrocardiography, or ECG, is a diagnostic technique for studying the electrical fields generated during the work of the heart. When diagnosing myocarditis, this research method is very informative, since changes in the electrocardiogram in case of disease are always noted, although they are not specific. They appear as nonspecific transient changes in the T wave (flattening or decreasing amplitude) and ST segment (displacement up or down from the isoelectric line). Pathological Q waves and a reduction in the amplitude of R waves in the right precordial leads (V1-V4) can also be recorded.

Often, the ECG also shows parasystole, ventricular and supraventricular extrasystole, and atrioventricular conduction pathology. An unfavorable prognosis is indicated by episodes of atrial fibrillation and blockade of the branches (usually the left) of the His bundle, which indicates extensive inflammatory foci in the myocardium.

• Echocardiography is an ultrasound method that examines morphological and functional abnormalities in the activity of the heart and its valves. Unfortunately, it is not possible to talk about specific signs of myocardial inflammation during echocardiography.

When diagnosing myocarditis, echocardiography can detect various disorders of the myocardium associated with its contractile function (primary or significant dilatation of the cardiac cavities, decreased contractile function, diastolic dysfunction, etc.), depending on the severity of the process, as well as identify intracavitary thrombi. It is also possible to detect an increased amount of fluid in the pericardial cavity. At the same time, cardiac contractility indicators during echocardiography may remain normal, which is why echocardiography has to be repeated several times.

Auxiliary methods for diagnosing myocarditis, allowing you to prove the correctness of the diagnosis, can also be the following:

The latter method today is considered by many doctors to be sufficient for an accurate diagnosis of “myocarditis”, however, this position still raises some doubts, since endomyocardial biopsy can give many ambiguous results.

Treatment of myocarditis

Treatment of myocarditis includes etiotropic therapy and treatment of complications. The main recommendations for patients with myocarditis will be hospitalization, providing rest and bed rest (from 1 week to 1.5 months - according to the severity), the prescription of oxygen inhalations, as well as the use of non-steroidal anti-inflammatory drugs (NSAIDs).

The diet during the treatment of myocarditis involves limited consumption of salt and liquid when the patient exhibits signs of circulatory failure. And etiotropic therapy - the central link in the treatment of myocarditis - is focused on eliminating the factors that caused the disease.

Treatment of viral myocarditis directly depends on its phase: Phase I – the period of pathogen reproduction; II – stage of autoimmune damage; III – dilated cardiomyopathy, or DCM, that is, stretching of the cardiac cavities, accompanied by the development of systolic dysfunction.

a consequence of the unfavorable course of myocarditis - dilated cardiomyopathy

The prescription of drugs for the treatment of viral myocarditis depends on the specific pathogen. Patients are indicated for maintenance therapy, immunization, reduction or complete elimination of physical activity until the symptoms of the disease disappear, functional indicators stabilize and the natural, normal size of the heart is restored, since physical activity promotes the resumption (replication) of the virus and thereby complicates the course of myocarditis.

1. Bacterial myocarditis requires antibiotics (vancomycin, doxycycline, etc.). The intake of cardiac glycosides (corglycone, strophanthin) should stabilize the functioning of the heart, and various antiarrhythmic drugs are prescribed for arrhythmia. Anticoagulants (aspirin, warfarin, chimes) and antiplatelet agents are intended to avoid thromboembolic complications, and metabolic therapy agents (asparkam, potassium orotate, preductal, riboxin, mildronate, panangin), ATP, and vitamins are intended to improve metabolism in the affected myocardium.
2. If therapy for viral myocarditis by treating heart failure (taking diuretics, ACE inhibitors, cardiac glycosides, β-blockers) does not give the expected results due to the high activity of the pathological process, the patient should be prescribed immunosuppressive therapy (in phase II of the disease), taking glucocorticosteroids (prednisolone ) and immunosuppressants (azathioprine, cyclosporine A, etc.).
3. Rheumatic myocarditis requires the prescription of NSAIDs - non-steroidal anti-inflammatory drugs (ibuprofen, diclofenac, etc.), as well as glucocorticosteroids.
4. Treatment of allergic myocarditis begins with a detailed history and immediate elimination of the allergen. Antibiotics in this case cannot play a significant role and can even pose a danger to the patient who is more likely to take antihistamines, for example, H1-blockers.
5. Toxic myocarditis is treated by eliminating the agent that led to the development of the disease and taking medications that relieve the main symptoms of the disease. Symptomatic therapy is also prescribed for burn myocarditis, for which there is no specific treatment yet.

The cardinal measure in the treatment of myocarditis is transplantation, i.e., heart transplantation: it is performed provided that the therapeutic measures taken have not improved functional and clinical indicators.

Prognosis for myocarditis

The prognosis for myocarditis, unfortunately, is very variable: from complete recovery to death. On the one hand, myocarditis often progresses latently and ends with absolute recovery. On the other hand, the disease can lead, for example, to cardiosclerosis, accompanied by the growth of connective scar tissue in the myocardium, deformation of the valves and replacement of myocardial fibers, which then leads to persistent disturbances in the heart rhythm and its conductivity. The likely consequences of myocarditis also include a chronic form of heart failure, which can cause disability and even death.

Therefore, after hospitalization, a patient with myocarditis is under clinical observation for another year. He was also recommended for sanatorium treatment in cardiological institutions.

Outpatient observation is mandatory, which involves examination by a doctor 4 times a year, laboratory tests of blood (including biochemical analysis) and urine, as well as ultrasound of the heart - once every six months, and a monthly ECG. Regular immunological studies and testing for viral infections are also recommended.

Measures to prevent acute myocarditis are determined by the underlying disease that caused this inflammation, and are also associated with particularly careful use of foreign serums and other drugs that can cause allergic and autoimmune reactions.

And one last thing. Considering how serious the complications of myocarditis can be, it is extremely imprudent to self-medicate inflammation of the heart muscle using “grandmother’s methods”, various folk remedies or medications without a doctor’s prescription, as it can lead to serious consequences. And vice versa: timely detection of myocarditis symptoms and appropriate comprehensive treatment in the cardiology department of a medical institution always has a positive effect on the prognosis of patients.

Myocarditis. Types of myocarditis. Rheumatic and non-rheumatic myocarditis. Idiopathic, autoimmune, toxic, alcoholic myocarditis

Types of myocarditis by localization

There are three layers in the structure of the heart walls:

• endocardium ( inner layer);
• myocardium ( middle layer represented by muscle tissue);
• epicardium ( outer layer).

The inner layer consists of endothelium, muscle fibers and loose connective tissue. These structures also form the heart valves. Simply put, the valves of the heart and major vessels are an extension of the endocardium. That is why, when the inner layer of the heart is damaged, the heart valves are also damaged. Inflammation of the endocardium is called endocarditis.

Myocarditis pericarditis

Myocarditis endocarditis ( rheumatic carditis)

Myocarditis endocarditis pericarditis ( pancarditis)

• dyspnea;
• severe weakness and malaise;
• decreased blood pressure;
• severe swelling;
• liver enlargement.

The radiograph shows a massive increase in the size of the heart, the electrocardiogram ( ECG) signs of insufficient blood supply ( ischemia). The mortality rate for pancarditis is up to 50 percent.

Focal and diffuse myocarditis

The difference between focal and diffuse myocarditis lies in the degree of intensity of symptoms and the severity of the disease. If only one area of ​​the myocardium is affected, there may be no symptoms at all, and changes in the structure of the heart muscle are detected only by an electrocardiogram or other studies. Sometimes with focal myocarditis, the patient is bothered by a heart rhythm disorder, fatigue without objective reasons, and shortness of breath. The prognosis for this disease is favorable ( especially with viral etiology). In the absence of treatment, the focal form of the disease often develops into diffuse myocarditis.

Each of the above types of myocarditis may have both general signs of the disease and symptoms unique to it. The course of the disease and prognosis are also determined by which microorganism initiated the inflammatory process.

Among all the probable causative agents of infectious myocarditis, viruses are of the greatest importance, since they are characterized by high cardiotropism ( ability to affect the heart). Thus, about half of all inflammation of the heart muscle develops due to the Coxsackie virus.

• The surge in incidence occurs in spring and autumn, because it is during these periods that the human body is most vulnerable to viruses.
• Approximately 60 percent of patients with this pathology are men. In women, the disease is often diagnosed during pregnancy or after childbirth. Coxsackie myocarditis during pregnancy can cause inflammation of the heart muscle in the fetus ( while in the womb, immediately after birth or in the first six months of life).
• Before cardiac symptoms appear ( shortness of breath, pain) the patient begins to experience low-intensity pain in the stomach area, near the navel, nausea with vomiting, and watery stools. Subsequently, paroxysmal chest pains, which intensify when inhaling or exhaling or coughing, are added to the general symptoms of myocarditis.
• In patients under 20 years of age, Coxsackie myocarditis occurs with severe symptoms. For patients over 40 years of age, a more blurred picture of the disease is typical. In the vast majority of cases, this type of myocarditis occurs without serious complications, and patients recover within a few weeks.

In addition to the Coxsackie virus, the cause of infectious myocarditis can be the influenza virus. Statistics show that mild forms of inflammation of the heart muscle are diagnosed in 10 percent of patients with influenza. Symptoms of myocarditis ( shortness of breath, rapid heartbeat) appear one and a half to two weeks after the onset of the underlying disease. Also, inflammation of the heart muscle can develop against the background of viral diseases such as hepatitis ( the characteristic difference is the absence of symptoms), herpes, polio ( diagnosed most often after the patient's death).

This form of myocarditis is caused by various bacterial infections. As a rule, this disease develops in patients with weak immunity and in those who have resistance ( sustainability) to antibiotics. Often with bacterial myocarditis, ulcers form on the myocardium, which significantly aggravates the course of the disease. This form of myocarditis is always a secondary disease, that is, it develops as a complication of various bacterial pathologies.

• Diphtheria. The infection enters the body through airborne droplets and, as a rule, affects the upper respiratory system. A characteristic sign of diphtheria is white, dense or loose films on the tonsils, which make breathing difficult. Inflammation of the heart muscle is diagnosed in approximately 40 percent of patients with diphtheria and is one of the most common causes of death. Signs of heart damage appear in acute form 7–10 days after the onset of the underlying disease.
• Meningococcal infection. Most often, this infection affects the nasal mucosa ( meningococcal pharyngitis), circulatory system ( meningococcal sepsis, that is, blood poisoning), brain ( meningitis). Inflammation of the myocardium due to meningococcal infection is more commonly diagnosed in men.
• Typhoid fever. A type of intestinal infection that is transmitted by food. Signs of myocarditis appear 2 to 4 weeks after the onset of the underlying disease. Most often, typhoid fever affects the intermediate tissue of the myocardium, which is accompanied by acute stabbing pain in the heart and increased sweating.
• Tuberculosis. This infection most often affects the lungs, and a characteristic symptom is a debilitating cough at night, which may be accompanied by coughing up blood. A distinctive characteristic of myocarditis, which develops against the background of tuberculosis, is the simultaneous damage to the right and left parts of the heart. Tuberculous myocarditis is characterized by a long course, often developing into a chronic form.
• Streptococcal infection. In most cases, this infection affects the respiratory tract and skin. The disease manifests itself as inflammation of the glands, a skin rash, which is localized mainly on the upper part of the body. Myocarditis that develops against the background of streptococcal infection is characterized by pronounced symptoms and frequent transition to a chronic form.

• Toxoplasmosis. The carriers of the disease are animals from the cat family. Toxoplasmosis manifests itself as general malaise, loss of appetite, and the appearance of a rash all over the body ( except for the head). Myocarditis develops, as a rule, if the infection occurs in an acute form. If improperly treated or not treated, inflammation of the myocardium due to toxoplasmosis leads to cardiac arrest.
• Chagas disease. This infection is carried by bedbugs, and a specific symptom is swelling and redness of one eyelid. Myocarditis becomes a complication in the acute form of the disease.
• Trichinosis. The causative agents of this infection belong to the class of helminths ( worms) and affect the digestive tract. Infection occurs by eating meat from infected animals. A distinctive symptom of trichinosis is swelling of the face ( in medical practice it is called “frog face”). Myocarditis is aggravated by severe forms of the disease, and damage to the heart muscle is the main cause of death in this infection.
• Sleeping sickness. The carrier of the disease is the tsetse fly, which, when bitten, releases pathogens into the human blood. A characteristic symptom of the disease is severe daytime sleepiness ( a person can fall asleep while eating).

Myocarditis of this type develops against the background of generalized ( affecting the entire body rather than just one organ) mycoses ( infections caused by fungal microorganisms). Fungal myocarditis is most common in patients who have been taking antibiotics for a long time. That is why the disease has become diagnosed in recent decades much more often than before. Also at risk are people with acquired immunodeficiency syndrome ( AIDS).

Infectious-allergic myocarditis

The key trigger for this form of myocarditis is infection, most often of the respiratory viral type. A bacterial infection can also initiate the inflammatory process in the myocardium ( streptococcal, for example).

With allergic inflammation of the myocardium, the pathological process is localized mainly in the right side of the heart. During instrumental examination, the focus of inflammation looks like a dense nodule. The lack of adequate treatment leads to the fact that myocarditis is complicated by irreversible changes in muscle tissue and cardiosclerosis.

Rheumatic ( rheumatoid) and non-rheumatic myocarditis

• nodular or granulomatous myocarditis;
• diffuse myocarditis;
• focal myocarditis.

Nodular myocarditis is characterized by the formation of small nodules in the heart muscle ( granulomas). These nodules are scattered throughout the myocardium. The clinical picture of such myocarditis is very poor, especially during the first attack of rheumatism. However, despite this, the disease progresses rapidly. Due to the presence of granulomas, the heart becomes flabby and its contractility decreases. With diffuse myocarditis, edema develops in the heart, the vessels dilate, and the contractility of the heart drops sharply. Shortness of breath, weakness rapidly increases, hypotension develops ( lowering blood pressure). The main characteristic of diffuse myocarditis is a decrease in the tone of the heart muscle, which provokes the symptoms described above. Due to decreased contractility of the heart, blood flow in organs and tissues decreases. Diffuse myocarditis is characteristic of childhood. With focal myocarditis, infiltration by inflammatory cells occurs locally, and not scattered, as with diffuse.

Symptoms of rheumatic myocarditis

With this pathology, the initial stage of the disease is manifested by general symptoms of the inflammatory process. Patients experience weakness for no obvious reason, increased fatigue, and muscle aches. An increased body temperature is noted, and tests may reveal an increase in the number of leukocytes and the appearance of C-reactive protein ( inflammatory marker).

In the focal form of the disease, the clinical picture is very poor, which greatly complicates the diagnosis. Some patients complain of weakness, irregular heart pain, and heart rhythm disturbances. Extrasystole may also appear inconsistently. The presence of heart problems in a patient is determined, as a rule, during examinations for rheumatism or other diseases.

Granulomatous myocarditis

Non-rheumatic myocarditis

The clinical manifestations of this disease depend on factors such as the localization of the inflammatory process, the volume of affected tissue, and the state of the patient’s immune system. The causes of inflammation also influence the nature of the symptoms. Thus, with a viral origin, myocarditis is more blurred, while the bacterial form is characterized by a more pronounced manifestation of symptoms.

• Violation of general condition. Unmotivated weakness, decreased ability to work, drowsiness - these symptoms are among the first and are observed in most patients with non-rheumatic myocarditis. Irritability and frequent mood swings may also be present.
• Changes in physiological parameters. A slight increase in body temperature is characteristic of infectious type myocarditis. Also, this form of the disease can manifest itself as intermittent downward changes in blood pressure.
• Discomfort in the heart area. Chest pain is experienced by more than half of patients with non-rheumatic inflammation of the myocardium. The pain syndrome has a different character ( sharp, dull, squeezing) and occurs without the influence of external factors ( fatigue, physical activity).
• Cardiac dysfunction. Deviations in cardiac activity can be either in the direction of increasing the frequency of contractions ( tachycardia), and in the direction of decrease ( bradycardia). Also, with non-rheumatic myocarditis, extrasystole may be present, which is manifested by the appearance of extraordinary cardiac impulses.
• Change in skin tone. Some patients experience pale skin due to poor circulation. Blue discoloration of the dermis may also be present ( skin) in the area of ​​the nose and lips, on the fingertips.

Diagnosis of non-rheumatic myocarditis

Modern diagnostic equipment makes it possible to detect myocarditis in the early stages. Therefore, people with an increased likelihood of developing heart pathologies need to undergo regular examinations.

• Electrocardiogram ( ECG). During the procedure, electrodes are attached to the patient's chest, transmitting heart impulses to special equipment that processes the data and forms a graphic image from them. Using an ECG, you can identify signs of tachycardia, extrasystole and other heart rhythm disturbances.
• Echocardiography ( ultrasound examination of the heart). This procedure can be performed superficially ( through the chest) or internal ( the sensor is inserted through the esophagus) method. The study shows changes in the normal structure of the myocardium, the size of the heart valves and their functionality, the thickness of the heart wall and other data.
• Blood analysis ( general, biochemical, immunological). Laboratory blood tests determine the volume of white blood cells ( types of blood cells), the presence of antibodies and other indicators that may indicate inflammation.
• Blood culture. It is carried out in order to determine the nature of the pathogenic microorganisms that provoked bacterial myocarditis. Blood culture also reveals the sensitivity of microbes to antibiotics.
• Scintigraphy. In this study, a radioactive liquid is injected into the patient's body, then an image is taken to determine the movement of this substance in the myocardium. Scintigraphy data show the presence and localization of pathological processes in the heart muscle.
• Myocardial biopsy. A complex procedure that involves removing myocardial tissue for subsequent study. Access to the heart muscle is through a vein ( femoral, subclavian).

Types of non-rheumatic myocarditis

• viral myocarditis;
• alcoholic myocarditis;
• septic myocarditis;
• toxic myocarditis;
• idiopathic myocarditis;
• autoimmune myocarditis.

Viral myocarditis

Symptoms of viral myocarditis are dull pain in the heart area, the appearance of extraordinary heart contractions ( extrasystoles), rapid heartbeat.

Alcoholic myocarditis

Septic myocarditis

Abramov-Fiedler myocarditis ( idiopathic myocarditis)

• intraventricular and atrioventricular blocks;
• extrasystoles ( extraordinary heart contractions);
• thromboembolism;
• cardiogenic shock.

The prognosis for idiopathic myocarditis is usually unfavorable and ends in death. Death occurs from progressive heart failure or embolism.

Toxic myocarditis

Autoimmune myocarditis

• systemic lupus erythematosus;
• dermatomyositis;
• rheumatoid arthritis.

Systemic lupus erythematosus is an autoimmune disease that occurs with generalized damage to connective tissue. In one case out of 10 it is diagnosed in childhood. Heart damage in this disease occurs in 70–95 percent of cases. The clinical picture of lupus myocarditis does not differ in any specific symptoms. Basically, diffuse damage to the myocardium and endocardium occurs, the pericardium is affected less frequently. However, the myocardium is most often affected. It reveals changes of an inflammatory and dystrophic nature. A persistent and long-lasting symptom of lupus myocarditis is rapid heartbeat ( tachycardia), pain syndrome is observed in the later stages of the disease.

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Non-rheumatic myocarditis a group of myocardial diseases of a predominantly inflammatory nature, arising under the influence of a number of etiological factors (infectious, physical, chemical, allergic, autoimmune), not associated with group A beta-hemolytic streptococcus and systemic connective tissue diseases.
There are acute (lasting up to 3 months) and subacute (from 3 to 6 months) forms of myocarditis, by prevalence - focal and diffuse, by severity - mild, moderate and severe,

Etiology, pathogenesis

Diagnostics, differential diagnosis

In the diagnosis of non-rheumatic myocarditis, the correct interpretation of anamnestic, clinical data and the results of laboratory and instrumental studies is important.
Laboratory tests for mild forms of myocarditis reveal: in the CBC - a slight increase in ESR (usually up to 30 mm/h), lymphocytosis, monocytosis, slight eosinophilia; BAC - moderate increase in AST, LDH, CPK, C-reactive protein, seromucoid, sialic acids. In moderate and severe forms, the changes are more pronounced, in the CBC - leukocytosis (with viral infections - leukopenia), a significant increase in ESR; in the LHC, the level of seromucoid, sialic acids, haptoglobin, alpha-2- and gamma-globulins, LDH and its isoenzymes - LDH 1-2, CPK, AST is increased. In 90% of cases, the basophil degranulation test is positive (2-3 times higher than normal).
In a third of patients, immunological examination reveals antimyocardial antibodies.
X-ray examination in patients with moderate and severe forms of myocarditis reveals an increase in the size of the left chambers of the heart, less often the boundaries of the cardiac shadow are expanded in all directions. In mild forms, the ECG shows a decrease in health. T or ST segment in several leads, there may be a moderate increase in the P-Q interval. In moderate forms, in several leads, in addition to a decrease in the ST segment, changes appear. T, which can be biphasic, negative, giant pointed. Concomitant pericarditis is characterized by monophasic ST elevation. In severe cases, in addition to the changes described, the ECG voltage is reduced. Various disturbances of heart rhythm (ventricular and atrial extrasystole, atrial flutter or fibrillation, paroxysmal tachycardia) and conduction (atrioventricular block of I-III degrees, bundle branch block) are recorded. Echocardiography in mild cases does not reveal changes; in moderate forms, there is a decrease in myocardial contractile function, an increase in residual heart volumes in systole and diastole with a decrease in ejection fraction.
Severe myocarditis is characterized by an increase in heart size | and expansion of its cavities, especially the left ventricle.
When diagnosing idiopathic Abramov-Fiedler myocarditis, intravital myocardial biopsy is used.
In contrast to signs of inflammation, as in infectious forms, the morphological characteristics of idiopathic myocarditis are hypertrophy of muscle fibers in the subendocardial layers of the myocardium and papillary muscles, the presence of significant areas of myolysis and their replacement with connective tissue, the presence of intracavitary thrombi, vasculitis of small branches of coronary burning infiltrates along the vessels.
The diagnostic criteria for non-rheumatic myocarditis are: a clear connection with an infection or other underlying disease (allergy, etc.), proven by clinical and laboratory data; ECG changes; increased activity LDH enzymes, LDH1-2, AST, CPK in blood serum; cardiomegaly confirmed by echocardiography or x-ray; picture of congestive heart failure. Presumptive, or “minor” signs of myocarditis include tachycardia, weakened 1st rut and gallop rhythm.
The diagnosis of non-rheumatic myocarditis presents certain difficulties and is often made by excluding other possible causes of myocardial pathology. It is very important to examine all patients who have suffered acute infections of the upper respiratory tract and infections of other localizations if they develop “cardiac” complaints by recording an ECG. If changes in the latter are detected, it is necessary to additionally examine the level of enzymes, and, if possible, the titers of viral (bacterial) antibodies.
To diagnose myocarditis, a combination of infection or other proven etiological factor with two main signs or with one main and two presumptive signs is sufficient,
It is necessary to differentiate non-rheumatic myocarditis primarily from rheumatic carditis, as well as from myocardial dystrophies of various origins, dilated cardiomyopathy, vegetative-vascular dystonia, thyrotoxicosis, angina pectoris, chronic diseases of the lungs and pulmonary vessels.

Treatment

Treatment of non-rheumatic myocarditis is carried out in a hospital setting and includes pathogenetic and symptomatic therapy. Bed rest (for a mild form, 2-4 weeks, for a moderate form, strict bed rest for the first 2 weeks, then extended for another 4 weeks, for a severe form, strict to the point of circulatory compensation and extended for another 4-6 weeks), its cancellation is carried out only after the size is normalized hearts. Diet No. 10 with restriction of table salt.
Non-steroidal anti-inflammatory drugs (NSAIDs) are widely used in therapy in individual dosages for a course of 4-5 weeks; withdrawal criteria: reduction to normal clinical and laboratory signs of inflammation.
With diffuse myocarditis, it is necessary to reduce the amount of fluid. In the presence of a chronic focus of infection, treatment may be ineffective due to constant sensitization of the body, which contributes to the occurrence of relapses and a protracted course of myocarditis. The earliest possible and complete sanitation of such lesions is indicated.
The use of glucocorticosteroids for non-rheumatic myocarditis is limited by the following situations: ineffectiveness of conventional anti-inflammatory drugs; the presence of exudative inflammation in the myocardium and/or exudate in the pericardium; autoimmune or allergic nature of the inflammatory process; recurrent and progressive course of the disease. Prednisolone is prescribed at a dose of 30-40 mg/day, followed by dose adjustment and gradual withdrawal with persistent improvement. A prolonged course requires the use of aminoquinoline drugs (delagil, plaquenil). If pain in the heart area increases due to these medications, they should be discontinued.
In order to restore impaired metabolic processes in the heart muscle, anabolic steroids (retabolil, methandrostenolone, etc.) are prescribed in the usual dosage for a course of 3-4 weeks, especially while taking it. If necessary, use cardiac glycosides (carefully, in small doses!), antiarrhythmic drugs, potassium supplements, diuretics.
During the first half of the year after discharge from the hospital, patients are contraindicated from work associated with significant physical stress, as well as hypothermia, and work in conditions of large temperature changes.

Clinical examination

Clinical examination is carried out by a rheumatologist (cardiologist) and a therapist. The duration of observation is at least 3 years after non-rheumatic myocarditis. If the chronic focus of infection is preserved in the body, patients are prescribed year-round bicillin prophylaxis for a period of 1-2 years (bicillin-5, 1.5 million units monthly).
In addition, to improve metabolic and reparative processes in the myocardium, a course of vitamins, creatine phosphate (or riboxin, mildronate, cocarboxylase) 1-2 times a year is used.