Myocarditis. Causes, symptoms and signs, diagnosis and treatment of the disease

Myocarditis- This inflammatory lesions myocardium arising in connection with an infectious or allergic disease.

Etiology

Cause of the majority non-rheumatic myocarditis is a tonsillogenic (streptococcal) or respiratory (viral) infection. Myocarditis often complicates pneumonia, cholangitis, tuberculosis, sepsis, etc. It has now been proven that myocarditis can be complicated by any infection, but it should be borne in mind that in addition to infection, myocarditis can also be caused by allergic and physical factors. Non-rheumatic myocarditis is quite common.

Pathogenesis

In the pathogenesis of myocarditis, a significant role is played by myocardial damage caused by direct invasion of the pathogen (bacteria, viruses, fungi, rickettsia, protozoa) or its toxins, as well as allergic mechanisms damage associated with invasion or previous sensitization of the myocardium. In pathogenesis the most severe forms myocarditis, autoimmune reactions of both delayed and immediate type are important.

Pathomorphology

Depending on the features morphological changes myocarditis is distinguished by: localization pathological process- parenchymal and interstitial; character inflammatory reaction- alternative, exudative or productive; specificity - specific or nonspecific; prevalence - focal or diffuse. The degree of severity of morphological changes varies within very wide limits: from mild nested lesions, difficult to establish histologically, to the most severe - total.

Classification

The international classification of myocarditis is compiled solely on the etiological principle (rheumatic, streptococcal, viral - indicating the type of virus, etc., see table).

Clinic and diagnostics

The clinical picture of non-rheumatic myocarditis is extremely variable and depends on the depth, extent and severity of myocardial damage. On the one hand, there are very mild, asymptomatic forms, when the diagnosis is made only on the basis of an electrocardiographic study; on the other hand, there are severe, uncontrollably progressing and ending fatal. The disease usually begins either during the period of convalescence, or (more often) 1-2 (less often, more) weeks after recovery from a particular infection.

One of the most common signs of the onset of the disease is pain. The pain often becomes angina-like in nature, which is a reason for the erroneous diagnosis of angina pectoris or myocardial infarction. In addition, there are stabbing or aching pain in the area of ​​the heart without irradiation, often becoming permanent. Pain accompanied by palpitations or irregular heartbeats heart rate, weakness and fatigue appear, shortness of breath during physical exertion.

Objective signs of the disease include: low-grade fever body (optional sign): tachycardia (less commonly, bradycardia); decline blood pressure. The borders of the heart are often expanded (usually moderately), and a systolic (muscle) murmur is heard above the apex. The tones are dull, the first tone is often split.

Enough common symptom- embryocardia. The liver is not enlarged; occasionally there is a moderate enlargement. In most cases there is no swelling. A blood test may (but not necessarily) detect moderate neutrophilic leukocytosis, eosinophilia, and a moderate increase in ESR. About a third of patients have a positive reaction to C-reactive protein.

Changes in the final part of the ECG are detected with great consistency ( S-T offset; changes T-flat, biphasic, negative: widening of the QRST complex).

First option infectious myocarditis- pain - usually not accompanied by heart failure and ends after 1-2 months. recovery. However, in some cases, pain and adynamia do not go away for a long time, and therefore treatment is delayed up to 3-6 months.

The second variant - arrhythmic - of infectious myocarditis is characterized by disturbances in heart rhythm and conduction. In the convalescence phase or 1-2 weeks after the end infectious process disorders of atrioventricular conduction are detected (electrocardiographically and clinically) up to complete blockade in severe cases), bundle branch block (often Wilson type), transient or permanent form of atrial fibrillation, paroxysmal tachycardia, WPW syndrome, etc.

It should be noted that atrioventricular conduction disorders are relatively less common than with rheumatic myocarditis. Circulatory disorders may initially be absent. They appear later, with the long-term existence of such severe types of rhythm disturbances as posterior atrioventricular block, atrial fibrillation, paroxysmal tachycardia. The prognosis for this option is usually less favorable, because we're talking about about more severe and pronounced myocardial damage.

The third variant of infectious myocarditis is characterized by the appearance of symptoms of circulatory failure from the very beginning. These are cases with severe diffuse myocardial damage, often in combination with rhythm and conduction disorders.

Circulatory failure often develops in the right ventricular type or is total (with stagnation in the systemic and pulmonary circulation). The examination reveals tachycardia, hypotension, expansion of the borders of the heart in diameter, dull tones, systolic murmur above the top.

Gallop rhythm, alternating pulse, and embryocardia are often observed. The ECG records a low-voltage waveform, a downward displacement of S-T, negative T, widening of the QRS and QRS-T. The prognosis is mostly unfavorable. In the case when myocardial damage develops during a particular infection, the phenomena may predominate vascular insufficiency, up to severe collapse.

This feature of hemodynamic disorders in patients with myocarditis was pointed out by G. F. Lang.

Clinical manifestations of the mixed variant largely depend on the combination of leading syndromes. The following combinations are more common: pain syndrome with rhythm disturbance; rhythm disturbance with circulatory failure. The prognosis is usually serious.

Finally, such variants of myocarditis are known when it is clinically impossible to establish any pathological changes from the heart, and the diagnosis is based solely on electrocardiographic data. These are usually mild, benign cases of myocarditis; however, it also happens sudden death from latent myocarditis.

The most severe course and prognosis is myocarditis of the Abramov-Fiedler type. There is reason to consider it as a polyetiological disease with autoimmune genesis. However, the details of the pathogenesis of this most severe form of myocarditis have not been disclosed, and the problem of treatment cannot be considered solved.

In practical work, the following diagnostic criteria for infectious myocarditis should be taken into account:

I. Basic: 1) connection with infection (epidemiological history, clinical and laboratory data); 2) signs of isolated (without the participation of the endo- and pericardium) myocardial damage - subjective (pain in the heart, palpitations), physical (tachycardia, shortness of breath, weakening of the first tone and muscle systolic murmur, enlarged heart size, hypotension, circulatory failure); instrumental (ECG changes in the T wave, increased electrical systole, rhythm and conduction disturbances).

II. Additional: 1) general manifestations- fever, weakness, weakness, fatigue; 2) laboratory indicators: the appearance of C-reactive protein, an increase in ESR, leukocytosis.

Differential diagnosis

In the process of making a diagnosis of infectious myocarditis, certain difficulties may occur. In this case, there is often a need for differential diagnosis With functional diseases cardiovascular system, coronary disease heart disease, thyrotoxicosis and rheumatic carditis.

In differential diagnosis with neurocirculatory dystonia it must be remembered that during various infections and in the convalescence phase, vasomotor balance is often disturbed, and the phenomena develop vascular dystonia. Infectious myocarditis usually occurs against the background of dystonia, the symptoms of which do not exclude signs of myocardial damage.

It is important to consider the following main features that distinguish NCD from myocarditis: 1) numerous complaints of irritability, bad dream, headaches, dizziness; 2) absence of objective changes in the heart; 3) lability of blood pressure and pulse; 4) absence from ECG signs myocardial damage; 5) the presence of signs of neurasthenia in many patients; b) normal indicators blood.

Subject to availability pain forms Myocarditis requires differential diagnosis with coronary heart disease, and the assessment of pain becomes important. In patients with ischemic disease, a typical anginal syndrome predominates; in patients with myocarditis, aching and stabbing, prolonged, sometimes almost constant pain without irradiation.

Pain syndrome with myocarditis, even if it resembles an anginal attack, differs from the latter in the lack of effect from taking validol and nitroglycerin and does not have the stereotypy characteristic of patients angina pectoris. In a number of patients with myocarditis, the pain syndrome is characterized by greater duration and persistence, reminiscent of the picture of myocardial infarction, but differs from it in the lower intensity of pain and the exceptional rarity of cardiogenic shock.

In differential diagnosis with a fresh heart attack, it also helps that symptoms such as fever, leukocytosis, etc., which are symptoms of the second day in case of a heart attack, exist from the very beginning of the disease in myocarditis (if they are present at all).

In contrast to myocardial infarction, which, as a rule, has typical ECG dynamics, with painful myocarditis there is for the most part a disproportion between the severity of the pain syndrome and the nature of the ECG changes: with significant pain syndrome, moderate changes ECG; infarction-like curves in myocarditis are a rare phenomenon.

The need for differential diagnosis of myocarditis with thyrotoxic myocardial dystrophy arises primarily in cases where clinical picture diffuse toxic goiter prevail cardiovascular disorders, and the appearance of other symptoms characteristic of thyrotoxicosis is delayed. Correct assessment of the symptom of tachycardia helps resolve the diagnostic problem.

It is important to highlight the resistance of tachycardia caused by thyrotoxicosis to anti-inflammatory and desensitizing therapy and, conversely, high sensitivity to antithyroid drugs. Function study thyroid gland confirms the diagnosis.

The greatest difficulties arise in differential diagnosis with primary rheumatic carditis. However primary rheumatic carditis distinguished from infectious myocarditis by less severe complaints, greater constancy of such signs as increased body temperature, tachycardia, systolic murmur over the apex of the heart, and combination with polyarthritis. In addition, rheumatic carditis is more characterized by myocardial lesions in combination with damage to the endo- and pericardium and a tendency to recurrent course.

Complications in patients with myocarditis most often manifest themselves in the form of acute heart failure and various violations rhythm.

Urgent medical care in acute myocarditis comes down to combating pain syndrome, rhythm and conduction disturbances, acute heart failure (see relevant sections). In the absence of contraindications, anti-inflammatory drugs can be prescribed ( acetylsalicylic acid, brufen, indomethacin, voltaren).

A patient with acute myocarditis is subject to urgent hospitalization V cardiology department hospital.

The prognosis of most infectious and infectious-allergic myocarditis is favorable. However, in 20% of cases, myocarditis ends with myocardial cardiosclerosis, a transition is possible acute myocarditis c chronic, recurrent.

Prevention

It involves the implementation of a set of measures aimed at preventing infectious myocarditis and its complications.

Primary prevention of infectious myocarditis consists of measures to prevent and treat infections, monitoring the condition cardiovascular system not only at the height of infection, but also in the convalescence phase. Persons who have suffered acute infection, it is advisable to release for 2-3 weeks from work associated with heavy physical exertion. Important Prevention also includes the rehabilitation of chronic foci of infection.

B.G. Apanasenko, A.N. Nagnibeda

Inflammatory diseases of the myocardium of various etiologies not associated with group A β-hemolytic streptococcus diseases connective tissue or others systemic diseases.

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 immune complexes, release of mediators and development of inflammation, activation of LPO.

Clinical, laboratory and instrumental data

Light form

Complaints: general weakness, moderately severe, pain in the heart area of ​​a constant, stabbing or aching nature, interruptions in the heart area, possible palpitations, slight shortness of breath with physical activity.

Objective examination: general condition is satisfactory, no edema, cyanosis, no 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.

Moderate form

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. General condition moderate severity. 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. II: positive reaction of 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.

Severe form

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). Muffled heart sounds, tachycardia, often a gallop rhythm, extrasystole, often paroxysmal tachycardia, atrial fibrillation, a systolic murmur at the apex is determined to be of muscular origin, a pericardial friction murmur (with concomitant pericarditis). When auscultating the lungs in lower parts You can listen to congestive fine bubbling 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 a significant enlargement of the heart, relative tricuspid valve insufficiency can develop; in this case, a systolic murmur is heard in the area of ​​the xiphoid process, 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 parameters, undergo significant changes, the nature of which is similar to those in moderate myocarditis, but the degree of change 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 lesion myocardium, normal boundaries heart, absence of circulatory failure, low severity of clinical and laboratory data, 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 lesion myocardium, severe course, cardiomegaly, severity of all clinical symptoms, congestive failure blood circulation

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 etc.).

plus

Signs of myocardial damage

I. “big”:

• 1. Pathological changes in the ECG (rhythm, conduction disturbances, changes S-T interval 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

II. "small":

• 1. Tachycardia
• 2. Weakened 1 tone
• 3. Gallop rhythm

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.

Formulation of diagnosis

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

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 of the population. Various factors contribute to the occurrence of the disease in question. 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, non-rheumatic myocarditis may occur as a complication of lupus, scleroderma, or endocarditis of infectious origin. Also, specialists have registered cases of UI occurring without apparent causes.

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

• painful sensations of various types in the chest area;
• significant increase in body temperature;
• feeling of heat;
• convulsions;
• malaise;
• drowsiness;
• various heart rhythm disturbances (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 mild and moderate form, subject to timely consultation with specialists, responds well to treatment and does not cause complications or consequences. However, in the absence of 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 of the serous membrane of the heart.

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, with this disease, arrhythmia occurs, to eliminate which the patient is given a pacemaker.

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

Subject to availability 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 a chronic form, so 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 illness, young patients are recommended to attend physical therapy classes to restore proper functioning of the cardiovascular system. During rehabilitation, foods that can cause allergic reactions should be excluded from the child’s diet.

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 your family doctor, who will measure the heart rate, check 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 sent to hospital for inpatient treatment. 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 for an average of 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 due to untimely contact with specialists or improper treatment of urinary incontinence. 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, reduce the amount of salt in the daily diet as much as possible, do not drink a lot of water and adhere to a protein diet to speed up the recovery 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 taking medications, you should consult a specialist.

Treatment with folk remedies

For the treatment of non-rheumatic myocarditis, various folk recipes are used as additional remedies:

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 of 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, alternative medicine recommends consuming several tablespoons of honey daily, brewing strawberry tea, and adding walnuts and raisins to the diet. Also, to normalize heart function, use a decoction of rose hips and hawthorn. But all of the above traditional medicine remedies should be used only after consultation with your doctor.

Prevention

At the moment, there are no special means to prevent the development of non-rheumatic myocarditis. But experts have compiled a list of recommendations that help strengthen both the cardiovascular system and the body as a whole:

• fortified proper nutrition;
• refusal to drink alcoholic beverages and cigarettes;
• regular exercise;
• timely access to specialists for the treatment of various ailments;
• compliance with preventive measures during viral epidemics.

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

Inflammation of the heart muscle is a rather dangerous disease, which, if not properly treated, can lead to the death of the patient. Therefore, for a complete cure and the absence of 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.

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

Etiology.

The division of myocarditis into rheumatic (caused by streptococcal infection) and non-rheumatic (viral) is the first stage of diagnosis.
Rheumatic myocarditis is an obligatory component of rheumatic carditis (rheumatic carditis) along with endocarditis and pericarditis. Under consideration
in the section on acute rheumatic fever.
The cause of non-rheumatic myocarditis in the vast majority of cases is viral infection(influenza viruses, parainfluenza, Coxsackie B, infectious hepatitis, ECHO, cytomegaloviruses, etc.).

Pathogenesis.

A viral infection at the stage of active viral replication triggers immunopathological reactions with the participation of cytotoxic cells and autoantibodies to various components of cardiomyocytes, which leads to their damage (hypothesis of autoimmune damage).
Diagnosis criteria.
I. Relationship with past infection, proven by clinical and laboratory data: isolation of the pathogen, results of the neutralization reaction, complement fixation reaction, hemagglutination reaction, acceleration of ESR, appearance of C-reactive protein.
II. Signs of myocardial damage.
Disturbance of repolarization processes in the anterior wall area
Big signs:
— Disturbance of repolarization processes on the ECG — a change in the final part of the ventricular complex in the form of depression of the ST segment and the appearance of a low-amplitude, smoothed or negative T wave, which, as a rule, are detected in precordial leads, but can also occur in standard leads
— Rhythm and conduction disorders
— Increased activity of cardioselective serum enzymes and isoenzymes (LDG and LDH1, CK and MB-CK, troponin T and I).
— Cardiomegaly
— Heart failure
Minor signs:
- tachycardia
— weakening of the 1st tone (important to confirm during phonocardiography)
- gallop rhythm

Treatment.

1. Etiotropic treatment. A method for treating non-rheumatic myocarditis with antiviral drugs has not yet been developed. Patients with bacterial myocarditis,
occurring during a sore throat (or other streptococcal infection), or shortly after its end, treatment with penicillin 1 million units intramuscularly is prescribed 8
once a day or semisynthetic penicillins (amoxicillin) in a daily dose of 2-3 g/day or macrolides (clarithromycin 1.0 per day) for 7-10 days.
2. More recently, non-steroidal anti-inflammatory drugs were considered the basis of pathogenetic treatment. However, at present, given the lack of evidence of their positive effect on the outcome of the disease, the slowdown of reparative processes in the myocardium as a result of their use, this group of drugs in the treatment of myocarditis is not recommended.
— Therapeutic (bed) rest for acute myocarditis is considered a pathogenetic method of treatment and is mandatory until the manifestations of the viral infection cease.
— Glucocorticoids, having a pronounced anti-inflammatory and immunosuppressive property, are indicated for severe myocarditis and the development of myopericarditis. Prednisolone is most often prescribed at a dose of 20-30 mg per day for 2-3 weeks, depending on the severity of the clinical manifestations of the disease.
— Anticoagulants are indicated for myocarditis with high clinical and laboratory activity. They have anticoagulant, anti-inflammatory
and antihypoxic effect. Heparin is prescribed 10,000 units 2 times a day subcutaneously for 7-10 days.
— Metabolic therapy aims to improve metabolism and tissue respiration in the myocardium, thereby reducing degenerative processes. Riboxin, panangin, anabolic drugs, cytochrome C, preductal, mildronate are prescribed. These drugs do not cause harm, are psychologically well accepted by patients and are highly appreciated by them.

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 occur latently.

Myocarditis is characterized by great variability in the 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;

For diffuse connective tissue diseases (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, infection with hepatitis C virus, 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;