Non-rheumatic myocarditis. Additional treatment for the development of complications of myocarditis

On the topic: Non-rheumatic myocarditis

Performed by an intern

Ostankova A. Yu.

Semipalatinsk

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

Classification

Etiology

Pathological data

Severity

Circulatory failure

Inflammatory lesions of the myocardium constitute a large group of diseases, the study of which until recently has been insufficient. This is due to the fact that the main attention was aimed at combating rheumatism, although in a significant group of patients myocarditis develops without connection with the rheumatic process. As pathological studies have shown, the prevalence of urinary incontinence among children is higher (6.8%) than among adults (4%).

Etiology. See classification.

Sometimes the etiology may not be established, in such cases they speak of idiopathic myocarditis.

Pathogenesis is different, which is associated with a variety of etiological factors. However, most UI does not arise as a result of direct exposure to infection, but in connection with a certain state of sensitization of the child’s body to various agents - bacterial, chemical, physical. Such myocarditis can be combined under the concept of infectious-allergic. When they occur, fixation of immune complexes in the walls of blood vessels occurs, and therefore damage cell membranes with activation of hydrolytic enzymes of lysosomes. All this leads to denaturation of proteins and their acquisition of autoantigenic properties.

In the pathogenesis of some myocarditis, purely allergic mechanisms(for serum sickness, reactions to medications, vaccinations).

During Coxsackie infection, the invasion of this virus into the myocardial cell, leading to its destruction and the release of lysosomal enzymes, is of key importance. At the same time, with influenza, the role of immunological mechanisms is more significant.

However, not all children who have had infectious diseases suffer from UI. The state of reactivity of the macroorganism plays a major role in the development of the disease. At an early age, the child’s reactivity can be influenced by the mother’s toxicosis of pregnancy, acute and chronic diseases, previous abortions and miscarriages, as well as various perinatal infections, constitutional abnormalities in the child. Children from the group of frequently and long-term ill patients are also susceptible to UI.

Age aspect. NM occurs in all age groups.

Family aspect. In the occurrence of UI in children, the factor of hereditary predisposition is important. It has been established that close relatives of a sick child have frequent cases of pathology cardiovascular system and allergic diseases.

Children brought up surrounded by carriers of chronic foci of infection (parents and other relatives) are more likely to get sick.

Diagnostic criteria

In practice, they use the criteria proposed by the New York Heart Association (1964, 1973) as modified by Yu.I. Novikova et al. (1979).

Supporting features:

previous infection, proven clinically and laboratory methods, including isolation of the pathogen, results of the neutralization reaction (RN), complement fixation (RSK), hemagglutination (RHA);

· signs of myocardial damage (increase in heart size, weakening of 1 tone, cardiac arrhythmia, systolic murmur);

presence of persistent pain in the heart area, often intractable vasodilators;

· pathological changes on the ECG, reflecting disturbances in excitability, conduction, and automaticity of the heart, which are resistant and often refractory to targeted therapy;

· early appearance signs of left ventricular failure followed by the addition of right ventricular failure and the development of total heart failure;

· increased activity of serum enzymes (CPK, LDH);

· changes in the heart with ultrasound echocardiography: enlargement of the left ventricular cavity; hypertrophy back wall left ventricle; hyperkinesia interventricular septum; decreased contractility of the left ventricular myocardium.

Optional signs:

· burdened heredity;

· previous allergic mood;

general weakness:

· temperature reaction;

· changes in blood tests characterizing the activity of the inflammatory process.

Laboratory and instrumental research methods

Basic methods:

· complete blood count (moderate leukocytosis, increased ESR);

· general urine analysis (normal), with congestion – proteinuria;

· biochemical analysis blood: increased levels of DPA, CRP, enzyme activity (LDH, CPK);

· laboratory tests to identify the pathogen: RN, RSK, RGA;

· ECG (decrease in wave voltage, rhythm disturbance, change S-T interval etc.);

· radiography of the heart (determining the size of the heart).

Additional methods:

· level determination total protein and its fractions in blood serum;

· Ultrasound of the heart;

· immunological studies (determination of the content of immunoglobulins, T- and B-lymphocytes, complement);

· polycardiography (polyCG).

Examination stages

In the family doctor's office: taking anamnesis (previous infectious or allergic diseases, hereditary history); objective examination (pulse pattern, blood pressure, presence of arrhythmia, changes in the boundaries of the heart, liver size, presence of edema).

At the clinic: general blood and urine tests, biochemical blood tests, chest x-ray, consultation with a cardiologist.

In the clinic: determination of enzyme levels, RSC, RGA, polyCG, ultrasound of the heart.

All blood tests are done on an empty stomach.

Course, complications, prognosis

Clinical course options

In severe forms of carditis, signs of intoxication are observed, and the child’s general condition suffers significantly. Body temperature can rise to 39°C. Signs of circulatory failure appear early. By percussion and x-ray, the expansion of the borders of the heart is determined. In some children, a rough systolic murmur is heard above the apex of the heart, which indicates relative insufficiency bicuspid valve. If such a noise persists for a long time during treatment and with a decrease in the size of the heart, this indicates damage to the valve apparatus (sclerosis of the papillary muscles and chords), hemodynamic or organic deformation of the valve leaflets.

In the case of pericarditis, tachycardia, dullness of heart sounds increase, and a pericardial friction noise is heard. Severe forms of UI include diseases that occur with complex disturbances in the rhythm and conduction of the heart.

This form of UI is more common in children early age(for congenital and acquired carditis).

The moderate form of UI can occur in both young and older children and is characterized by subfebrile body temperature for 1-2 weeks, pallor skin, fatigue. The degree of intoxication is less pronounced. All the symptoms of carditis are present. Signs of circulatory disorders correspond to Art. II A.

The mild form occurs in older children and is extremely rare in early childhood. It is characterized by a paucity of signs of the disease. The general condition of such children is slightly impaired. The borders of the heart are normal or expanded to the left by 0.5-1 cm. There is a slight tachycardia, more pronounced in young children with rhythm disturbances. Clinical signs circulatory failure corresponds to Art. I. or missing. There are changes in the ECG.

A feature of UI in children is the variety of types of their course, which can be acute, subacute, chronic (see classification).

In an acute course, the onset of myocarditis is rapid, a clear connection is established between its development and an intercurrent disease, or it occurs soon after preventive vaccination. The leading place at the onset of the disease is occupied by non-cardiac symptoms: pallor, irritability, poor appetite, vomiting, abdominal pain, etc. And only after 2-3 days, and sometimes later, signs of heart damage appear.

In young children, the onset of the disease may be attacks of cyanosis, shortness of breath, and collapse.

The subacute type of urinary incontinence develops gradually and is accompanied by moderately severe clinical symptoms. The disease manifests itself asthenization 3-4 days after a viral or bacterial infection. Initially appear general signs illnesses: irritability, fatigue, poor appetite, etc. Body temperature may be normal. Cardiac symptoms develop gradually and in some children they appear against the background of repeated ARVI or preventive vaccination.

The chronic course of UI is more common in older children and occurs as a consequence of acutely or subacutely onset myocarditis or in the form of a primary chronic form that develops gradually with an asymptomatic initial phase.

In young children chronic course may have carditis developed in utero.

Myocarditis is inflammation of the myocardium (heart muscle). The disease is common among children of various ages, but more often in 4–5 year olds and adolescents. The disease can occur in hidden form absolutely asymptomatic. Often it is recognized only after pronounced changes that are detected on the ECG.

Exists the following types diseases that differ in symptoms and processes occurring in the body:

Infectious myocarditis– is directly related to infection of the body, appears against the background of illness or immediately after it. Infectious form begins with persistent heart pain, interruptions in its work, shortness of breath, pain in the joints. The temperature may rise slightly. With progression infectious process symptoms are more acute. The heart increases in size, the rhythm of heart contractions is disrupted;
Idiopathic– has a more severe form, often with a malignant course. Characteristic symptoms: heart enlargement, beating rhythm is greatly disturbed. Complications are possible in the form of blood clots, heart failure, thromboembolism and;
Allergic– occurs 12 hours to 2 days after the vaccine or drug that provokes an allergy in the patient was administered. For rheumatism, pathologies connective tissue myocarditis is a symptom of an underlying disease.

There are the following forms of the disease:

Downstream: acute myocarditis in children, subacute, chronic;
According to the prevalence of inflammation: isolated and diffuse;
By severity: mild degree, moderate and heavy;
According to clinical manifestations: erased, typical, asymptomatic forms.

Reasons

The reasons for the development of myocarditis in early age are varied and are caused by the influence of various factors.

Infections: bacterial, viral, fungal, spirochetal, rickettsial, caused by protozoa.
Worm infestations for: trichinosis, cysticercosis, echinococcosis.
Toxic, chemical factors: wasp bite, snake bite, exposure to mercury, carbon monoxide, arsenic, drug and alcohol use.
Physical factors: hypothermia, ionizing radiation, overheating.
Impact medicines : sulfonamide drugs, antibiotics, vaccines, serums, spironolactone.

Myocarditis often develops in children with rheumatism, diphtheria, and scarlet fever. The disease is noted at the time of allergic reactions, when exposed to toxins, congenital. With autoimmune myocarditis, the child’s body produces antibodies to the cells of the heart muscle.

By origin, the disease can be of a rheumatic or non-rheumatic nature.

Rheumatic myocarditis develops as a result. Non-rheumatic myocarditis is caused by inflammatory processes of different nature. The non-rheumatic form often appears after or.

Rheumatic myocarditis has both acute and chronic forms. Has symptoms such as general weakness, mood swings. If there are no changes in the heart area, then a lot of time sometimes passes before a disease such as rheumatic myocarditis is identified. It has the first symptoms such as shortness of breath during physical activity, strange sensations in the heart area.

Symptoms

There is no clinical symptom that would allow one hundred percent accuracy to diagnose myocarditis– this disease in children is characterized by severity and a rapid increase in existing symptoms. Symptoms of the clinical manifestation of the disease may vary depending on:

Immediate cause;
Depth of damage;
The extent of inflammation in the heart muscle;
A certain flow variant.

The prevalence of inflammation has an impact on clinical manifestations of this disease. At the neonatal stage (4 weeks after the birth of the child), congenital myocarditis is severe and has the following symptoms:

The skin is pale with a gray tint;
Weakness;
Weight gain is very slow.

Symptoms such as palpitations and shortness of breath appear during bathing, feeding, defecation, and changing. Swelling may also occur. The liver and spleen enlarge. There is a reduction in the daily amount of urine.

In infants, the disease usually develops against the background of an ongoing infection or after a week. The temperature rises to 37.5° C, and sometimes higher.

Myocarditis in infants may well begin with shortness of breath. Initial symptoms in children after 2 years of age they have the appearance of severe abdominal pain. The baby's hands and feet become cold. The child is lethargic. There is an enlargement of the heart and liver. The child has a delay in physical development. A dry cough may occur.

At serious illness Symptoms such as fever and swelling in the alveoli of the lungs may appear, which can result in death.

In older age, the disease occurs in acute, subacute, chronic recurrent form, and has a more benign course. After an infection, myocarditis has no symptoms for 2-3 weeks. After which symptoms such as weakness, fatigue, pale skin, and weight loss appear.

The temperature may be normal or slightly increased. Children may be bothered by joints and muscles.

In preschool and school age There are heart pains and shortness of breath. Initially, these appear during physical activity, then at rest. The pain in the heart is not pronounced, but it is long-lasting and difficult to relieve with medications. Rapid heartbeat and expansion of the borders of the heart are noted less frequently. But heart rhythm disturbances, swelling in the extremities, and enlarged liver may appear.

Diagnostics

For diagnosis, 24-hour Holter ECG monitoring is used. Echocardiography allows you to determine the size of the heart cavities. Diagnosis of myocarditis has major and minor criteria. It is imperative to identify 1-2 major or 2 minor criteria, as well as an anamnesis.

Diagnostics uses antimyosin scintigraphy or gallium techniques, as well as magnetic resonance with gadolinium.

Diagnosis is especially difficult in the absence of clear specific diagnostic criteria.

According to clinical guidelines treatment of myocarditis in children acute form carried out in a hospital. Characterized by strict bed rest, the duration of which is determined individually. Bed rest is also required in the absence of manifestations of heart failure. Severe cases are characterized by the use of oxygen therapy.

Treatment of myocarditis must be comprehensive. Specific treatment not developed. The main focus is the therapy of the disease that caused this disease hearts.

The main components of complex therapy for the disease are:

For bacterial infections, antibiotics are used (Doxycycline, Monocycline, Oxacillin, Penicillin);
For myocarditis caused by a viral infection, use antiviral drugs(Interferon, Ribavirin, Immunoglobulins). An immunomodulator is often prescribed without side effects and contraindications.

At intravenous administration gammaglobulin increases the survival rate of children and improves the recovery of myocardial function.

Complex treatment includes such anti-inflammatory non-steroidal drugs , such as: salicylates and pyrazolone drugs (Indomethacin, acetylsalicylic acid, Methindol, Butadione, Brufen, Hydroxychloroquine). Such drugs are mandatory in the treatment of a disease with a protracted or recurrent course. Some of these medications relieve heart pain.

For persistent pain, Anaprilin is prescribed minimum dose. Such products have a powerful anti-inflammatory and antiallergic effect. hormonal drugs like glucocorticoids. Prednisolone, Dexamethasone, Hydrocortisone, Triamcinolone are used to treat severe forms of the disease. Hormonal therapy is applicable for heart failure, autoimmune myocarditis,. The dosage and duration of use of hormones is determined individually.

When treating with hormonal drugs, potassium supplements are prescribed; the following foods are rich in it: dried apricots, raisins, carrots.

In case of heart failure, after stopping inflammation in the myocardium, digitalis preparations are used. In case of severe deficiency, Dopamine and Dobutamine are used. And for edematous syndrome, the following are applicable: Hypothiazide, Fonurit, Novurit, Lasix, fasting diet. Required in complex treatment vitamin preparations are included: B vitamins, . For anxiety, headaches, and sleep disturbances, symptomatic treatment is provided.

If there is a disturbance in the rhythm of cardiac activity, a selection occurs antiarrhythmic drugs. For persistent arrhythmias, surgical method Treatment: transvenous cardiac pacing or pacemaker implantation. In case of chronic recurrent myocarditis after hospital treatment, regular preventive trips to a specialized sanatorium are recommended.

Myocarditis - acute, subacute or chronic inflammatory lesion myocardium of predominantly 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;

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, infection with hepatitis C virus, cytomegalovirus) or come to the fore in clinical picture and determine the prognosis (myocarditis due to 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- weakly expressed, 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;

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 specific 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 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. Various degrees The localization/prevalence of the inflammatory process in the heart muscle also allows us 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. Yes, the reason rheumatic myocarditis is, 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 severe course diseases - also acute left ventricular failure in the form of alveolar pulmonary edema, accompanied by moist rales in the lungs. Over time, it 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 pathogen: 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, medicinal, serum, post-vaccination, burn, transplantation, or nutritional. Most often it is caused by a reaction immune system humans to vaccines and serums that contain proteins from other organisms. TO pharmacological drugs, which can provoke allergic myocarditis include some antibiotics, sulfonamides, penicillins, catecholamines, as well as amphetamine, methyldopa, novocaine, spironolactone, etc.

Toxic myocarditis happens as a consequence toxic effect on the myocardium - with alcoholism, hyperfunction of the thyroid gland (hyperthyroidism), uremia, toxic poisoning 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, elevated (37-39°C) or normal temperature. Also sometimes there are disturbances in intracardiac conduction and heart rhythm: tachycardia, bradycardia (less often).

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, that is, by a significant increase in the size of the heart (the reason for which is pronounced), serious disturbances in 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 analysis blood 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 or symptoms of left and right ventricular failure, a weakening of the first tone and a gallop rhythm, and listens to a systolic murmur at the apex.

A laboratory blood test is also informative in diagnosing myocardial inflammation. General blood test may show left shift leukocyte formula, increase , increase number ().

demonstrate dysproteinemia (abnormalities in quantitative ratio blood protein fractions) with hypergammaglobulinemia ( increased level immunoglobulins), presence, increased content of seromucoid, sialic acids, fibrinogen.

Blood culture able to testify bacterial origin diseases. During the analysis, the antibody titer indicator is also determined, informing about their activity.

Radiography chest shows expansion of the boundaries of the heart, and sometimes congestion in the lungs.
, or ECG, is a diagnostic technique for studying the electric fields generated during the work of the heart. When diagnosing myocarditis this method The study is very informative, since changes in the electrocardiogram in case of illness 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 ventricular and supraventricular extrasystole. An unfavorable prognosis is indicated by episodes and, which indicates extensive inflammatory foci in the myocardium.

– 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 may reveal various disorders myocardial work 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 blood clots. 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 one to prove the correctness of the diagnosis, can also be the following:

Isotope study of the heart.
Endomyocardial biopsy and others.

The latter method is today considered by many doctors to be sufficient for precise setting diagnosis of “myocarditis”, however, this situation 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 - depending on the severity), the prescription of oxygen inhalations, as well as the use of non-steroidal anti-inflammatory drugs (NSAIDs).

Diet during the treatment of myocarditis involves limited consumption salts and liquids when the patient exhibits signs of circulatory failure. A etiotropic therapy is the central link in the treatment of myocarditis– 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 autoimmune damage; III – dilatation, 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 prescribed maintenance therapy, immunization, reduction or complete elimination of physical activity - until the symptoms of the disease disappear, stabilization functional indicators and restoration of natural normal sizes heart, since physical activity promotes the renewal (replication) of the virus and thereby complicates the course of myocarditis.

The cardinal measure in the treatment of myocarditis is transplantation, i.e.: it is performed on the condition that the therapeutic measures taken did not improve functional and clinical indicators.

Prognosis for myocarditis

The prognosis for myocarditis, unfortunately, is very variable: from full 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, 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 heart rhythm and its conductivity. To the number likely consequences myocarditis also applies chronic form 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 research blood (including biochemical analysis) and urine, as well as ultrasound of the heart - once every six months, monthly ECG. Regular immunological studies and testing for viral infections are also recommended.

Prevention measures 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 complications of myocarditis can be, self-medicate inflammation of the heart muscle using “grandmother’s methods”, various folk remedies or medical supplies Without a doctor’s prescription, it is extremely imprudent, as it can lead to serious consequences. And vice versa: timely detection of symptoms of myocarditis and appropriate comprehensive treatment in cardiology department medical facilities always have a positive effect on the prognosis of patients.

Video: myocarditis in the program “Live Healthy!”

MYOCARDITIS. This is predominantly an inflammatory lesion of the myocardium that occurs against the background of the action of infectious agents, physical and chemical factors or allergic and autoimmune diseases. Non-rheumatic myocarditis combines inflammatory diseases of the myocardium of various etiologies, not associated with group A beta-hemolytic streptococcus and systemic diseases connective tissue. Myocarditis occurs more often in spring and autumn, as well as during epidemics of viral infections. There is no reliable information on the prevalence of non-rheumatic myocarditis.

To designate myocarditis non-rheumatic etiology Until now, the term “infectious-allergic myocarditis” is often used. However, focusing only on the clinical manifestations of the disease, when all myocarditis is considered infectious-allergic, deprives the doctor of the possibility of an individual approach to the patient, taking into account etiological factor.

Etiology. In recent decades, most common cause myocarditis are transmitted viral infections. The damaging effect on the myocardium of Coxsackie viruses A and B, influenza, parainfluenza, adenoviruses, infectious mononucleosis, cytomegaly, herpes, measles, ECHO viruses, etc. Viral myocarditis has noticeably overshadowed myocardial damage due to bacterial infections (staphylococcal and pneumococcal sepsis, diphtheria, typhoid and typhus, etc.). Among all the viruses that cause myocarditis, Coxsackie viruses account for 1/3 of cases.

Possible inflammatory changes in the myocardium with allergic conditions (drug allergy, serum sickness, etc.), against the background of chemical or physical influences(radiation, toxic, etc.). Myocarditis occurs unknown etiology(idiopathic).

Pathogenesis. In the development of non-rheumatic infectious myocarditis, the leading pathogenetic role is played by immune and toxic-allergic mechanisms. The direct entry of the pathogen into the myocardium is of certain importance. Each etiological factor has its own predominant mechanisms in the development of myocarditis. Even with different viral infections, the mechanism of myocardial damage may be different. For example, in case of Coxsackie infection, the leading role is played by the invasion of viruses into the cell, its destruction and the release of lysosomal enzymes, and in case of influenza - immunological disorders. When viruses enter the myocardium, the functions of myocardial cells and viral replication are inhibited.

Most common features in the mechanisms of development of myocarditis of non-rheumatic etiology can be imagined as follows. Etiological factors have a direct or indirect damaging effect on the myocardium through the neuroendocrine system. This may be the action of antigens or toxins. Predominantly alterative (parenchymal) changes develop in the myocardium. In the future included defense mechanisms. The production of interferon increases, T-lymphocytes and macrophages are activated, inhibiting the introduction of viruses into unaffected myocardial cells. The number of virus-neutralizing antibodies to IgM increases. Whenever autoimmune disorders the disease becomes progressive and protracted.

As a result of damaging effects, metabolic changes occur in the myocardium, manifested primarily by a decrease in the synthesis of contractile proteins, macroergs and adenylate cyclase, and the transport of calcium ions is disrupted. Significant importance is attached to the disruption of the formation of creatine phosphate, the final product of energy processes in the mitochondria of myocardial cells.

Clinical picture. Non-rheumatic myocarditis is most often diagnosed in patients aged 30-40 years, and both sexes are affected equally often. The disease begins, as a rule, against the background of or immediately after an infection (ARVI, influenza, exacerbation chronic tonsillitis etc.). The “light” interval characteristic of rheumatism after an infection is not observed in non-rheumatic myocarditis. Long-term lesions contribute to the development of myocarditis chronic infection(tonsillitis, sinusitis, otitis media), allergic reactions in the form of drug intolerance, food allergies.

The main and most early sign non-rheumatic myocarditis - stabbing, aching, less often pressing and squeezing pain in the precordial region to the left of the sternum, occurring in 80% of patients.

The pain is often constant, its intensity is not related to physical activity, it is not relieved by nitroglycerin, and in approximately 20% of patients it radiates to the left hand, shoulder and under the left shoulder blade.

Cardialgia is characterized by great persistence, severity, diversity, and resistance to the therapy used. The pain is often localized not in the heart area, but spreads to left half chest. With concomitant pericarditis, it intensifies with inhalation, swallowing, and bending of the body.

Next important symptom: shortness of breath at rest or with little physical activity (up to 50% of patients). It is associated with damage to the heart muscle and the appearance of signs of heart failure. Patients often experience palpitations, interruptions in heart function, and asthenovegetative syndrome. The latter appears general weakness, fatigue, sweating, desire to lie in bed for a long time, etc. In some patients, signs of asthenia can be expressed very sharply, up to adynamia. With myocarditis, some patients may complain of headaches and dizziness. About 5% of patients suffer from joint pain (arthralgia), but there are no signs of arthritis. With viral myocarditis, myalgia is possible.
In some patients, myocarditis can occur without any subjective manifestations.
A physical examination of patients with myocarditis reveals a change in the boundaries of relative cardiac dullness. The expansion of boundaries may be absent, barely noticeable, or significant. This depends on the severity of inflammatory changes in the myocardium. Auscultation reveals tachycardia, weakening or splitting of tones, gentle systolic murmur at the apex and at Botkin's point, and sometimes extrasystoles. Diffuse myocarditis may be accompanied by symptoms of congestive heart failure and hypotension.

Approximately half of patients with myocarditis experience persistent low-grade fever, which can often be caused by foci of chronic infection rather than by myocardial damage.

Laboratory indicators. With non-rheumatic myocarditis, there may be slight increase ESR (usually up to 30 mm/h), lymphocytosis, monocytosis, slight eosinophilia. The level of acute phase indicators (C-reactive protein, seromucrid, sialic acids, etc.) increases moderately. In most cases, changes in laboratory parameters indicate an underlying infectious disease that has not yet ended, and not the severity of inflammatory manifestations in the myocardium.

With diffuse myocarditis in the blood serum, the level of LDH and its isoenzymes - LDH 1-2, creatine phosphokinase, and less often - AST increases. In 90% of patients, the basophil degranulation test exceeds the norm by 2-3 times. In 20-30% of patients, anticardiac antibodies are detected in the blood serum.

Instrumental data. X-ray examination reveals an increase in the size of the left chambers of the heart in approximately half of the patients, much less frequently in the left and right chambers.

ECG changes. On a regular ECG, in approximately 3/4 of patients, changes in the T wave appear in the form of its flattening, biphasicity or inversion, in some patients - a pointed giant T wave, often - a decrease in the 5T interval below the isoline. With concomitant pericarditis, an increase in the 5U interval in leads aVL, V, -V6 may be observed. A number of patients have a low-voltage ECG. Changes in the ECG are more often recorded in leads V, -V6, less often in leads II, III, aVF, I and aVL.

Typical heart rhythm disturbances are: ventricular and atrial extrasystole, atrial flutter or fibrillation, paroxysmal tachycardia. Atrioventricular conduction disorders I-III degrees are less common, but intraventricular blocks are often diagnosed. ECG changes in myocarditis are quite stable.

Echocardiographic changes. Often there is a decrease in myocardial contractile function, an increase in residual heart volumes in systole and diastole with a decrease in ejection fraction. At severe forms Myocarditis reveals dilatation of the cavities of the heart, especially the left ventricle, in connection with this the appearance of signs of relative mitral valve insufficiency is characteristic.

The frequency of detection and the severity of individual symptoms of non-rheumatic myocarditis depend on the etiological factor, the location and size of the myocardial lesion, on physical activity in the acute period of the disease, the state of the heart muscle before the disease.

Classification. We present the most common classification of non-rheumatic myocarditis (Table 1).
The division into acute and subacute myocarditis is made depending on the rate of development of the disease. In practical terms, it is necessary to divide myocarditis according to severity. Depends on it therapeutic tactics and the duration of the patient’s temporary disability.

Table 1. Classification of non-rheumatic myocarditis

By etiology:
Viral, caused by Coxsackie viruses, ECHO, polio, influenza, parainfluenza, adenoviruses, infectious mononucleosis, mumps, measles, chickenpox, psittacosis, herpes simplex, cytomegalovirus infection, infectious hepatitis, measles rubella Protozoans for toxoplasmosis, amebiasis, trepanosomiasis, syphilis, borreliosis

Bacterial at infective endocarditis, septicemia, diphtheria, abdominal and typhus Allergic drug reactions, serum sickness and other diseases Caused by physical, chemical, radiation, toxic and other influences Idiopathic

According to clinical and morphological manifestations:

Myocarditis: acute, subacute Myocardial cardiosclerosis

By severity:

Light, medium and heavy forms

Complications:

Rhythm and conduction disorders Circulatory failure stages I, II and III
The mild form is manifested by subjective sensations from the heart. The size of the heart and its function do not change. This form may occur without patient complaints, subclinically, but with characteristic ECG data and signs of past infection, different favorable course. Complete normalization of the resting ECG and other manifestations of the disease in most patients occurs within a period of several weeks to 6 months.

In the moderate form, the size of the heart increases, but without signs congestive failure blood circulation at rest. There are diffuse changes in the myocardium, sometimes symptoms of myopericarditis. There are typical subjective and objective signs of myocarditis. Recovery in most cases occurs after 2 months or later, relapses of the disease are possible. After the elimination of signs of myocarditis, in some patients, pathological ECG changes or the phenomenon of myocardial cardiosclerosis may permanently persist.

The main difference between severe and moderate forms of myocarditis is congestive heart failure at rest. Against the background of cardiomegaly, such patients often exhibit rhythm and conduction disturbances. In most patients, the severe form of myocarditis ends with the development of myocardial cardiosclerosis. Due to persistent heart failure or severe violations rhythm may result in death.

Diagnosis of myocarditis is associated with certain difficulties, which is due to the lack of pathognomonic signs of the disease and clear diagnostic criteria. Particular difficulties arise when diagnosing mild forms of myocarditis. The diagnosis of non-rheumatic myocarditis of infectious origin can be based on the analysis of anamnestic information (indication of an infection suffered the day before), clinical laboratory data and instrumental examination sick. In some cases, the diagnosis of myocarditis is established only after excluding other similar heart diseases.

Every patient with “cardiac” complaints after colds or other infectious diseases, fever of unknown origin should be examined to exclude heart damage (ECG recording). If pathology is detected, the level of serum enzymes and, if possible, titers of viral and bacterial antibodies are examined.

Differential diagnosis is carried out primarily with rheumatism (rheumatic carditis), as well as with myocardial dystrophies of various origins, neurocirculatory dystonia, thyrotoxicosis, coronary heart disease, chronic diseases of the lungs and pulmonary vessels. Particular difficulties are presented by the differential diagnosis of severe forms of myocarditis with dilated cardiomyonation.

The greatest difficulties arise in the differential diagnosis of myocarditis and myocardial dystrophy. The main consideration in this case is dynamic monitoring of the patient and conducting functional pharmacological tests. For myocardial dystrophies functional tests pidsral and potassium are positive in most cases.

An important treatment method is to limit physical activity. Duration of bed rest mild form myocarditis is 2-4 weeks. For moderate myocarditis, strict bed rest is prescribed in the first 2 weeks, and then extended - 4 weeks. Bed rest is canceled only after the heart size has normalized. In severe forms of myocarditis, strict bed rest is prescribed until the blood circulation is compensated, and then extended until clear signs of reverse development of cardiomegaly appear (usually within 4-6 weeks). Limiting physical activity allows you to reduce the load on the myocardium, which helps prevent the development of dilatation of the heart cavities, rhythm disturbances and heart failure. People suffering from myocarditis should receive adequate nutrition, rich in vitamins, but with a limitation table salt(10th table, according to Pevzner). With diffuse myocarditis, fluid should also be limited in order to further reduce the load on the myocardium.

An essential aspect of treatment is timely sanitation of chronic foci of infection, and for bacterial myocarditis, the prescription of antibiotics acts as etiotropic therapy. For toxoplasmosis, a combination of sulfonamides and antiprotozoal agents is used. For myocarditis of known etiology, specific therapy can be carried out.

As pathogenetic therapy, most patients are prescribed non-steroidal anti-inflammatory drugs (NSAIDs) for a period of 4-5 weeks until the severity of clinical and laboratory signs inflammatory process. Any NSAID can be prescribed pharmacological group, however, the patient’s individual reaction to a specific drug is taken into account. NSAIDs have not only an anti-inflammatory, but also an analgesic effect in the presence of cardialgia.

Glucocorticosteroid hormones for non-rheumatic myocarditis are prescribed only according to strict indications. In many cases, they are even contraindicated, since they reduce the body’s resistance to persistent viruses localized in the myocardium and contribute to their spread. In addition, glucocorticoids may enhance dystrophic processes in the myocardium. Indications for the prescription of corticosteroid hormones for myocarditis of non-rheumatic etiology should be considered: 1) ineffectiveness of conventional anti-inflammatory therapy; 2) pronounced exudative phenomena in the heart muscle; 3) the presence of exudate in the pericardium; 4) pronounced immune disorders or concomitant allergies; 5) recurrent and progressive course of the disease.

The initial dose of methylprednisolone in such cases is 24-32 mg/day or prednisolone 30-40 mg/day. At reverse development pathological process dose hormonal drugs gradually decreases until completely eliminated.

In case of prolonged myocarditis, aminoquinoline drugs (Delagil, Plaquenil) are needed due to their weak anti-inflammatory, immunosuppressive and antiarrhythmic effect. In some patients, while taking quinoline derivatives, pain in the heart area may increase, which requires discontinuation of the drug. The effect of using aminoquinoline drugs, as a rule, occurs several weeks after the start of treatment.

To normalize disturbed metabolic processes in the myocardium, anabolic steroids (retabolil, phenobolin, methandrostenolone, etc.) are used in the usual dosage for 3-4 weeks. Anabolic hormones are especially indicated for moderate and severe forms of myocarditis, as well as while taking corticosteroid hormones to reduce the catabolic effect of the latter.

Used according to indications symptomatic therapy cardiac glycosides, antiarrhythmic drugs, potassium salts, diuretics and other drugs. Cardiac glycosides are used with some caution, low dosages of drugs are used. This is due to the high sensitivity of the inflamed myocardium to their toxic effects.

The infectious focus leads to constant sensitization of the body, which contributes to a protracted and recurrent course of myocarditis; in this regard, timely sanitation of foci of chronic infection is of great importance.

Primary prevention of myocarditis mainly involves prevention and timely treatment infectious and other diseases, ECG monitoring when Kirlial complaints appear.

Persons who have had non-rheumatic myocarditis should be under clinical observation for 3 years. The persistence of a focus of chronic infection in the body serves as an indication for year-round bicillin prophylaxis for 1-2 years (bicillin-5 1.5 million units monthly).

And an inactive period of illness for the purpose of recovery functional state myocardium, courses of vitamins, creatine phosphate (or riboxin, mildronate, cocarboxylase) are carried out 1-2 times a year.

For the first 6 months after myocarditis of any etiology, the patient should not perform work associated with significant physical stress. Hypothermia and work in conditions of large temperature fluctuations are also contraindicated.