Dilated cardiomyopathy (I42.0). Neuromuscular asthenia syndrome: weakness, adynamia, fatigue

a common part

Myocarditis is inflammatory disease myocardium. Myocarditis is described as inflammatory infiltration of the myocardium with necrosis or degeneration of adjacent myocytes, not characteristic of ischemic damage caused by diseases coronary arteries. Myocarditis typically occurs in otherwise healthy people and can lead to rapidly progressive (and often fatal) heart failure and arrhythmias. Myocarditis can have a wide range of clinical manifestations, from practically asymptomatic to severe heart failure.

Etiology and pathogenesis

Myocarditis is usually caused by a wide range of different infectious microorganisms, autoimmune disorders, and exogenous influences.

The development of the disease is also influenced by genetic background and environmental influences.

Most cases of myocarditis are caused by autoimmune mechanisms, although direct cytotoxic effects of the pathogen and changes caused by the expression of cytokines in the myocardium may play a significant role in the etiology of myocarditis.

A number of microorganisms are able to invade the cardiomyocyte. This is especially true for the Coxsackie B virus, the main infectious agent that causes myocarditis.

The Coxsackie B virus not only penetrates the cardiomyocyte, but also replicates in it. Penetration of the Coxsackie B virus into the cardiomyocyte occurs after its interaction with receptors located on the surface of the cardiomyocyte. The virus then replicates in the cytoplasm and can further invade unaffected cardiomyocytes. Under the influence of infection, the production of interferons α and β by lymphocytes and fibroblasts is stimulated, which increase the resistance of unaffected cardiomyocytes to viral infection and stimulate the activity of macrophages and natural killer cells. Influenza and hepatitis C viruses and toxoplasma can also penetrate into the cardiomyocyte. Viral RNA in coxsackievirus-infected myocardium.

Bacterial flora is also capable of invading cardiomyocytes.

Staphylococci are most often found in the myocardium during septic conditions. The introduction of an infectious agent into a cardiomyocyte causes its damage, destruction of lysosomal membranes and the release of acid hydrolases from them, aggravating myocardial damage. These processes also create the prerequisites for the formation of autoantigens in the myocardium and the formation of autoimmune reactions.

Toxins released by infectious agents can also directly affect the myocardium, causing significant degenerative changes in it.

Metabolic processes are disrupted and cardiomyocyte organelles are damaged. Toxins keep things going inflammatory process. In addition, toxins produced by infectious agents contribute to the development of a toxic-allergic process in the myocardium due to the formation of antibodies to them.

A secondary immune response that can be triggered by a causative factor.

Damaged myocardium becomes a source of autoantigens, which induce the formation of autoantibodies against the myolemma, sarcolemma, but most often against the α and β chains of myosin.

There is an opinion that with myocarditis, antibodies are produced not only to damaged, but also to undamaged cardiomyocytes, while new antigens are released that stimulate the formation of antibodies to the components of cardiomyocytes.

Expression of cytokines in the myocardium (eg, tumor necrosis factor-alpha, nitricoxide synthase).

Cytokine imbalance plays a major role in the development of myocarditis. A correlation was found between increased levels of cytokines in the blood and inflammatory changes in the myocardium.

Cytokines are low molecular weight glycoproteins and peptides secreted by activated cells of the immune system, sometimes by epithelium, fibroblasts, regulating interactions and activating all parts of the immune system and influencing various organs and fabrics. In patients with myocarditis, the blood level of pro-inflammatory cytokines - interleukin-1, interleukin-6, tumor necrosis factor-α, which support the inflammatory process in the myocardium, significantly increases. At the same time, the level of interleukin-2 and the content of interferon-γ increase significantly in the blood plasma of patients with myocarditis.

Aberrant induction of apoptosis.

Apoptosis is programmed cell death. The process by which damaged, end-of-life, or unwanted cells are removed from a multicellular organism.

Apoptosis occurs without damage to the cellular microenvironment. Cardiomyocytes are highly and terminally differentiated cells, and cardiomyocyte apoptosis is not normally observed. With myocarditis, apoptosis develops. Apoptosis in myocarditis can be induced by cytotoxic T lymphocytes, tumor necrosis factor-α, free radicals, toxins, viruses, and excessive accumulation of calcium ions in cardiomyocytes. The final role of cardiomyocyte apoptosis in myocarditis has not been clarified. It is assumed that it is most pronounced in the most severe forms of the disease, accompanied by circulatory disorders, and in dilated cardiomyopathy.

Activation of lipid peroxidation in the myocardium.

The myocardium contains many free fatty acids - substrates for peroxide (free radical) oxidation. Under conditions of inflammation, local acidosis, diselectrolyte disorders, and lack of energy in the myocardium, the peroxidation of free fatty acids increases, resulting in the formation of free radicals and peroxides that directly damage cardiomyocytes.

An effect on lysosomal hydrolases is also observed - their permeability increases and acid hydrolases, which have a proteolytic effect, enter the cell and extracellular space. As a result, proteins are damaged cell membrane cardiomyocytes and their degradation products, the so-called R-proteins, accumulate in the blood. High titers of R proteins in circulating blood correlate with the severity of myocarditis.

• Phases of myocarditis pathogenesis
  • Acute phase(first 4-5 days).

    It is characterized by the fact that a pathogenic agent that has penetrated into cardiomyocytes causes lysis of cardiac cells and at the same time replicates in them. In this phase, macrophages are activated and express, releasing a number of cytokines (interleukin-1 and 2, tumor necrosis factor, interferon-γ). In the same phase, viremia is observed and viruses are detected in myocardial biopsies. Myocyte destruction occurs, which then repeatedly causes myocardial damage and dysfunction.

  • Subacute phase (from 5-6 days).

    Inflammatory infiltration of the myocardium by mononuclear cells is observed: natural killer cells, cytotoxic T-lymphocytes and B-lymphocytes. A secondary immune response occurs. Cytotoxic T lymphocytes also participate in the lysis of cardiomyocytes containing viruses. B lymphocytes produce antibodies to viruses and components of cardiomyocytes.

    From the 5th day of the pathological process, collagen synthesis begins, reaching a maximum after the 14th day. After 14 days, the virus is no longer detectable in the myocardium, and inflammation gradually subsides.

  • Chronic phase (after 14-15 days).

    Fibrosis begins to actively progress, myocardial dilatation develops, dilated cardiomyopathy gradually forms, and circulatory failure develops.

    There is no viremia.

    The destruction of myocytes of an autoimmune nature continues, associated with pathological discharge human leukocyte antigen (HLA) into myocytes. In the case of viral myocarditis, persistence of the viral genome in the myocardium is possible.

Clinic and complications

In most cases, myocarditis is subclinical, so patients rarely seek treatment. medical care during the acute period of the disease.

In 70-80% of patients, myocarditis manifests itself as mild malaise, fatigue, mild shortness of breath and myalgia.

A small number of patients present with an acute clinical picture with fulminant development of congestive heart failure, with massive involvement of pathological process myocardial tissue.

In isolated cases, small and pinpoint foci of inflammation in electrically sensitive areas can cause sudden death.

• Clinical symptoms of myocarditis
  • Acute respiratory viral infection.

    More than half of patients with myocarditis have a previous viral syndrome - respiratory manifestations, high fever, headaches. The manifestation of cardiac symptoms is observed mainly in the subacute phase of viral elimination, and therefore usually occurs 2 weeks after acute viremia.

  • Chest pain.
    • The development of pain in the heart area is characterized by stages (in the first days of the disease, the pain is short-term, then, after a few hours or days, it becomes constant).
    • Localization of pain in the apex of the heart, in the left half of the chest or precordial region.
    • The nature of the pain is stabbing or pressing.
    • The pain is constant in most patients (less often it is paroxysmal).
    • Most often, the pain intensity is moderate (however, with myopericarditis, the pain intensity can be significantly pronounced).
    • The intensity of pain usually does not change during the day, and also depending on physical and emotional stress.
    • There is often increased pain with deep breath(especially if the patient has myopericarditis), lifting the left arm up.
    • Usually there is no irradiation of pain to the area of ​​the left arm, but in some patients such irradiation is observed.
  • Shortness of breath when moving.
    • Shortness of breath is especially common in older adults age group and for more severe forms of the disease. Focal myocarditis may not be accompanied by shortness of breath either during exercise or at rest.
    • Severe forms of myocarditis are characterized by severe shortness of breath at rest, sharply increasing even with slight movements.
    • Orthopnea and shortness of breath at rest may be a sign of heart failure.
  • Palpitations and a feeling of interruptions in the functioning of the heart.
    • Palpitations and a feeling of interruptions in the functioning of the heart are observed in 40-50% of patients. Occur both during physical activity and at rest, especially when severe course myocarditis.
    • The sensations of interruptions and fading in the heart area are caused by extrasystole.
    • In some patients, severe palpitations occur paroxysmally, often at rest, and are associated with paroxysmal tachycardia. Heart rhythm disturbances are common.
    • The appearance of syncope may indicate high-grade atrioventricular block or risk sudden death.
  • Dizziness.

    Darkening in the eyes, severe weakness up to the development of fainting states are usually caused by severe bradycardia due to the development of sinoatrial or complete atrioventricular block. More often, these phenomena are observed in severe cases of diphtheria and viral myocarditis. Sometimes dizziness is associated with arterial hypotension, which can develop with myocarditis.

  • Increased body temperature.
    • An increase in body temperature is accompanied by sweating.
    • Body temperature usually does not exceed 38 C°.
    • High fever is rare and is usually associated not with myocarditis, but with the underlying disease against which myocarditis developed.
  • Blood pressure in myocarditis is usually normal.
  • Development of heart failure.
    • With the development of acute cardiac decompensation:
      • Tachycardia.
      • Gallop rhythm.
      • Mitral regurgitation.
      • Edema.
      • With the development of concomitant pericarditis, a pericardial friction rub may occur.
    • With the gradual development of heart failure:
      • Bradycardia may occur.
      • More pronounced increase in temperature.
      • More pronounced respiratory disorders.
      • Poor appetite, or in case of decompensation, sweating when eating.
      • Cyanosis.

Diagnostics

• Diagnostic goals
  • Confirm the presence of myocarditis.
  • Establish the etiology of myocarditis.
  • Determine the severity of the disease to determine the amount of therapy required.
  • Determine the clinical course of the disease.
  • Identify the presence of complications.

• Diagnostic methods
  • Anamnesis

    Facts to pay attention to when collecting anamnesis:

    • Indications in the medical history of the connection of cardiac symptoms with previous episodes of respiratory viral and bacterial infections and unknown fever.
    • The connection between cardiac symptoms and various allergic reactions, contacts with toxic substances, food poisoning, and skin rashes.
    • The connection of the disease with previous exposure to radiation, with trips to foreign countries and other possible etiological factors indicated in the section etiology of myocarditis.
    • The presence of foci of chronic infection, primarily nasopharyngeal.
    • Presence of previous allergic diseases - drug allergy, urticaria, bronchial asthma, Quincke's edema, hay fever, etc.

    Attention should be paid to the age of the patient, since myocarditis is characterized by the development of cardiac symptoms mainly in middle-aged people.

  • Physical examination findings

    Physical examination findings can range from normal to signs of severe cardiac dysfunction.

    Patients in mild cases may appear without signs of intoxication. Tachycardia and tachypnea are most often observed. Tachycardia is most often proportional to the increase in temperature.

    Patients with more severe forms may exhibit signs of left ventricular circulatory failure. When widespread, inflammation can be observed classic symptoms cardiac dysfunction, such as swelling of the jugular veins, crepitus at the bases of the lungs, ascites, peripheral edema, a third tone or gallop rhythm is heard, which can be observed when both ventricles are involved in the pathological process.

    The severity of the first tone may be reduced.

    Possible cyanosis.

    Hypotension caused by left ventricular dysfunction is not typical for the acute form and indicates a poor prognosis.

    Mitral and tricuspid regurgitation murmurs indicate ventricular dilatation.

    As dilated cardiomyopathy progresses, signs of pulmonary embolism may appear.

    Diffuse inflammation can lead to the development of pericardial effusion, without tamponade, which is manifested by friction sounds when surrounding structures are involved in the process.

  • • X-ray examination of the chest.

      With mild myocarditis, the size of the heart is not changed, its pulsation is normal. With moderate and severe myocarditis, the size of the heart is significantly increased; with severe cardiomegaly, the heart seems to blur on the diaphragm, its arcs are smoothed, and the pulsation weakens. In the lungs one can detect moderately pronounced venous congestion, wide roots (they may be blurred, unclear), and an increased venous pattern.

      Picture of myocarditis.
    • Echocardiography.

      Echocardiography is performed to exclude other causes of cardiac decompensation (eg, valvular, congenital, amyloidosis) and to determine the degree of cardiac dysfunction (usually diffuse hypokinesia and diastolic dysfunction).

      Echocardiography can also help localize the extent of inflammation (wall motion abnormalities, wall thinning, pericardial effusion).

      Echocardiography can help in the differential diagnosis between fulminant and acute myocarditis. It is possible to identify paranormal left ventricular diastolic measurements and the appearance of septal thinning in fulminant myocarditis. In acute myocarditis with increased left ventricular pressure, normal thickness of the ventricular septum is noted.

      Echocardiographic picture of myocarditis.
    • Antimyosin scintigraphy (using injections of antimyosin antibodies).

      This method has high specificity but low sensitivity for diagnosing myocarditis.

      Antimyosin scintigraphy for myocarditis.
    • Gallium scanning.

      This technique is used to image severe cardiomyocyte infiltration and has a good negative predictive value, but the specificity of this method is low.

    • Gadolinium-enhanced magnetic resonance imaging.

      This imaging technique is used to detect the spread of inflammation. although, this study It has rather low specificity and is used for research purposes.

    • Cardioangiography.

      Cardiac angiography often shows coronary ischemia as a consequence of cardiac dysfunction, especially when the clinical picture is similar to acute myocardial infarction. Usually detected high pressure filling and decreased cardiac output.

      Coronary ischemia in myocarditis.
    • Electrocardiography.

      The ECG is characterized by nonspecific changes (for example, sinus tachycardia, nonspecific changes in ST and T waves).

      Sometimes blockades (atrioventricular block or intraventricular conduction delay), ventricular arrhythmia, or changes characteristic of damage to myocardial tissue in ST T waves, similar to those in myocardial ischemia or pericarditis (pseudoinfarction picture) may be observed, which may indicate a poor prognosis.

      The electrocardiogram may show the following: block right branch with or without blockade of both bundles (in 50% of cases), complete blockade(7-8%), ventricular fibrillation (7-10%), and ventricular arrhythmia (39%).

      EGC of a patient with myocarditis.
    • Myocardial biopsy.

      A right ventricular endomyocardial biopsy (EMB) is performed. This is the standard criterion for diagnosing myocarditis, although it is somewhat limited in sensitivity and specificity, since the inflammation can be widespread or focal.

      Standard EMB confirms the diagnosis of myocarditis but is rarely useful in guiding treatment options.

      Because this method involves sampling, its sensitivity increases with multiple biopsies (50% for 1 biopsy, 90% for 7 biopsies). Typically, 4 to 5 biopsies are taken, although the false negative rate is 55%.

      Frequency false positive results is quite high, due to the small number of lymphocytes normally present in the myocardium, and the difficulties in differentiating lymphocytes and other cells (such as eosinophils in eosinophilic endocarditis).

      The large dependence of the result on the interpretation of the data also causes false positive or false negative results.

      Granulomas in sarcoid myocarditis are observed in 5% of cases with a single biopsy, and in at least 27% of cases with multiple biopsies.

      Sarcoid myocarditis. Active granulomas.

• Examination program for suspected myocarditis

  The given examination program is not strictly mandatory. The list of studies is determined by the clarity and severity of the clinical picture of myocarditis, as well as the technical equipment and capabilities of the medical institution.

  • All patients with suspected myocarditis undergo next research:
    • Clinical blood and urine tests.
    • Biochemical blood test: determination of total protein, protein fractions, bilirubin, glucose, creatinine, urea, aminotransferases (AST, ALT), total lactate dehydrogenase and its fractions, creatine phosphokinase and its MB fraction, troponin, seromucoid, haptoglobin, sialic acids.
    • Electrocardiography.
    • Echocardiography.
    • X-ray of the heart and lungs.
  • Patients in whom the disease develops predominantly involving autoimmune mechanisms are additionally treated with the following: immunological studies:
    • Determination of the content of T- and B-lymphocytes and their functional activity, as well as determination of subpopulations of T-lymphocytes.
    • Determination of lupus cells, antinuclear antibodies, titers of antistreptococcal and virus-neutralizing antibodies, anti-myocardial antibodies.
  • At unclear diagnosis and deterioration of the patient's condition, if it is impossible to make a diagnosis by other available research methods, an endomyocardial myocardial biopsy is performed.

• Diagnostic algorithm for suspected myocarditis

  Reliable diagnosis of myocarditis is one of the most complex tasks modern practical medicine.

  Currently, to make a diagnosis of myocarditis, a diagnostic algorithm is recommended based on the following clinical and instrumental criteria for myocardial damage syndrome:

  • Relationship of the disease with previous infection.
  • Clinical symptoms: tachycardia, weakening of the first tone, gallop rhythm.
  • Pathological changes on the ECG (repolarization disturbances, rhythm and conduction disturbances).
  • Increased blood concentrations of cardioselective enzymes and proteins (CPK, CPK-MB, LDH, troponin T and I).
  • Increased heart size as determined by radiography or echocardiography.
  • Signs of congestive heart failure.
  • Changes in immunological parameters (increased CD4/CD8 ratio, CD22 and CEC counts, positive RTML reaction).

Differential diagnosis if myocarditis is suspected, it is carried out with the following diseases:

• Rheumatic myocarditis.

  Most often it is necessary to carry out differential diagnosis between rheumatic and non-rheumatic myocarditis.

  Differential diagnostic differences between rheumatic and non-rheumatic myocarditis.

  Signs	Rheumatic myocarditis	Non-rheumatic myocarditis
  Diseases and conditions preceding the development of myocarditis	Acute nasopharyngeal infection or exacerbation chronic tonsillitis	Often symptoms of acute respiratory viral infection, acute gastroenteritis, drug allergies, urticaria, vasomotor rhinitis, acute nasopharyngeal infection
  The duration of the latent period between acute nasopharyngeal infection and the development of myocarditis	2-4 weeks	1-2 weeks, sometimes myocarditis develops during the infection itself
  Age of patients	Primary rheumatic carditis usually develops at the age of 7-15 years (childhood, adolescence)	Mostly average age
  Availability articular syndrome	Characteristic	Not typical
  Onset of the disease	Mostly acute or subacute	Gradual development in most patients
  Features of systolic murmur in the apex of the heart	May gradually intensify and become musical when mitral regurgitation develops	Usually quiet, not musical, gradually weakens and disappears during successful treatment of myocarditis
  Condition of the valvular apparatus of the heart according to ultrasound examination	Possible development of valvulitis mitral valve(thickening of the chordal leaflets, limited mobility of the posterior leaflet, decreased systolic excursion of the closed mitral valves, slight prolapse of the leaflets at the end of systole, mitral regurgitation)	Without changes
  Associated pericarditis	Occurs frequently	Rarely seen
  High titers of antistreptococcal antibodies in the blood	Characteristic	Not typical
  Increase in titers of antiviral antibodies in the blood	Not typical	Characteristic of viral myocarditis
  “Active”, “persistent” nature of cardiac complaints	Rarely observed	Occurs frequently

• Cardiopsychoneurosis.

  It is usually necessary to differentiate myocarditis from neurocirculatory dystonia in mild forms of myocarditis in young people.

  There are some similarities in the symptoms of these two diseases - general weakness, asthenia, pain in the heart, extrasystole, sometimes a feeling of lack of air, changes in the T wave and ST interval on the electrocardiogram.

  Myocarditis can be excluded based on the absence of its characteristic signs: a clear connection with a previous viral infection; laboratory signs of inflammation, increased levels of cardiac-specific enzymes in the blood; troponin; cardiomegaly and echocardiographic signs of impaired contractile function of the left ventricular myocardium; clinical manifestations of circulatory failure. In addition, it should be taken into account that neurocirculatory dystonia is not characterized by disturbances in atrioventricular conduction, atrial fibrillation.

• Idiopathic dilated cardiomyopathy.
  • Acute myocarditis and idiopathic dilated cardiomyopathy.

    It is not difficult to differentiate between acute myocarditis and idiopathic dilated cardiomyopathy. Acute myocarditis, in contrast to dilated cardiomyopathy, is characterized by a connection with a previous viral infection, an increase in body temperature, the presence of laboratory signs of inflammation (leukocytosis, a shift in the leukocyte formula to the left, an increase in ESR, an increase in the content of seromucoid, fibrin, sialic acids, haptoglobin in the blood), clear positive dynamics of the patient’s condition and clinical manifestations of the disease under the influence of treatment, an increase in titers of specific virus-neutralizing antibodies in the patient’s paired blood sera (with viral myocarditis).

    If we are talking about myocarditis, as one of the manifestations of a systemic disease connective tissue, then there are symptoms of inflammation and autoimmune damage to other organs (polyarthralgia, polyserositis, polyneuropathy, nephritis).

  • Chronic myocarditis and idiopathic dilated cardiomyopathy.

    Significant difficulties arise in the differential diagnosis of chronic myocarditis and idiopathic dilated cardiomyopathy. The similarity between the two diseases in this situation lies in the presence of cardiomegaly and the gradual development of symptoms of circulatory failure. Differential diagnosis is also complicated by the fact that with a long course of myocarditis, the severity of the laboratory inflammation syndrome decreases somewhat. In addition, there is the possibility of transformation of chronic myocarditis into dilated cardiomyopathy.

    When differentially diagnosing these two diseases, it is necessary to analyze the anamnesis and medical documents patient, which in some cases will make it possible to clarify the etiological factors of myocarditis and clarify the features of the course of the pathological process in the myocardium over many years. In patients with chronic myocarditis, it is often possible to establish a connection between the development of the disease and its exacerbations with a previous viral infection, taking medications or other etiological factors, while dilated cardiomyopathy develops gradually without connection with any known etiological factor.

    Myocarditis is also supported by the presence of laboratory manifestations of exacerbation (inflammatory syndrome) both at the onset of the disease and subsequently when the patient’s condition worsens, which is not typical for dilated cardiomyopathy.

    To a certain extent, analysis of the effectiveness of ongoing treatment measures can help in differential diagnosis. The lack of positive dynamics from the treatment, persistent persistence of congestive heart failure and cardiomegaly for a long time, diffuse hypokinesia of the ventricular walls according to echocardiography indicate in favor of dilated cardiomyopathy.

    In the most difficult cases, it is necessary to resort to endomyocardial biopsy. At the same time, it should be noted that in the most severe situation (severe cardiomegaly, refractory to treatment, congestive heart failure), the differential diagnosis of chronic myocarditis and dilated cardiomyopathy ceases to be relevant, since treatment for both diseases will consist of transplantation hearts.

• Acute myocarditis and coronary heart disease.

  The need for differential diagnosis of myocarditis and coronary heart disease usually occurs in elderly people and is caused, first of all, by the presence of pain in the heart area, heart rhythm disturbances and changes in the electrocardiogram in both diseases. In addition, the development of myocarditis is possible against the background of coronary heart disease.

  Differential diagnosis of myocarditis and ischemic heart disease.

  Signs	Myocarditis	IHD
  Relationship of the disease or its exacerbation with a previous viral infection	Characteristic	Absent
  Age	Mostly under 40 years of age	More often after 40-50 years
  Pain in the heart area	Cardialgia type	Type of angina
  ECG changes, horizontal ST interval depression	Uncharacteristic	Characteristic
  Negative symmetrical T waves	Uncharacteristic	Characteristic
  Focal scar changes	Absent (occurs in in rare cases in severe myocarditis)	Occur frequently
  Positive dynamics of the T wave and ST interval during tests with nitrates and β-blockers	Absent	Characteristic
  Presence of zones of hypokinesia in the myocardium of the left ventricle (according to echocardiography)	Less typical (occurs with severe myocarditis)	Happens often (after myocardial infarction)
  Presence of laboratory signs of inflammation	Characteristic	Uncharacteristic
  Increased blood activity of LDH, CPK, MB-CPK	May be in severe cases	Not typical for chronic ischemic heart disease
  Presence of atherogenic hyperlipoproteinemia	Uncharacteristic	Characteristic
  Severe signs of aortic atherosclerosis (according to radiography and echocardiography)	None	Always present
  Fast development total heart failure	Happens often with severe myocarditis	Uncharacteristic

• Other diseases.
  • With a long course of myocarditis, the development of severe cardiomegaly, and heart failure, there is a need for differential diagnosis with ischemic cardiomyopathy.
  • Echocardiography can also diagnose different kinds heart defects, with which myocarditis also sometimes has to be differentiated.
  • Mild myocarditis must be differentiated from metabolic cardiomyopathies, since such variants of myocarditis can only manifest themselves as ECG changes, like metabolic cardiomyopathies. In this case, first of all, it is necessary to take into account that metabolic cardiomyopathies occur against the background of various diseases accompanied by impaired metabolism of proteins, fats, carbohydrates, and electrolytes ( toxic goiter, diabetes mellitus, obesity, hypokalemia, etc.), and are not accompanied by inflammatory manifestations (laboratory and clinical).

Treatment

• Treatment Goals
  • Treatment of the cause of the disease.
  • Reducing the workload on the heart.
  • Treatment of the consequences of changes in the heart that resulted from inflammation.

• Treatment conditions

  All patients with acute moderate and severe myocarditis, as well as mild myocarditis with an unclear diagnosis, are subject to hospitalization.

  Some adults lung patients acute myocarditis with an established diagnosis, as well as patients with chronic myocarditis (in the inactive phase) can be treated at home according to the conclusion and under the supervision of a cardiologist. In the latter case, patients with acute myocarditis are provided with ECG registration at home at least once every 3 days until stable positive dynamics are detected.

• Treatment methods
  • Non-drug treatments
    • Bed rest.

      For a mild form, 2-4 weeks; for a moderate form, the first 2 weeks are strict bed rest, then another 4 weeks - extended; for severe forms, strict - until the blood circulation is compensated, and another 4-6 weeks - extended. Complete abolition of bed rest is permissible only after restoration of the original size of the heart.

    • Stop smoking.
    • Diet therapy. Diet No. 10 is recommended with restriction of table salt, and for diffuse myocarditis - and fluids.
    • Stop drinking alcohol and any drugs.
    • General strengthening therapy, vitamin therapy.
  • Drug treatment

    The strategy and duration of etiotropic therapy depends on the specific pathogen and the individual course of the disease in the patient.

    TREATMENT OF MYOCARDITIS CAUSED BY INFECTIOUS AGENTS
    Etiology	Treatment
    Viruses
    Enteroviruses: Coxsackie viruses A and B, ECHO viruses, polio virus
    Mumps, measles, rubella virus
    Influenza A and B virus	Rimantadine: 100 mg orally 2 times a day for 7 days. Prescribed no later than 48 hours from the onset of symptoms
    Dengue fever virus	Supportive and symptomatic therapy
    Varicella zoster virus, virus herpes simplex, virus Epstein-Bar, cytomegalovirus	Acyclovir: 5-10 mg/kg IV infusion every 8 hours; Ganciclovir: 5 mg/kg IV infusion every 12 hours (if cytomegalovirus infection
    HIV infection	zidovudine (: 200 mg orally 3 times daily. Note: zidovudine itself may cause myocarditis
    Organisms, bacteria and fungi
    Mycoplasma pneumoniae	Erythromycin: 0.5-1.0 g, IV infusion every 6 hours
    Chlamydia	Doxycycline
    Rickettsia	Doxycycline: 100 mg IV infusion every 12 hours
    Borella burgdortery (Lyme disease)	Ceftriaxone: 2 g IV infusion once daily, or Benzylpenicillin: 18-21 million IU/day, IV infusion divided into 6 doses
    Staphylococcus aureus	Before antibiotic sensitivity testing - Vancomycin
    Corynebacterium diphtheriae	Antibiotics + emergency administration of diphtheria toxin
    Mushrooms (Cryptococcus neoformans)	Amphothirecin B: 0.3 mg/kg/day + fluorocytosine: 100-150 mg/kg/day orally in 4 divided doses
    Protozoa and helmins
    Trypanosoma cruzi (Chagas disease)	No specific treatment has been developed. Supportive and symptomatic therapy
    Trichinella spiralis (trichinosis)	Mebendazole. In severe cases, corticosteroids
    Toxoplasma gondii (toxoplasmosis)	pyrimethamine (Fansidar): 100 mg/day orally, then 25-50 mg/day orally + sulfadiazine 1-2 g orally 3 times a day - for 4-6 weeks. Folic acid: 10 mg/day to prevent hematopoiesis inhibition

    • Symptomatic therapy acute heart failure is carried out using diuretics, nitrates, sodium nitroprusside, and ACE inhibitors (angiotensin-converting enzyme). Inotropic medications (eg, dobutamine, milrinone) may be necessary in cases of severe decompensation, although they may cause arrhythmias.

      Further treatment is carried out in a similar drug regimen, including ACE inhibitors, beta blockers, and aldosterone receptor antagonists. Although, according to some sources, some of these drugs may cause hemodynamic instability.

      • Immunomodulatory drugs.

        Immunomodulatory substances are the most promising group of drugs that affect the immune response in myocarditis, involving immune modulators that interact with individual parts of the immune cascade, without interfering with the body’s ability to defend itself against the virus. Tumor necrosis factor plays a major role in this treatment approach.

        Drug name	Intravenous immunoglobulins (Gamimune, Gammaguard, Gamma-P, Sandoglobulin) - neutralize circulating myelin antibodies through anti-idiotypic antibodies, reduce the regulation of pro-inflammatory cytokines, inf-gamma inclusions, block Fc receptors of macrophages, suppress the induction of T and B cells and add T cell suppressors, block compliment cascade; causes remyelination, may increase the concentration of IgA in the cerebrospinal fluid (10%).
        Adult dose	2 g/kg IV, 2-5 days
        Child dose	Not installed
        Contraindications	Hypersensitivity, IgA deficiency
        Interactions	Globulins may interfere with the immune response to live virus vaccines and reduce effectiveness.
        Pregnancy
        Cautions	Monitoring of serum IgA is necessary (use of a product without IgA, such as Gammaguard); infusions may increase serum viscosity and cause thromboembolism; infusions can cause migraine attacks, aseptic meningitis (10%), urticaria, petechial rashes (2-30 days after infusion); increased risk of renal tubular necrosis in elderly patients and diabetics, decreased volume; results laboratory research may change in the following way- increased titer of antiviral and antibacterial antibodies for 1 month, 6-fold increase in erythrocyte sedimentation coefficient for 2-3 weeks, and obvious hyponatremia.

      • Angiotensin-converting enzyme inhibitors.

        Angiotensin-converting enzyme inhibitors are indicated for correction blood pressure and the work of the left ventricle in cardiac decompensation. Captopril is particularly indicated in the treatment of severe left ventricular dysfunction.

        Drug name	Captopril (Capoten) - prevents the conversion of angiotensin 1 to angiotensin 2, a strong vasoconstrictor, which leads to an increase in plasma renin levels and a decrease in aldosterone secretion
        Adult dose	6.25-12.5 mg orally 3 times a day; no more than 150 mg 3 times a day
        Child dose	0.15-0.3 mg/kg orally 2-3 times a day
        Contraindications	Hypersensitivity, renal failure Cautions	Category D in the second and third trimester of pregnancy, caution is required in case of renal failure, valvular stenosis, or severe cardiac decompensation.

        Other ACE inhibitors did not show such an effect in experiments on biological models.

      • Calcium channel blockers.

        Calcium channel blockers - while they have limited use in cases of ischemic cardiac dysfunction, calcium channel blockers are useful in myocarditis. Amlodipine (Norvasc, Tenox), in particular, possibly due to nitric oxide, has shown good results in animal models, and in placebo-controlled studies.

        Drug name	Amlodipine (Norvasc) - relaxes smooth muscles coronary vessels, and causes dilation of the coronary vessels, which in turn increases the delivery of oxygen to the myocardium. Indicated in patients with systolic dysfunction, hypertension, or arrhythmia.
        Adult dose	2.5-5 mg orally 4 times a day; no more than 10 mg 4 times a day
        Child dose	Not installed
        Contraindications	Hypersensitivity
        Interactions	NSAIDs can reduce the hypotensive effect of captopril, ACE inhibitors can increase the concentration of digoxin, lithium and allopurinol; Rifampicin reduces captopril levels; probenecid may increase captopril levels; the hypotensive effects of ACE inhibitors may be enhanced if they interact competitively with diuretics.
        Pregnancy	There is no data on the safety of use during pregnancy
        Cautions	It is necessary to select a dose for renal-hepatic dysfunction; it may cause slight swelling; in rare cases, allergic hepatitis may occur.

      • Loop diuretics.

        Diuretics reduce preload and afterload on the heart, eliminate congestion during internal organs and peripheral edema. The effectiveness of their action depends on which part of the nephron they affect. The most powerful diuretics are furosemide and uregit, as they act throughout the loop of Henle, where the main reabsorption of sodium occurs.

        Drug name	Furosemide (Lasix) - increases water excretion by reducing soda and chloride reabsorption in the ascending loop of Henley and the distal renal tubule.
        Adult dose	20-80 mg/d IV IM; up to 600 mg d for severe edematous conditions
        Child dose	1-1 mg/kg not exceeding 5 mg/kg do not give >q6h 1 mg/kg IV IM slowly under close supervision; not exceeding 6 mg/kg
        Contraindications	Hypersensitivity, hepatic coma, anuria, condition sharp decline electrolytes
        Interactions	Metformin reduces furosemide concentrations; furosemide reduces the hypoglycemic effect of antidiabetic drugs, and is antagonistic to the muscle-relaxing effect of tubocurarine; ototoxicity occurs when aminoglycosides interact with furosemide, hearing loss of varying degrees may occur, the anticoagulant activity of warfarin can be increased by the interaction, plasma lithium levels increase and toxicity is possible due to the interaction.
        Pregnancy	There is no data on the safety of use during pregnancy
        Drug name	Digoxin (Digoxin, Digitek, Lanoxicaps, Lanoxin) is a cardiac glycoside with a direct inotropic effect with additional indirect effects on cardiovascular system. Acts directly on the heart muscle, increasing systolic contractions of the myocardium. His indirect action manifests itself in an increase in the activity of the nerves of the carotid node, and an increase in sympathetic innervation, which is manifested in an increase in blood pressure.
        Adult dose	0.125-0.375 mg 4 times a day
        Child dose	10 years: 10-15 mcg/kg. Maintenance dose: 25-35% of the administered dose is used
        Contraindications	Hypersensitivity, beriberi disease, idiopathic hypertrophic subaortic stenosis, constrictive pericarditis, carotid sinus syndrome
        Interactions	Many drugs can alter the levels of digoxin, which has a very narrow therapeutic window.
        Pregnancy	There is no data on the safety of use during pregnancy
        Cautions	Patients with myocarditis are particularly sensitive to the toxic effects of digoxin.

      • Anticoagulants.
      • Immunosuppressants.

        Data on the effect of immunosuppressants on natural history There is no infectious myocarditis. There have been three large studies of immunosuppressive strategies for myocarditis, and none have shown significant benefit (National Institutes of Health Prednisone Study, Myocarditis Treatment Study, and Myocarditis and Acute Cardiomyopathy Study (MIAC)). Empirical therapy with immunosuppressants for systemic autoimmune diseases, especially giant cell myocarditis and sarcoid myocarditis, is often used as a baseline in a small number of cases.

      • Antiviral drugs.

        There is no justified basis for the use of antiviral drugs, although they have been shown to be effective in a small number of cases.

• Criteria for the effectiveness of treatment of myocarditis
  • Good general health.
  • Normalization of laboratory parameters.
  • Normalization or stabilization of ECG changes.
  • X-ray: normalization or reduction in heart size, absence of venous congestion in the lungs.
  • Normalization of cardiac activity clinically, and with the use of special research methods.
  • Absence of complications and transplant rejection after heart transplantation.

Long-term observations of a large group of children allow us to identify the following diagnostic criteria for non-rheumatic myocarditis:

A) a connection between the development of the disease and an infection, especially a viral one, proven clinically or laboratory, or a clear indication of the possibility of a connection with non-infectious factors (administration of vaccines, serums, long-term use medicines, etc.);

B) signs of myocardial damage: increase in heart size (clinically and radiologically), weakening of the first tone, rhythm disturbance;

C) the presence of persistent cardialgia that is not relieved by vasodilators;

G) pathological changes on the ECG, reflecting disturbances in excitability, conductivity or automaticity and others, characterized by resistance, and often refractoriness to targeted therapy;

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

E) increased activity of serum enzymes and cardiac isoenzyme fractions.

Additional criteria for non-rheumatic myocarditis may include: family history, previous allergic mood, minimal or moderate degree activity of the process, according to laboratory indicators, a tendency to a protracted course of the disease despite the therapy. The combination of medical history, clinical and electrocardiographic signs of myocardial damage arising in connection with an infection, with one or more additional criteria allows the diagnosis of non-rheumatic myocarditis.

I.M. Vorontsov believes that the following signs indicate myocarditis:

1) connection between the clinical picture of myocardial damage and infection (against the background of the latter or within 4-6 weeks after it);

2) variability of combinations of clinical and especially electrocardiographic symptoms of heart damage in the dynamics of the disease;

3) addition of damage to other membranes of the heart;

4) simultaneous development of inflammatory changes in other organs and systems (vasculitis, glomerulonephritis, polyserositis);

5) the presence of paraclinical signs of inflammation;

6) a clear positive effect on the clinical picture, changes in the ECG and contractile function myocardial therapy with anti-inflammatory drugs for a period of 2 to 6 weeks.

The development of myocarditis at any age, the variety of clinical variants and types of course require careful, often individual approach to carry out a differential diagnosis.

So, in preschool and school age The clinical picture of acute and subacute non-rheumatic myocarditis is similar to that of primary rheumatic carditis.

Myocarditis, which is asymptomatic (especially primary chronic), must be distinguished from myocardial dystrophy.

In the arrhythmic variant of non-rheumatic myocarditis, arrhythmias caused by extracardiac causes (functional cardiopathy), in which extrasystole, paroxysmal tachycardia, lengthening of atrioventricular conduction is combined with symptoms of autonomic disorders: increased sweating, transient acrocyanosis, a tendency to bradycardia, hypotension, etc.

The following signs indicate the dystrophic nature of myocardial damage:

1. Development of a picture of damage to the heart muscle (in the absence of symptoms typical of myocarditis) in direct connection with an acute violation of vital signs important functions- breathing, nutrition, electrolyte metabolism or with diseases causing metabolic disorders in the myocardium, its functional overload.

2. The presence of positive dynamics: in the treatment of the underlying disease, restoration of the function of affected organs, correction of metabolism; reducing physical activity; during therapy with cardiac drugs and functional tests with them.

With a functional disorder of the heart, single transient extrasystoles are noted, emanating from one source (atrial, right ventricular). The boundaries of the heart are not changed, the tones are loud. Under the influence of physical activity, functional arrhythmia decreases or disappears.

It is necessary to differentiate myocarditis in children of senior school age and neurocirculatory dystonia. The similarity of these diseases is determined by the presence of cardialgia. However, in patients with neurocirculatory dystonia, it is combined with other typical complaints: headache, increased irritability, dizziness, sleep disturbance, fainting, lack of fullness of inspiration, sweating, etc. The boundaries of the heart are not changed, the tones are clear, a systolic murmur of a functional nature is rarely heard. The ECG reveals a decrease in the amplitude of the T wave and changes in the S-T segment, which are characteristic of myocardial dystrophy, which develops secondary to vascular disorders and impaired regulation of blood circulation. Rhythm disturbances are rare, are transient in nature, disappear after physical activity and during a test with Inderal. When analyzing the phase structure of systole, hyperdynamia syndrome is revealed, while hypodynamia syndrome is characteristic of patients with myocarditis.

In young children, myocarditis is similar to endomyocardial fibroelastosis. The latter is characterized early manifestation clinical signs (in the first 6 months of life), often without a clear connection with intercurrent diseases. Its clinical symptoms are: tachycardia, early developing cardiac hump, enlargement of the heart predominantly to the left percussion and radiologically, sharply reduced pulsation, significant weakening of tones, on the ECG - high voltage of the QRS complex, signs of isolated hypertrophy of the left ventricular myocardium, displacement of the 5-T segment below the isoline , negative T wave in the left precordial leads, often rhythm disturbances. Signs of heart failure are observed early - first left ventricular (cough, shortness of breath, cyanosis), and then right ventricular (liver enlargement, swelling in the lower extremities).

Treatment for endomyocardial fibroelastosis gives a short-term effect. Cardiomegaly, weakening of heart sounds, left ventricular or right and left ventricular failure of the heart remain persistent.

It is often necessary to distinguish subacute, chronic and intrauterine myocarditis from congenital heart defects.

Cardiomegaly with a spherical heart shape with x-ray examination, frequent violation cardiac rhythm and conductivity bring the non-cyanotic variant of Ebstein’s anomaly closer to myocarditis. However, in the anamnesis of such patients there are indications of the presence of signs of heart disease from birth; there is no connection between its development and infectious diseases. Typical signs of Ebstein's anomaly, according to ECG, are: enlargement of the right atrium, incomplete block of the right bundle branch, absence of left ventricular myocardial hypertrophy.

The chronic course of non-rheumatic myocarditis in children must be distinguished from primary hypertrophic cardiomyopathy, which is characterized by: shortness of breath, fainting, and in older children - pain in the heart area, palpitations. The apical impulse is elevating, pulsation is often observed cervical vessels. In the fourth intercostal space at the left edge of the sternum, a systolic murmur of varying intensity is often heard. The ECG shows signs of left ventricular myocardial hypertrophy and interventricular septum. It is very difficult to distinguish these diseases, although it is possible with a comprehensive examination of the child and monitoring over time.

Complex treatment of patients with non-rheumatic myocarditis depends on the etiology, characteristics of pathogenesis, clinical picture and includes two stages: inpatient - during the acute period and outpatient or sanatorium - during the period of convalescence and remission.

In the acute period of myocarditis, patients need a strictly limited motor regimen, the duration of which is determined by the positive dynamics under the influence of therapy and averages 2-4 weeks. The transfer of patients to limited, gentle and tonic motor regimens is carried out gradually, taking into account the clinical picture of the disease and the functional capacity of the cardiovascular system, determined using functional tests.

Exercise therapy is prescribed from the first days of treatment in a hospital when body temperature decreases and edema is eliminated. As the patients' condition improves, the complexes of therapeutic exercises become more complicated.

The nutrition of patients should be complete, meet age-related needs, balanced in the content of proteins, fats, carbohydrates and vitamins according to age. During the acute period, the disease is somewhat limited table salt, carbohydrates, during treatment with corticosteroid drugs, increase the content of animal protein, vegetables and fruits rich in potassium salts (potatoes, raisins, dried apricots, prunes, etc.) in food. If there are symptoms of circulatory disorders with a tendency to develop edema or the presence of the latter, follow a certain drinking regimen. The daily amount of fluid in such patients should be 200-300 ml less than the daily amount of urine excreted during the previous day.

For patients with severe myocarditis and circulatory disorders, with symptoms of stagnation in the pulmonary circulation, oxygen therapy is indicated.

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Version: MedElement Disease Directory

Dilated cardiomyopathy (I42.0)

Cardiology

general information

Short description

Dilated cardiomyopathy Cardiomyopathies (syn. cardiopathy) are myocardial diseases in which the heart muscle is structurally and functionally changed in the absence of pathology of the coronary arteries, arterial hypertension and damage to the valve apparatus
* (DCM) is a syndrome characterized by dilation of the heart cavities and systolic dysfunction of the left or both ventricles.

According to a working group of experts from WHO and the International Society of Cardiology, the diagnosis of idiopathic DCM can be established only after excluding specific cardiomyopathies. Based only clinical examination The existence of specific cardiomyopathies such as inflammatory, ischemic or alcoholic, as well as cardiomyopathies associated with metabolic disorders, cannot be excluded.

* ABOUT WHO/IFC definition, 1995

Classification

According to the WHO/IFC classification (1995), by origin There are 5 forms of dilated cardiomyopathy:

Idiopathic;
- family-genetic;
- immunoviral;
- alcohol-toxic;
- associated with a recognized cardiovascular disease, in which the degree of myocardial dysfunction does not correspond to its hemodynamic overload or the severity of ischemic damage.

Some experts (for example, Gorbachenkov A.A., Pozdnyakov Yu.M., 2000) designate dilated cardiomyopathies with the term “dilated heart disease.” The same authors highlight the following etiological groups(forms) of dilated cardiomyopathy:

Ischemic;
- hypertensive;
- valve;
- dismetabolic (for diabetes mellitus, thyrotoxicosis, hypothyroidism, hemochromatosis);
- nutritional-toxic (alcohol, with beriberi disease - vitamin B deficiency);
- immunoviral;
- family-genetic;
- at systemic diseases;
- tachyarrhythmic;
- peripartum;
- idiopathic.

Etiology and pathogenesis

For a long time, the causes of the development of the idiopathic (sporadic) form of dilated cardiomyopathy (DCM) remained unknown. It is currently believed that in at least 30-40% of cases the disease is inherited. Important factors in pathogenesis are also poor nutrition (malnutrition), deficiency of thiamine and protein in the body, as well as the effect of anthracycline derivatives (for example, doxorubicin) on the myocardium.

It is assumed that the bulk of secondary forms of DCM (alcoholic, hypertensive or ischemic DCM) develops when, against the background of a genetic predisposition to the disease, the hemodynamic load on the cardiovascular system increases (for example, during pregnancy) or factors arise that have a direct damaging effect on the myocardium (for example, ethyl alcohol).

In the absence of a family history, DCM may occur due to acute myocarditis. In the autoimmune model of DCM development, the main role in myocardial damage is given immune system. When using polymerase chain reaction (PCR), the presence of Coxsackie B viruses, hepatitis C virus, herpes, and cytomegalovirus is detected in some patients.

The formation of DCM is based on primary damage and death of cardiomyocytes, resulting in the following hemodynamic consequences:
- progressive decrease in contractility;
- pronounced dilatation of the heart cavities;
- development of compensatory myocardial hypertrophy and increase in heart mass (without thickening of the walls of the ventricles);
- in severe cases - the occurrence of relative insufficiency of the mitral and tricuspid valves;

Stagnation of blood in the pulmonary and systemic circulation;
- relative coronary insufficiency and the development of myocardial ischemia;
- the appearance of focal and diffuse fibrosis in the myocardium;
- peripheral vasoconstriction.

Due to excessive activation of neurohumoral systems (sympathoadrenal system, renin-angiotensin-aldosterone system, endothelial factors, etc.), cardiac remodeling and various hemodynamic disorders develop.

Epidemiology

Dilated cardiomyopathy accounts for 60% of all cardiomyopathies and up to 9% of all cases of heart failure. Found in most countries of the world. Due to its high mortality rate, DCM is the main indication for heart transplantation.

Clinical picture

Symptoms, course

The clinical course of dilated cardiomyopathy (DCM) is highly variable, and the symptoms of the disease are not specific.
Complaints most often associated with manifestations of congestive biventricular heart failure:
- shortness of breath - in 99.1% of cases, shortness of breath at rest - 37.9%;
- general weakness, fatigue - 85.7%;
- rapid heartbeat - 83.9%;
- peripheral edema - 81.7%;
- heaviness in the right hypochondrium and epigastrium - 71.0%;
- pain in the heart area - 64.3%; the pain is of the nature of mild and short-term cardialgia Cardialgia is pain localized by the patient in the area of ​​the projection of the heart onto the anterior chest wall
, which appears to be associated with pericardial stretching Pericardium (heart sac) - tissue membrane surrounding the heart, aorta, pulmonary trunk, mouths of the vena cava and pulmonary veins
as a result of dilatation Dilatation - persistent diffuse expansion the lumen of any hollow organ.
cavities of the heart, and does not require special therapy;
- anginal pain - observed only in 4.5% of cases, associated with a discrepancy between the increased need of the dilated left ventricle for oxygen and the limited expansion reserve of the coronary arteries of the heart.

The most important clinical feature of DCM is rapid and steady progression of the disease and signs of decompensation, as well as refractoriness Refractoriness (from the French refractaire - unresponsive) is a transient state of reduced excitability of the nervous or muscle tissue, arising after their excitation
To traditional treatment chronic heart failure (CHF).

Main clinical manifestations of DCM:

1. Systolic CHF (left ventricular or biventricular) with signs of stagnation in the pulmonary and systemic circulation.

2. Frequent occurrence of rhythm and conduction disturbances (ventricular arrhythmias, atrial fibrillation, AV block Atrioventricular block (AV block) is a type of heart block that indicates a violation of the conduction of electrical impulses from the atria to the ventricles (atrioventricular conduction), often leading to disturbances in heart rhythm and hemodynamics
, bundle branch block).

3. Thromboembolic complications in the form of pulmonary embolism and embolism in the systemic circulation. Develop in 20% of patients, most often occurring against the background of atrial fibrillation Atrial fibrillation (syn. atrial fibrillation) is a cardiac arrhythmia characterized by complete asynchrony of contractions of atrial myofibrils, manifested by cessation of their pumping function
.
According to available data, thromboembolism is diagnosed intravitally in 10-44% of cases of DCM. The detection rate of DCM at autopsy reaches 80%, which is caused by the asymptomatic course of many thromboembolic episodes or the masking of these episodes by signs of congestive heart failure.
The sources of thromboembolism are parietal thrombi Parietal thrombus - a thrombus attached to the wall of a vessel or endocardium and incompletely covering the lumen of the vessel or heart cavity
in dilated cavities of the heart, which are diagnosed intravitally using echocardiography in 30-45% of such patients and postmortem - in 60-75% of cases.

On auscultation weakening of 1 tone at the apex is detected. If pulmonary hypertension develops Pulmonary hypertension - increased blood pressure in the vessels of the pulmonary circulation
the accent and splitting of 2 tones is determined. At the apex, a protodiastolic gallop rhythm is often heard, which is associated with severe volume overload of the ventricles.

Diagnostics

Diagnostic criteria idiopathic dilated cardiomyopathy (Mestroni et al., 1999)

Major diagnostic criteria:

1. Dilatation of the heart.

2. Ejection fraction less than 45% and/or fractional shortening of the anteroposterior dimension of the left ventricle< 25%.

Minor diagnostic criteria:

1. Unexplained supraventricular (atrial fibrillation or other sustained arrhythmias) or ventricular arrhythmias before the age of 50 years.
2. Dilatation of the left ventricle (the end-diastolic size of the left ventricle is more than 117% of the calculated norm, taking into account age and body surface).
3. Unexplained conduction disturbances: 2-3 degree atrioventricular block, complete block of the left bundle branch, sinoatrial block.

4. Unexplained sudden death or stroke before age 50.

Electrocardiography.Changes on the ECG with DCM are quite nonspecific. According to Holter monitoring, various disturbances of heart rhythm and conduction are observed in almost 100% of cases of DCM. Ventricular arrhythmias are the most frequently recorded. Atrial fibrillation Atrial fibrillation is an arrhythmia characterized by fibrillation (rapid contraction) of the atria with complete irregularity of the intervals between heartbeats and the force of contraction of the ventricles of the heart.
Among patients with DCM, it occurs on average in only 24-35%.
An unfavorable prognostic sign is the occurrence of atrial fibrillation, since this condition is associated with increased mortality and progression of heart failure in any type of cardiomyopathy.
Of the conduction disorders for DCM, the most typical are complete blockade of the left bundle branch or its anterosuperior branch.

2D EchoCG with Doppler analysis- the most important method for diagnosing DCM. The main signs are significant dilatation of the left ventricle with normal or reduced thickness of its walls and a decrease in ejection fraction below 30-20%. Based on this indicator, cardiomyopathies are classified by severity into severe (LVEF ≤30%), moderate (LVEF 30-45%) and non-severe (LVEF ≥45%). There is often an expansion of other chambers of the heart, as well as total hypokinesia Hypokinesia - 1. Limitation in the number and range of movements due to lifestyle, characteristics of professional activity, bed rest during the period of illness and accompanied in some cases by physical inactivity; 2. syn. Hypokinesis is a movement disorder manifested by limitation of their volume and speed.
walls of the left ventricle. Parietal intracardiac thrombi are often visualized.

X-ray examination. Signs:
- an increase in the size of the heart due to its left sections or more often - total, the degree of which varies from relatively small to pronounced, like cor bovinum;
- the shadow of the heart acquires spherical shape; with a significant increase in the left atrium, its configuration may approach the mitral one;
- along with its dilatation of the left ventricle, as a rule, there are also signs of its hypertrophy;

The predominance of the phenomena of venous stagnation on the part of the vessels of the pulmonary circulation, more rarely - signs of pulmonary arterial hypertension.

MRI of the heart- a new standard for assessing ventricular volumes, ejection fraction, myocardial mass and regional contractility. When using a paramagnetic agent, disturbances in regional contraction of the myocardium and areas of non-viable myocardium, which are characterized by late filling with a contrast agent, are detected. This method has higher sensitivity compared to thallium scintigraphy.

Coronary angiography Coronary angiography is an X-ray examination of the coronary arteries of the heart after filling them with a contrast agent, for example through a catheter inserted into the ascending aorta
- allows you to exclude the atherosclerotic process in the coronary arteries and is a necessary diagnostic procedure when diagnosing DCM.
When performing coronary angiography, important additional information can be obtained about the state of cardiac output, myocardial wall tension, as well as the characteristics of the pulmonary arteries (dilatation, compliance and pressure). Parameters such as wedge pressure or pulmonary vascular resistance may be used for risk stratification.
Cardiac catheterization is a diagnostic procedure, but it is not performed if the patient is already being treated for DCM.

Endomyocardial biopsy. The histological picture of the obtained samples is nonspecific: hypertrophy of cardiomyocytes is detected Cardiomyocytes - muscle cells hearts
, increased nuclear size and interstitial fibrosis Fibrosis is the proliferation of fibrous connective tissue, occurring, for example, as a result of inflammation.
.

Laboratory diagnostics

General clinical and biochemical research blood tests do not reveal pathological changes characteristic of DCM.

Determination of neurohormones

A generally accepted marker that allows determining further treatment tactics for a patient is currently considered brain natriuretic peptide, released in response to cardiomyocyte stretching. An increase in its concentration in blood plasma by 2 times compared to the norm is a predictor of an unfavorable prognosis in patients with chronic heart failure.

Interleukin-6 concentration in the blood - another predictor of high cardiovascular mortality in stable severe chronic heart failure, correlating with the severity clinical symptoms diseases.

It is also considered a predictor of cardiovascular morbidity and mortality. norepinephrine content in blood plasma.

Differential diagnosis

Differential diagnosis of idiopathic dilated cardiomyopathy (DCM) is carried out with the following diseases:
- ischemic cardiomyopathy;
- severe myocarditis (including Fiedler's myocarditis);
- myocardial damage in diffuse connective tissue diseases (mainly with systemic scleroderma and systemic lupus erythematosus);
- rheumatic mitral heart defects;
- non-rheumatic mitral insufficiency;
- stenosis of the aortic mouth.
The clinical manifestations of DCM also have certain similarities with such rarer pathologies as exudative pericarditis, cardiac damage due to amyloidosis, hemochromatosis and sarcoidosis, and some other cardiomyopathies.

1. Coronary heart disease(IHD)
Most often, DCM is differentiated from IHD, especially in males aged 40-50 years.

The main differences between DCM and IHD:

1.1 In DCM, the pain syndrome is of the nature of cardial pain:
- more often aching pain;
- pain is localized mainly in the left half of the chest, does not radiate;
- pain is not always relieved by nitroglycerin;
- pain syndrome appears against the background of already developed decompensation and cardiomegaly.
With angina pectoris, the pain is paroxysmal in nature and is associated with physical activity, are localized behind the sternum and have typical irradiation, relieved by nitrates.
In myocardial infarction, severe pain precedes the development of heart failure.

1.2 With DCM, expansion of all boundaries of the heart is observed, which is confirmed by percussion, X-ray studies, ECG, EchoCG.
With ischemic heart disease in the later stages of development, there is a predominant expansion of the left border of relative cardiac dullness.

1.3 In case of coronary artery disease, the ECG reveals signs of chronic coronary insufficiency or scar changes, which indicate a myocardial infarction.
With DCM, ECG signs of hypertrophy and overload of the heart are observed.
In some cases, with cardiomyopathy, signs of focal cicatricial changes are recorded - pathological Q and QS waves associated with focal fibrosis of non-coronarogenic origin. In this case, ECG mapping with registration of 35 leads is used.

1.4 Coronary angiography in patients with coronary artery disease, as a rule, reveals signs of atherosclerotic lesions of the coronary arteries; with DCM, the arteries of the heart are intact.

1.5 A gallop rhythm is more typical for DCM.

2. True left ventricular aneurysm - is formed after extensive anterior myocardial infarction and is characterized by pronounced diastolic protrusion and dyskinesia of the anterior wall of the left ventricle. As a result, there is a significant expansion of the heart shadow and a decrease in the left ventricular ejection fraction to very low values ​​during isotope ventriculography with erythrocytes labeled with 99mTc.
It is possible to identify the focal nature of myocardial damage using echocardiography, which reveals normal contractility of the lower and lateral walls.

3. Aortic stenosis. In patients with severe aortic stenosis in the decompensation stage, pronounced dilatation of the left ventricle and a decrease in its contractility may be observed. As cardiac output falls, the murmur of aortic stenosis becomes weaker and may even disappear.

4. Aortic insufficiency . Aortic regurgitation leads to left ventricular volume overload.

5. Mitral regurgitation. Of all the acquired heart defects, mitral regurgitation is the most difficult to distinguish from DCM. This is because mitral annulus dilation and papillary muscle dysfunction, which are almost always present in DCM, themselves cause mitral regurgitation.
The primary nature of mitral regurgitation and the fact that it was it that led to dilatation of the left ventricle, and not vice versa, can be assumed if mitral regurgitation is moderate or severe, if it is known that it occurred before dilatation of the left ventricle, or if pronounced changes in the mitral valve are detected during EchoCG.

6. Mitral stenosis. Severe enlargement of the right ventricle in some cases occurs with severe mitral stenosis, high pulmonary hypertension and right ventricular failure. As a result of the enlargement of the right ventricle, an enlarged shadow of the heart is visible on the chest x-ray, and a palpable and audible third heart sound appears.

7. Exudative pericarditis. Pericardial effusion can cause significant expansion of the cardiac shadow and heart failure, which raises suspicion of the presence of DCM. Normal ventricular contractility can rule out cardiomyopathy. Exudative pericarditis must be excluded first of all, since it is curable.

Complications

The most serious complications of dilated cardiomyopathy include sudden cardiac death, as well as the development of thromboembolism, including pulmonary embolism. PE - pulmonary embolism (blockage of the pulmonary artery or its branches by blood clots, which often form in the large veins of the lower extremities or pelvis)
.

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1. Evidence-based medicine is a set of methodological approaches to conducting clinical trials, evaluating and applying their results. In a narrow sense, “evidence-based medicine” is a method (type) of medical practice when a doctor uses only those methods in caring for a patient whose usefulness has been proven in benign research. The problem of evidence-based medicine is deeper than just collecting, processing and accumulating information . In fact, we can talk about a change in the doctor’s worldview, about the emergence of a new medical code based on evidence. However, evidence-based medicine is not limited to the analysis of the results of randomized clinical trials. Its boundaries are applicable to any area of ​​medical science, including general problems of organizing an optimal healthcare system

2. Cardiomyopathies.

CARDIOMYOPATHIES are primary non-inflammatory myocardial lesions of unknown etiology (idiopathic), not associated with valve defects or intracardiac shunts, arterial or pulmonary hypertension, coronary heart disease or systemic diseases (collagenosis, amyloidosis, hemochromatosis, etc.). The pathogenesis of cardiomyopathy is unclear. The involvement of genetic factors, enzyme and endocrine disorders (in particular in the sympathetic-adrenergic system) is assumed; the role of viral infection and immunological changes is not excluded. The main forms of cardiomyopathy: hypertrophic (obstructive and non-obstructive), congestive (dilated) and restrictive (rare).

Hypertrophic cardiomyopathy. The non-obstructive form is characterized by an increase in the size of the heart due to diffuse hypertrophy of the walls of the left ventricle, less often only the apex of the heart. At the apex of the heart or at the xiphoid process, a systolic murmur is heard, often a presystolic gallop rhythm. With asymmetric hypertrophy of the interventricular septum with narrowing of the outflow tract of the left ventricle (obstructive form), symptoms of muscular subaortic stenosis occur: pain behind the sternum, attacks of dizziness with a tendency to faint, paroxysmal shortness of breath at night, loud systolic murmur in the third or fourth intercostal space at the left edge of the sternum, not carried out on the carotid arteries, with a maximum in mid-systole, sometimes combined with a systolic regurgitation murmur caused by “papillary” mitral insufficiency. Arrhythmia and intracardiac conduction disturbances (blockade) are not uncommon. The progression of hypertrophy can lead to the development of heart failure, first left ventricular, then total (at this stage a proto-diastolic gallop rhythm often appears). The ECG shows signs of hypertrophy of the left ventricle and interventricular septum: deep, non-widened Q waves in II, III, aVF, V 4 .g leads in combination with a high R wave. Echocardiography is the most reliable method identifying hypertrophy of the ventricular walls and interventricular septum. Probing of the heart cavities and radionuclide ventriculography helps in diagnosis.

Stagnant(dilated) cardiomyopathy is manifested by a sharp expansion of all chambers of the heart in combination with their slight hypertrophy and steadily progressing heart failure, refractory to therapy, the development of thrombosis and thromboembolism. Differential diagnosis is carried out primarily with myocarditis and myocardial dystrophies, i.e. with those conditions that are sometimes called secondary cardiomyopathies without proper reason.

Treatment. For hypertrophic cardiomyopathy, beta-blockers (anaprilin, inderal) are used, and surgical correction of subaortic stenosis is performed. With the development of heart failure, physical activity is limited, a diet with a reduced salt and fluid content, cardiac glycosides (not effective enough), vasodilators, diuretics, calcium antagonists (isoptin, etc.) are prescribed.

The prognosis for the development of progressive heart failure is unfavorable. In severe forms, cases of sudden death are observed. Until circulatory failure develops, the ability to work suffers little.

3. . Myocarditis.

MYOCARDITIS - inflammatory damage to the heart muscle.

Symptoms, course. Infectious-allergic myocarditis(the most common form of non-rheumatic myocarditis) begins, unlike rheumatic myocarditis, usually against the background of infection or shortly after it; there is malaise, pain in the heart area, sometimes persistent, palpitations and “interruptions”, shortness of breath, and in some cases moderate pain in the joints. Body temperature is often subfebrile or normal. The onset of the disease may be asymptomatic or hidden. The severity of symptoms is largely determined by the prevalence and severity of the progression of the process. In diffuse forms, the size of the heart increases relatively early. Important, but not constant signs of myocarditis are disturbances in heart rhythm (tachycardia, less often bradycardia, ectopic arrhythmias) and intracardiac conduction, as well as presystolic, and in later stages protodiastolic gallop rhythm. A short functional systolic murmur at the apex of the heart or at the fifth point and muffling of tones are not reliable signs of myocarditis, while the disappearance of functional systolic murmur during treatment, due to the cessation of prolapse of the mitral valve leaflet, as well as the restoration of the sonority of heart sounds, indicates improving the condition of the myocardium.

Idiopathic myocarditis differs in a more severe, sometimes malignant course with the development of cardiomegaly (due to pronounced dilatation of the heart), severe violations rhythm and conduction, heart failure; Often, parietal blood clots form in the cavities of the heart with thromboembolism in the systemic and pulmonary circulation.

At myocarditis associated with collagen diseases, viral infection(viruses of the Coxsackie group, etc.), concomitant pericarditis often develops. The course of myocarditis can be acute, subacute and chronic (recurrent). The ECG shows various disturbances of heart rhythm and conduction; in the acute stage of myocarditis, signs of myocardial changes are usually detected, sometimes resembling ischemic ones (in the absence of angina!). Laboratory signs of inflammation may be absent. Differential diagnosis should be made with coronary heart disease (especially in the elderly), myocardial dystrophy, cardiomyopathies, and pericarditis.

Treatment. The regime is usually bed rest. It is advisable to early combine glucocorticoids (prednisolone, starting from 20-30 mg/day, in decreasing doses, etc.) with non-steroidal anti-inflammatory drugs in the following daily doses: acetylsalicylic acid - 3-4 g, amidopyrine - 1.5-2 g, butadione -0.45-0.6 g, ibuprofen (brufen) - 0.8-1.2 g, indomethacin - 75-100 mg. For heart failure - Celanide, digoxin (0.25-0.5 mg/day) and other cardiac glycosides, taking into account the increased sensitivity of patients with myocarditis to glycosides. Diuretics - furosemide (Lasix) 0.04 g per day, etc. Antiarrhythmic drugs (novocainamide 1-1.5 r/day, etc.). Agents that improve metabolism in the myocardium: potassium orotate (1 g per day), methandrostenolone (0.005-0.01 g per day), B vitamins (thiamine chloride, riboflavin). In case of prolonged course, quinoline drugs are indicated - delagil at 0.25 r/day, etc.

4. Differential diagnosis of mitral heart defects and dilated cardiomyopathy

Diagnostics mitral valve insufficiency . Direct signs:

Systolic murmur at the apex in combination with weakening of the first tone

The appearance of the third tone at the apex and its combination with systolic murmur and weakening of the first tone

Indirect signs: Hypertrophy and dilatation of the left ventricle and left atrium

Symptoms of pulmonary hypertension and the phenomenon of backflow in the systemic circulation

Enlargement of the left borders of the heart: “heart hump”, displacement of the apical impulse to the left and down with significant dilatation of the left ventricle Some clinical signs mitral stenosis : Pulsus differens - appears when the left atrium compresses the left subclavian artery. Hoarseness of voice is Ortner's sign (as a result of compression of the left recurrent nerve).

Anisocoria is a result of compression sympathetic trunk enlarged left atrium.

Diagnosis of mitral stenosis Direct signs: Increased first tone, diastolic murmur

Mitral valve opening tone Quail rhythm Displacement of the upper border relative stupidity heart upward (due to enlargement of the left atrium appendage) Palpation “cat purring” (diastolic tremor) at the apex of the heart Indirect signs:

“Pulmonary:” Cyanosis Accent of the second tone over the pulmonary artery Diastolic murmur on the left edge of the chest (Graham-Still murmur) Objective data on DCM : required cardiomegalyauscultationhepatomegaly.

5. Differential diagnosis of myocarditis and dilated cardiomyopathy.

DCM : required cardiomegaly, the percussion boundaries of the heart are expanded in all directions, the apical impulse is shifted to the left and down, diffuse. At auscultation Heart sounds are muffled, a “gallop rhythm” is possible due to the III and IV sounds. A systolic murmur of relative mitral and tricuspid insufficiency is often heard. Swelling of the neck veins, edema syndrome, hepatomegaly.Myocarditis Physical examination varies from moderate tachycardia to symptoms of decompensated right and left ventricular failure (swelling of the jugular veins, edema, weakening of the first tone, gallop rhythm, systolic murmur at the apex, congestion in the lungs). It is currently believed that the diagnosis of myocarditis can only be confirmed by endomyocardial biopsy,

6. Pulmonary edema.

Most often, the life-threatening acute development of alveolar pulmonary edema is caused by: 1) an increase in hydrostatic pressure in the capillaries of the lungs (left heart failure, mitral stenosis) or 2) increased permeability of the pulmonary membrane. Specific factors cause cardiogenic pulmonary edema in patients with compensated CHF or even in the absence of a cardiac history.

Physical symptoms. The patient's condition is serious, he sits upright, covered in sweat, often cyanosis. Wheezing is heard in the lungs on both sides, above the heart - III heart tone. The sputum is foamy and bloody.

Laboratory data. In the early stages of edema, when studying CBS, a decrease in Pao 2, Paco 2 is noted; later, as DN progresses, hypercapnia increases in the structure of acidosis. A chest x-ray shows an increase in the vascular pattern of the lungs, diffuse shading of the lung fields, and the appearance of a “butterfly” in the area of ​​the hilum of the lungs.

Treatment of pulmonary edema. To save the patient's life, urgent intensive therapy. The following activities should be implemented almost simultaneously:

1. Sit the patient down to reduce venous return.

2. Administer 100% oxygen through a mask to achieve Pao 2 > 60 mm Hg. Art.

3. Introduce loop diuretics intravenously (furosemide 40-100 mg or bumetanide 1 mg); Smaller doses can be used if the patient does not take diuretics regularly

4. Morphine 2-5 mg intravenously repeatedly; often used to lower blood pressure and reduce shortness of breath; Naloxone should be on hand to counteract the effects of morphine.

5. Reduce afterload [intravenous sodium nitroprusside (20-300 mcg/min) if systolic blood pressure > 100 mm Hg. st]; establish direct blood pressure measurement.

If there is no rapid improvement, additional therapy is required:

1. If the patient has not received digitalis regularly, 75% of the full therapeutic dose is administered intravenously.

2. Aminophylline (6 mg/kg intravenously over 20 minutes, then 0.2-0.5 mgDkg x h); reduces bronchospasm, increases myocardial contractility and diuresis; can be applied to initial stage instead of morphine if it is unclear whether the breathing problem is due to pulmonary edema or significant obstructive disease (prior to chest x-ray).

3. If the administration of diuretics does not cause rapid diuresis, it is possible to reduce the volume of blood volume by exfusion venous blood(250 ml from the cubital vein) or by applying venous tourniquets to the limbs.

4. If hypoxemia and hypercapnia persist, tracheal intubation is performed.

The causes of pulmonary edema, especially acute arrhythmia or infection, should be found and eliminated.

Some noncardiogenic causes may cause pulmonary edema despite the absence of left ventricular failure; in this case, treatment should be aimed at eliminating the cause.

7. . Pericarditis.

PERICARDITIS is an acute or chronic inflammation of the pericardial sac. There are fibrinous, serous-fibrinous, hemorrhagic, xanthomatous, purulent, putrefactive pericarditis.

Pathogenesis is often allergic or autoimmune; with infectious pericarditis, infection can be a trigger; Direct damage to the membranes of the heart by bacterial or other agents cannot be ruled out.

Symptoms and course are determined by the underlying disease and the nature of the effusion, its quantity (dry, effusion pericarditis) and the rate of accumulation. Initial symptoms: malaise, increased body temperature, substernal or precordial pain, often associated with respiratory phases, and sometimes reminiscent of angina pectoris. A pericardial friction rub of varying intensity and extent is often heard. The accumulation of exudate is accompanied by the disappearance of precordial pain and pericardial friction noise, the appearance of shortness of breath, cyanosis, swelling of the neck veins, weakening of the cardiac impulse, and expansion of cardiac dullness, however, with a moderate amount of effusion, heart failure is usually moderate. Due to a decrease in diastolic filling, the stroke volume of the heart decreases, heart sounds become muffled, the pulse is small and frequent, often paradoxical (a drop in filling and pulse tension during inspiration). With constrictive (compressive) pericarditis, atrial fibrillation or atrial flutter often occurs as a result of deforming adhesions in the atria; At the beginning of diastole, a loud pericardial tone is heard. With the rapid accumulation of exudate, cardiac tamponade may develop with cyanosis, tachycardia, weakening of the pulse, painful attacks of shortness of breath, sometimes with loss of consciousness, rapidly increasing venous stagnation. With constructive pericarditis with progressive cicatricial compression of the heart, circulatory disorders in the liver and in the system increase portal vein. High central venous pressure, portal hypertension, ascites (Pick's pseudocirrhosis) are detected, peripheral edema appears; Orthopnea is usually absent. The spread of the inflammatory process to the mediastinal tissue and pleura leads to mediastinopericarditis or pleurisy; when inflammation passes from the epicardium to the myocardium (superficial layers), myopericarditis develops.

On the ECG in the first days of the disease, a concordant rise of the 8T segment in standard and chest leads is noted, subsequently the ST segment shifts to the isoelectric line, the T wave flattens or undergoes inversion; with a significant accumulation of effusion, the voltage of the QRS complex decreases. X-ray examination reveals an increase in the diameter of the heart and a trapezoidal configuration of the cardiac shadow with a weakening of the pulsation of the cardiac circuit. With long-term pericarditis, calcification of the pericardium (armored heart) is observed. Echocardiography is a reliable method for detecting pericardial effusion; jugular venography and phonocardiography are also used for diagnosis. Differential diagnosis is carried out with the initial period of acute myocardial infarction and acute myocarditis.

The prognosis is most unfavorable for tumor and purulent pericarditis.

8. Pleurisy.

Pleurisy is an inflammation of the pleural layers, which, as a rule, is a complication of certain pathological processes in the lungs, less often in other organs and tissues located close to the pleural cavity, or is a manifestation of systemic diseases.

Etiology . There are infectious and non-infectious (aseptic). Infectious diseases are caused by pathogens that cause a pathological process in the lung tissue. Aseptic ones are most often associated with damage to the pleura by malignant neoplasms, trauma, pulmonary infarction, exposure to pancreatic enzymes in pancreatitis, and systemic connective tissue diseases.

Pathogenesis . Penetration of the pathogen into the pleura during infarction pleurisy most often occurs directly from the subpleural focus in lung tissue; along lymphatic ducts during penetrating wounds and operations. In some forms (tuberculosis), sensitization under the influence of the previous course of a specific process plays a significant role.

Pathanatomy. With pleurisy, inflammatory edema and cellular infiltration of the pleural layers and accumulation of exudate (fibrinous, serous, hemorrhagic, purulent) between them are observed. As pleurisy progresses, serous exudate is prone to resorption, and fibrinous exudate undergoes organization by elements of connective tissue, as a result of which fibrinous deposits (moorings) are formed on the surface of the pleural layers. Purulent exudate is not prone to resorption and can only be eliminated as a result of surgical manipulation or spontaneous breakthrough through the chest wall.

Classification. Depending on the nature of the exudate, they are distinguished: fibrinous (dry), serous-fibrinous, serous, hemorrhagic, purulent, putrefactive, eosinophilic, chylous pleurisy. According to the characteristics and phase of the course: acute, subacute, chronic. Depending on the prevalence in the pleural cavity: diffuse (total) or organic (encysted).

Clinic. There are 3 main syndromes: dry (fibrinous) pleurisy syndrome; syndrome of effusion (exudative) pleurisy; purulent pleurisy syndrome (pleural empyema).

With dry pleurisy, patients complain of acute pain in the chest when breathing, which intensifies with a deep breath and bending in the opposite direction. There are usually no changes to percussion, and on auscultation a pleural friction rub is usually heard. Dry pleurisy in itself does not give radiological symptoms. The course of isolated dry pleurisy is usually short-lived (from several days to 3 weeks). A longer recurrent course, as well as transformation into exudative pleurisy, is sometimes observed with tuberculosis.

With exudative (effusion) pleurisy, patients, against a background of general malaise, feel a feeling of heaviness, fullness in the affected side of the chest, and sometimes a dry cough. With a significant accumulation of exudate, shortness of breath appears, the patient takes a forced position on the sore side. Percussion in lower sections a massive dullness is determined with a convex upward border, which has its highest point along the posterior axillary line. The percussion boundaries of the heart and mediastinum shift to the opposite side. Vocal tremors and respiratory sounds in the area of ​​dullness are usually sharply weakened or not detected at all. X-ray examination reveals massive shading in the lower parts of the lungs with an oblique upper border and a shift of the mediastinum to the “healthy” side.

The most important diagnostic method is pleural puncture, which makes it possible to judge the presence and nature of the effusion. In the punctate, the amount of protein and relative density are examined (inflammatory exudate is characterized by a relative density of more than 1.018 and an amount of protein of more than 3%). The Rivalta test (a drop of punctate in weak solution acetic acid at inflammatory nature the effusion produces a “cloud” due to the loss of seromucin).

The punctate sediment is examined cytologically (an increase in the number of neutrophils may indicate a tendency to suppuration of the exudate, multinucleated atypical cells may indicate its tumor nature). Microbiological examination allows confirmation and identification of infectious pathogens.

Treatment. For fibrinous pleurisy, it is aimed at relieving the underlying disease. The goal of treatment is to relieve pain and accelerate the resorption of fibrin, to prevent the formation of extensive cords and adhesions in the pleural cavity. First of all, etiotropic treatment of the underlying disease (pneumonia, tuberculosis, etc.) is started.

For this purpose, antibiotics, anti-tuberculosis drugs, and chemotherapy are prescribed. Desensitizing and anti-inflammatory drugs, salicylates are widely used; They usually also relieve pain. For very severe pain, narcotic painkillers are prescribed. In case of accumulation large quantity fluid in the pleural cavity conservative methods, as a rule, do not lead to positive results and in this case they resort to puncture of the pleural cavity with removal of exudate, which is repeated after 1-2 days. For purulent exudative pleurisy, aspiration and surgical treatment methods are used.

Differential diagnosis of mitral heart defects and dilated cardiomyopathy

Diagnostics mitral valve insufficiency . Direct signs:

Systolic murmur at the apex in combination with weakening of the first tone

The appearance of the third tone at the apex and its combination with systolic murmur and weakening of the first tone

Indirect signs: Hypertrophy and dilatation of the left ventricle and left atrium

Symptoms of pulmonary hypertension and the phenomenon of backflow in the systemic circulation

Enlargement of the left borders of the heart: “heart hump”, displacement of the apical impulse to the left and down with significant dilatation of the left ventricle Some clinical signs mitral stenosis : Pulsus differens - appears when the left atrium compresses the left subclavian artery. Hoarseness of voice is Ortner's sign (as a result of compression of the left recurrent nerve).

Anisocoria is the result of compression of the sympathetic trunk by the enlarged left atrium.

Diagnosis of mitral stenosis Direct signs: Increased first tone, diastolic murmur

Mitral valve opening tone Quail rhythm Shift of the upper limit of the relative dullness of the heart upward (due to an increase in the left atrial appendage) Palpation “cat purring” (diastolic tremor) at the apex of the heart Indirect signs:

“Pulmonary:” Cyanosis Accent of the second tone over the pulmonary artery Diastolic murmur on the left edge of the chest (Graham-Still murmur) Objective data on DCM

Differential diagnosis of myocarditis and dilated cardiomyopathy.

DCM: cardiomegaly is obligatory, the percussion boundaries of the heart are expanded in all directions, the apical impulse is shifted to the left and down, diffuse. On auscultation, heart sounds are muffled, a “gallop rhythm” is possible due to the III and IV sounds. A systolic murmur of relative mitral and tricuspid insufficiency is often heard. Swelling of the neck veins, edema syndrome, and hepatomegaly are detected. Myocarditis Physical examination varies from moderate tachycardia to symptoms of decompensated right and left ventricular failure (swelling of the jugular veins, edema, weakening of the first tone, gallop rhythm, systolic murmur at the apex, congestion in the lungs). It is currently believed that the diagnosis of myocarditis can only be confirmed by endomyocardial biopsy,

6. Pulmonary edema.

Most often, the life-threatening acute development of alveolar pulmonary edema is caused by: 1) an increase in hydrostatic pressure in the capillaries of the lungs (left heart failure, mitral stenosis) or 2) an increase in the permeability of the pulmonary membrane. Specific factors cause cardiogenic pulmonary edema in patients with compensated CHF or even in the absence of a cardiac history.

Physical symptoms. The patient's condition is serious, he sits upright, covered in sweat, often cyanosis. Wheezing is heard in the lungs on both sides, and a third heart sound is heard above the heart. The sputum is foamy and bloody.

Laboratory data. In the early stages of edema, when studying CBS, a decrease in Pao 2, Paco 2 is noted; later, as DN progresses, hypercapnia increases in the structure of acidosis. A chest x-ray shows an increase in the vascular pattern of the lungs, diffuse shading of the lung fields, and the appearance of a “butterfly” in the area of ​​the hilum of the lungs.

Treatment of pulmonary edema. To save the patient's life, urgent intensive care is necessary. The following activities should be implemented almost simultaneously:

1. Sit the patient down to reduce venous return.

2. Administer 100% oxygen through a mask to achieve Pao 2 > 60 mm Hg. Art.

3. Introduce loop diuretics intravenously (furosemide 40-100 mg or bumetanide 1 mg); Smaller doses can be used if the patient does not take diuretics regularly

4. Morphine 2-5 mg intravenously repeatedly; often used to lower blood pressure and reduce shortness of breath; Naloxone should be on hand to counteract the effects of morphine.

5. Reduce afterload [intravenous sodium nitroprusside (20-300 mcg/min) if systolic blood pressure > 100 mm Hg. st]; establish direct blood pressure measurement.

If there is no rapid improvement, additional therapy is required:

1. If the patient has not received digitalis regularly, 75% of the full therapeutic dose is administered intravenously.

2. Aminophylline (6 mg/kg intravenously over 20 minutes, then 0.2-0.5 mgDkg x h); reduces bronchospasm, increases myocardial contractility and diuresis; may be used initially instead of morphine if it is unclear whether the breathing disorder is due to pulmonary edema or significant obstructive disease (prior to chest x-ray).

3. If the administration of diuretics does not cause rapid diuresis, the volume of blood volume can be reduced by exfusion of venous blood (250 ml from the cubital vein) or by applying venous tourniquets to the extremities.

4. If hypoxemia and hypercapnia persist, tracheal intubation is performed.

The causes of pulmonary edema, especially acute arrhythmia or infection, should be found and eliminated.

Some noncardiogenic causes may cause pulmonary edema despite the absence of left ventricular failure; in this case, treatment should be aimed at eliminating the cause.

7. . Pericarditis.

PERICARDITIS is an acute or chronic inflammation of the pericardial sac. There are fibrinous, serous-fibrinous, hemorrhagic, xanthomatous, purulent, putrefactive pericarditis.

Pathogenesis is often allergic or autoimmune; with infectious pericarditis, infection can be a trigger; Direct damage to the membranes of the heart by bacterial or other agents cannot be ruled out.

Symptoms and course are determined by the underlying disease and the nature of the effusion, its quantity (dry, effusion pericarditis) and the rate of accumulation. Initial symptoms: malaise, increased body temperature, substernal or precordial pain, often associated with respiratory phases, and sometimes reminiscent of angina pectoris. A pericardial friction rub of varying intensity and extent is often heard. The accumulation of exudate is accompanied by the disappearance of precordial pain and pericardial friction noise, the appearance of shortness of breath, cyanosis, swelling of the neck veins, weakening of the cardiac impulse, and expansion of cardiac dullness, however, with a moderate amount of effusion, heart failure is usually moderate. Due to a decrease in diastolic filling, the stroke volume of the heart decreases, heart sounds become muffled, the pulse is small and frequent, often paradoxical (a drop in filling and pulse tension during inspiration). With constrictive (compressive) pericarditis, atrial fibrillation or atrial flutter often occurs as a result of deforming adhesions in the atria; At the beginning of diastole, a loud pericardial tone is heard. With the rapid accumulation of exudate, cardiac tamponade may develop with cyanosis, tachycardia, weakening of the pulse, painful attacks of shortness of breath, sometimes with loss of consciousness, and rapidly increasing venous stagnation. With constructive pericarditis with progressive cicatricial compression of the heart, circulatory disturbances in the liver and in the portal vein system increase. High central venous pressure is detected, portal hypertension, ascites (Pick's pseudocirrhosis), peripheral edema appears; Orthopnea is usually absent. The spread of the inflammatory process to the mediastinal tissue and pleura leads to mediastinopericarditis or pleurisy; when inflammation passes from the epicardium to the myocardium (superficial layers), myopericarditis develops.

On the ECG in the first days of the disease, a concordant rise of the 8T segment in standard and chest leads is noted, subsequently the ST segment shifts to the isoelectric line, the T wave flattens or undergoes inversion; with a significant accumulation of effusion, the voltage of the QRS complex decreases. X-ray examination reveals an increase in the diameter of the heart and a trapezoidal configuration of the cardiac shadow with a weakening of the pulsation of the cardiac circuit. With long-term pericarditis, calcification of the pericardium (armored heart) is observed. Echocardiography is a reliable method for detecting pericardial effusion; jugular venography and phonocardiography are also used for diagnosis. Differential diagnosis is carried out with the initial period of acute myocardial infarction and acute myocarditis.

The prognosis is most unfavorable for tumor and purulent pericarditis.

8. Pleurisy.

Pleurisy is an inflammation of the pleural layers, which, as a rule, is a complication of certain pathological processes in the lungs, less often in other organs and tissues located near the pleural cavity, or is a manifestation of systemic diseases.

Etiology . There are infectious and non-infectious (aseptic). Infectious diseases are caused by pathogens that cause a pathological process in the lung tissue. Aseptic ones are most often associated with damage to the pleura by malignant neoplasms, trauma, pulmonary infarction, exposure to pancreatic enzymes in pancreatitis, and systemic connective tissue diseases.

Pathogenesis . Penetration of the pathogen into the pleura during infarction pleurisy most often occurs directly from the subpleural focus into the lung tissue; along lymphatic ducts during penetrating wounds and operations. In some forms (tuberculosis), sensitization under the influence of the previous course of a specific process plays a significant role.

Pathanatomy. With pleurisy, inflammatory edema and cellular infiltration of the pleural layers and accumulation of exudate (fibrinous, serous, hemorrhagic, purulent) between them are observed. As pleurisy progresses, serous exudate is prone to resorption, and fibrinous exudate undergoes organization by elements of connective tissue, as a result of which fibrinous deposits (moorings) are formed on the surface of the pleural layers. Purulent exudate is not prone to resorption and can only be eliminated as a result of surgical manipulation or spontaneous breakthrough through the chest wall.

Classification. Depending on the nature of the exudate, they are distinguished: fibrinous (dry), serous-fibrinous, serous, hemorrhagic, purulent, putrefactive, eosinophilic, chylous pleurisy. According to the characteristics and phase of the course: acute, subacute, chronic. Depending on the prevalence in the pleural cavity: diffuse (total) or organic (encysted).

Clinic. There are 3 main syndromes: dry (fibrinous) pleurisy syndrome; syndrome of effusion (exudative) pleurisy; purulent pleurisy syndrome (pleural empyema).

With dry pleurisy, patients complain of acute pain in the chest when breathing, which intensifies with a deep breath and bending in the opposite direction. There are usually no changes to percussion, and on auscultation a pleural friction rub is usually heard. Dry pleurisy in itself does not give radiological symptoms. The course of isolated dry pleurisy is usually short-lived (from several days to 3 weeks). A longer recurrent course, as well as transformation into exudative pleurisy, is sometimes observed with tuberculosis.

With exudative (effusion) pleurisy, patients, against a background of general malaise, feel a feeling of heaviness, fullness in the affected side of the chest, and sometimes a dry cough. With a significant accumulation of exudate, shortness of breath appears, the patient takes a forced position on the sore side. Percussion reveals a massive dullness in the lower parts with a border convex upward, having highest point along the posterior axillary line. The percussion boundaries of the heart and mediastinum shift to the opposite side. Vocal tremors and respiratory sounds in the area of ​​dullness are usually sharply weakened or not detected at all. X-ray examination reveals massive shading in the lower parts of the lungs with an oblique upper border and a shift of the mediastinum to the “healthy” side.

The most important diagnostic method is pleural puncture, which makes it possible to judge the presence and nature of the effusion. In the punctate, the amount of protein and relative density are examined (inflammatory exudate is characterized by a relative density of more than 1.018 and an amount of protein of more than 3%). Certain implications for judgment of character pleural fluid has a Rivalta test (a drop of punctate in a weak solution of acetic acid with an inflammatory nature of the effusion gives a “cloud” due to the precipitation of seromucin).

The punctate sediment is examined cytologically (an increase in the number of neutrophils may indicate a tendency to suppuration of the exudate, multinucleated atypical cells may indicate its tumor nature). Microbiological examination allows you to confirm and identify infectious pathogens.

Treatment. For fibrinous pleurisy, it is aimed at relieving the underlying disease. The goal of treatment is to relieve pain and accelerate the resorption of fibrin, to prevent the formation of extensive cords and adhesions in the pleural cavity. First of all, etiotropic treatment of the underlying disease (pneumonia, tuberculosis, etc.) is started.

For this purpose, antibiotics, anti-tuberculosis drugs, and chemotherapy are prescribed. Desensitizing and anti-inflammatory drugs, salicylates are widely used; They usually also relieve pain. At very severe pain narcotic painkillers are prescribed. When a large amount of fluid accumulates in the pleural cavity, conservative methods, as a rule, do not lead to positive results and in this case, they resort to puncture of the pleural cavity with removal of exudate, which is repeated after 1-2 days. For purulent exudative pleurisy, aspiration and surgical treatment methods are used.