Viral myocarditis

Introduction to viral myocarditis Viral myocarditis (viralmyocarditis) is a localized or diffuse acute, subacute or chronic inflammatory cardiomyopathy associated with viral infection and is the most common infectious myocarditis. Almost every group of viruses can cause specific corticoviral diseases, among which the long-term virus infection of the committee that causes intestinal and upper respiratory tract infections is most common, but many are subclinical. The clinical manifestations of mild myocarditis are few and the diagnosis is difficult, so the pathological diagnosis is much higher than the clinical incidence. In recent years, with the improvement of detection technology, it has been found that a variety of viruses can cause myocarditis, and its incidence rate is increasing year by year, and it is a common disease and frequently-occurring disease all over the world. basic knowledge The proportion of illness: 0.004% Susceptible people: no specific people Mode of infection: non-infectious Complications: arrhythmia heart failure dilated cardiomyopathy

Cause of viral myocarditis

Almost every group of viruses can cause specific corticoviral diseases. Among them, the virus that causes intestinal and upper respiratory tract infections is most common, but many are subclinical. The viruses that have been confirmed to cause myocarditis include:

Arbovirus (20%):

Such as yellow fever virus, dengue virus, fever virus, epidemic hemorrhagic fever virus, etc., arbovirus is a group of arthropod vector viruses, which are classified into the togaviridae, the yellow virus family, the Bunia virus family and the sand grains. Some members of the virus family. The main arboviruses classified as the genus of the togavirus family are the eastern equine encephalitis virus, the western equine encephalitis virus and the Venezuelan encephalitis virus, mainly distributed in Africa and the Americas. Japanese encephalitis virus, forest encephalitis virus, dengue virus, yellow fever virus, St. Louis encephalitis virus, and West Nile encephalitis virus are classified into the genus Flavivirus of the genus togavirus.

Hepatitis virus (10%):

Including hepatitis A, B, C and hepatitis viruses, hepatitis virus refers to the pathogen causing viral hepatitis. The human hepatitis virus is classified into type A, type B, non-A, B and D viruses. Hepatitis A virus is spherical, non-enveloped, and the nucleic acid is single-stranded RNA. Hepatitis B virus is spherical, has a double-shell structure, and the outer layer is quite a general viral envelope. The nucleic acid is double-stranded DNA. Non-A, non-B hepatitis and hepatitis D viruses are currently under investigation.

Rabies virus (10%):

It is a serum/genotype 1 virus in the Rhabdoviridae Lyssavirus, and Type 2-6 is called a "rabies-associated virus" and is currently only found in Africa and Europe. Rabies virus is a link between wild animals (wolves, foxes, moles, bats, etc.) and domestic animals (dogs, cats, cattle, etc.) and humans. People are mainly infected by diseased animals or poisoned animals. Once infected, if effective prevention and treatment measures are not taken in time, it can lead to serious central nervous system acute infectious diseases, and the mortality rate is high. Tens of thousands of people die in rabies every year in developing countries in Asia, Africa and Latin America.

Influenza virus (20%):

Influenza virus, abbreviated as influenza virus, is an RNA virus that causes influenza in people, dogs, horses, pigs and poultry. In taxonomy, influenza virus belongs to the family of positive mucus, which causes acute upper respiratory tract. Infection, and through the rapid spread of air, there is often a cyclical pandemic around the world. The virus was first discovered in 1933 by the Englishman Wilson Smith, who called H1N1. H stands for hemagglutinin and N stands for neuraminidase. The numbers represent different types.

Lymphocytic choriomeningitis virus, etc., among the above-mentioned many viruses, Coxsackie virus group B type 1 to 5 (especially type 3 most common) and Coxsack group A virus 1,4,9,16 and Type 23 virus, group B of Coxsackie virus is the first pathogen of human myocarditis, according to its classification, the most common in group 2, 4, followed by type 5, 3, 1; group 1, 4, 9, 16 23, each type is easy to invade babies, occasionally invade adult myocardium, viruses of 6,11,12,16,19,22 and 25 in Echovirus, influenza virus, mumps and poliovirus are most common .

Pathogenesis

First, the virus directly acts

In the experiment, the virus can be injected into the blood circulation and can be myocarditis. The virus directly invades the myocardium through the blood flow. The virus itself causes cytolysis. It is also called the viral replication phase. It is the early stage of the virus. The virus actively replicates in the cardiomyocytes and directly acts on the myocardium, causing the myocardium. Injury and dysfunction, some people infected the Coxsackie B virus for 3 days, it can be found that the myocardium has scattered necrotic lesions, there are obvious inflammatory cell infiltration and myocardial necrosis after 5-7 days of infection, the virus caused infection after the body Receptors mainly rely on the cell membrane of the body, it has been confirmed that the receptor of Coxsackie B virus is located on human chromosome 19, because Coxsackie virus B, type A receptor exists on the human myocardial cell membrane, It can translate this kind of virus information, so this kind of virus can proliferate and replicate in cardiomyocytes, leading to myocardial damage. In addition, the virus may also produce toxins locally, resulting in myocardial fiber dissolution, necrosis, edema and inflammatory cell infiltration. Most scholars believe that acute fulminant viral myocarditis and viral death within 1 to 2 weeks of sudden death, the virus directly invades the myocardium, Myocardial damage may be the main pathogenesis, based on the fact that the virus is found in the myocardium from the autopsy. Inoculation of the virus by myocardial isolation may cause the disease, and the titer of the neutralizing antibody of the same type of virus in the serum is increased, in addition, in the acute During the period, mainly within 9 days of onset, the virus can be isolated from the myocardium of the patient or animal, the virus fluorescent antibody test results are positive, or virus particles are found during electron microscopy.

Second, the immune response for most viral myocarditis, especially chronic myocarditis, is currently believed to cause disease mainly through immune allergies, experimental and human viral myocarditis after 9 days of onset can no longer find the virus in the myocardium, but myocarditis continues It indicates that the immune response plays an important role in the pathogenesis. Some patients have mild symptoms of viral infection and myocarditis is quite serious. In some cases, the symptoms of myocarditis appear after the beginning of other symptoms of viral infection, and some patients may have myocardium. The discovery of antigen-antibody complexes, all of which suggest the existence of immune mechanisms, the mouse cardiomyocytes infected with a small amount of Coxsackie virus in the experiment, the cytotoxicity is not significant, such as the addition of the same kind of immune spleen cells, the cytotoxicity is enhanced, such as When the spleen cells were treated with anti-thoracic antibodies and complement, the cytotoxicity was not enhanced. If the spleen cells were treated with Coxsackie B antibody and complement in advance, the cytotoxicity was increased. Experiments show that there is a cell-mediated immune mechanism in viral myocarditis. The study also suggests that cytotoxicity is mainly mediated by T lymphocytes. Clinically, viral myocarditis prolongs unhealed, E-flowered, lymphocyte transformation rate, complement C It is lower than normal, anti-nuclear antibody, anti-myocardial antibody and anti-complement are higher than normal, indicating that the immune function is low in viral myocarditis. Recently, the activity of natural killer cells and alpha interferon in viral myocarditis have been found. It was also significantly lower than normal, gamma interferon was higher than normal, and it also reflected the loss of cellular immunity. In mice, experimental myocarditis increased the severity of the disease and increased mortality after the immunosuppressant cyclosporine A. After 1 week of infection, Administration reduces mortality.

Viral myocarditis prevention

1. Correct the cause and cause

The relationship between intestinal infection and upper respiratory tract infection and viral myocarditis has been relatively clear, so it should be actively prevented, focusing on enhancing physical fitness and improving immunity. Coxsackie B virus (CVB) is most closely related to myocardial disease in enterovirus. Therefore, CVB vaccine has important significance in the prevention of viral myocarditis. The research and application of inactivated vaccine, synthetic peptide vaccine, genetic engineering vaccine and DNA vaccine will be of great significance in preventing the occurrence of viral myocarditis.

2, pay attention to rest

Bed rest is the best way to reduce the heart load, and is also an important treatment for the acute phase of viral myocarditis. Rest can reduce the heart rate and blood pressure of patients with myocarditis. Generally, the general routine is 3 months, and the rest is 3 months. Severe myocarditis should be Strict bed rest until normal temperature, ECG and chest X-ray changes return to normal and then gradually get up, strengthen physical exercise, improve the body's disease resistance, avoid fatigue to prevent viruses, bacterial infections, pay attention to rest after the onset, into a nutritious diet, Eli recovered the heart.

Spring to prevent myocarditis:

In recent years, due to the wide application of antibiotics, the rheumatic fever caused by streptococcal infection is gradually reduced, the incidence of rheumatic myocarditis is significantly reduced, and the incidence of viral myocarditis is increasing. Viral myocarditis can be caused by a variety of viral infections, among which Koza Base virus B is the most common, chickenpox and EB virus can also be caused. According to the study, about 5% of infected people can affect myocarditis in the heart after infection. It can directly invade the myocardium after viral infection, or it can be caused by viral infection. Caused by autoimmune reaction, the former is more common in children, the latter is more common in adolescents, and spring is a high season of viral myocarditis, which should cause people to be vigilant.

Symptoms of upper respiratory tract infection or intestinal infection, 7-10 days later, chest tightness, palpitations, extreme fatigue, easy sweating and other symptoms. At this time, if you do an electrocardiogram, you may find arrhythmia and myocardial damage in premature beats. ESR, myocardial enzyme assay may increase, after 2-4 weeks, the Coxsackie virus antibody is detected, and the anti-myocardial antibody may be positive.

Viral myocarditis complications Complications, arrhythmia, heart failure, dilated cardiomyopathy

The disease often has complications such as arrhythmia, heart failure, sudden cardiac death and dilated cardiomyopathy, and severe cases can be life-threatening.

Viral Myocardial Inflammatory Symptoms Common Symptoms Muscle soreness, apical beats, diffuse tachycardia, left ventricular diastolic dysfunction, palpitations, weight loss, diarrhea, palpitations, fever, cardiac output, increased sinus node disease

The clinical manifestations of this disease depend on the patient's age, gender, type of virus infection, body reactivity and range of lesions. The severity of the disease varies greatly and is not specific. It is easy to cause misdiagnosis or missed diagnosis. The diagnosis of viral myocarditis must be established. Based on evidence of myocarditis and evidence of viral infection, mild cases are asymptomatic and subclinical, or mild symptoms; severe cases may occur with enlarged heart, cardiac insufficiency, severe arrhythmia, shock, and even sudden death.

1. History of viral infection: 50% to 80% of patients have fever, burnout, body muscle aches, runny nose and other upper respiratory tract infections caused by "cold" symptoms or nausea, vomiting, diarrhea and other gastrointestinal symptoms; some patients Symptoms are mild and neglected. Although there are no obvious prodromal symptoms at this time, it is not possible to exclude viral infections. It is also caused by other viral infections (such as hepatitis, mumps, etc.). Cardiac involvement is often preceded by viral infections. Symptoms appear gradually after 1 to 3 weeks.

2, Symptoms: Most patients have mild symptoms and subclinical or concealed type. Only electrocardiogram changes and suspected and diagnosed, or pathological changes of myocarditis found in death due to car accident or death from other diseases. A few patients are pervasive due to pathology. There is a large area of myocardial necrosis and a fulminant episode, manifested as acute heart failure, cardiogenic shock or sudden death.

Among the clinical patients, about 90% of the patients with arrhythmia as the main complaint or the first symptom, often complained of fever, diarrhea or flu symptoms, palpitations, fatigue, chest tightness, dizziness, etc., severe cases may appear syncope or A-S syndrome, Heart enlargement, arrhythmia or heart failure are manifestations of significant impairment of the heart. Some patients may have varying degrees of chest pain. The reasons may be:

(1) accompanied by pericarditis.

(2) Myocardial necrosis is extensive.

(3) Decreased cardiac output causes relative coronary insufficiency.

(4) Viral infection causes occlusive coronary arteritis.

3, signs:

(1) arrhythmia: the most common, and often the first performance of the patient's attention, a variety of arrhythmia can occur, pre-contraction is the most common, followed by atrioventricular block, severe arrhythmia is the main cause of sudden death .

(2) Heart rate change: visible persistent sinus tachycardia that is not proportional to body temperature. If manifested as bradycardia, attention should be paid to the presence of atrioventricular block.

(3) Heart sound changes: the first heart sound is reduced or split, and it is a fetal heart sound. It can smell the third heart sound or the fourth heart sound. In severe cases, there may be galloping, and when pericarditis can be heard, the pericardial friction sound.

(4) murmur: apical area audible and systolic hairy murmur, and fever, anemia caused by increased blood flow velocity and expansion of the heart cavity; can also smell diastolic murmur, the relative mitral valve caused by the expansion of the heart cavity Due to the narrowness, the intensity of the noise is not more than 3, and the disease can disappear after the condition is improved.

(5) Heart enlargement: The heart of patients with mild disease does not enlarge or expand significantly, and the heart of the severe heart is obviously enlarged.

(6) Heart failure: In severe cases, acute heart failure can occur, and even cardiogenic shock can occur.

Examination of viral myocarditis

1, routine testing and serum enzymology immunological examination

(1) Leukocytes can be slightly increased, but the left shift is not obvious, and the blood sedimentation rate of 1/3 to 1/2 cases is mild to moderately fast.

(2) In the acute phase or chronic myocarditis, there may be serum aspartate aminotransferase (AST), aspartate aminotransferase (GOT), lactate dehydrogenase (LDH), creatine phosphokinase (CK) and its isoenzymes. (CK-MB) increased, some patients with serum transaminase, creatine phosphokinase increased, reflecting myocardial necrosis.

(3) Serum cardiac troponin I (cTnI) or troponin T (cTnT) increased (based on quantitative determination) has greater value.

(4) Plasma myoglobin, myocardial myosin light chain can also be increased, indicating myocardial necrosis, the degree of increase is often positively correlated with the severity of the disease.

(5) The activity of superoxide dismutase (SOD) in erythrocytes of viral myocarditis has been found to be low.

Viral myocarditis leukocyte immunoassay, often found that peripheral blood natural killing (NK) cell viability decreased, alpha interferon titer low, while gamma interferon titer increased, E rosette and lymphocyte conversion rate decreased, total blood T cells (OKT3), T helper cells (OKT4) and suppressor T cells (OKT8) were lower than normal, while OKT4/OKT8 ratio was unchanged, complement C3 and CH50 decreased, antinuclear factor, anti-myocardial antibody, rheumatoid factor, anti-complement antibody The positive rate is higher than normal.

2, ECG

The diagnosis of this disease is highly sensitive, but the specificity is low. Some people think that if there is no ECG change, it is difficult to diagnose myocarditis in clinical practice. Arrhythmia, especially pre-systolic contraction, is the most common, and ventricular premature contraction accounts for various stages. 70% of the anterior contraction, followed by the atrioventricular block (AVB), with a degree of atrioventricular block more common, usually return to normal within 1 to 2 weeks after treatment, II degree and III degree AVB is not uncommon, Sometimes accompanied by bundle branch block, mostly indicating a wide range of lesions, most of the conduction block is temporary, disappeared after 1-3 weeks, but a few cases can exist for a long time, even must install a permanent pacemaker, in addition, some cases After the conduction block is restored, if the virus is infected again or relapse due to excessive fatigue, etc.

About 1/3 of the cases have repolarization abnormalities, which can be manifested as ST-T changes. In addition, ventricular hypertrophy, prolonged QT interval, and low voltage changes may also occur. Viral myocarditis produces multiple arrhythmias. The possible cause is myocardial Changes in cell membrane properties, in addition, fibrotic rupture after myocardial lesions, myocardial fibrosis, myocardial fiber bundles separated by collagen fibers can reduce the lateral conduction velocity of impulse, viable cardiomyocytes in necrotic myocardium can also become conduction abnormalities and as ventricular rhythm An abnormal pacemaker.

(1) ST-T changes: T wave inversion or reduction is common, sometimes it can be changed by ischemic T wave, and ST segment can be slightly displaced.

(2) arrhythmia: in addition to sinus tachycardia and sinus bradycardia, ectopic rhythm and conduction block are common, atrial, ventricular, atrioventricular junction premature beats can occur, about 2 / 3 patients With ventricular premature beats as the main manifestation, premature beats may have a fixed interval of joints, but most of the unfixed joint spacing, partially consistent with parallel contraction, this premature beat without fixed interval may reflect ectopic excitability, patients except There are no other findings other than premature beats, which may be from focal lesions. Premature beats may be monogenic or multi-source, supraventricular or ventricular tachycardia is relatively rare, but ventricular tachycardia may cause fainting. Atrial fibrillation and flutter are also seen, and flutter is relatively rare. The above-mentioned various rapid heart rhythms can be repeated in a short burst, and it is also sustainable. Ventricular fibrillation is rare, but for the cause of sudden death, one to three degrees of sinus, Atrioventricular, bundle or branch conduction block can occur, about 1/3 of patients rapidly develop into third-degree atrioventricular block after onset, which becomes another mechanism of sudden death. These arrhythmias can be combined, heart rhythm Malfunction can be seen in the acute phase, in recovery The disappearance of the relapse can also cause persistent arrhythmia with the formation of scars, which is one of the foundations for the recurrence of premature beats.

3, X-ray inspection

About 1/4 of patients have different degrees of heart enlargement, and the pulsation is weakened. The degree of enlargement is consistent with the degree of myocardial damage. Sometimes there is pericardial effusion (viral myocardial pericarditis). In severe cases, there is pulmonary congestion or pulmonary edema due to left ventricular dysfunction. .

4, echocardiography

Echocardiographic changes in viral myocarditis are not specific. Due to the wide spectrum of the disease and the different clinical manifestations, echocardiography (UCG) can vary from completely normal to obvious abnormalities. Generally, the following changes can be made:

(1) Cardiac enlargement: It is usually a general increase, but it can also be mainly left ventricular or right ventricular enlargement. Depending on the severity and extent of the ventricular lesions involved in the virus, the ventricular wall beat is weakened, and the generality is weakened. If it is focal or localized myocarditis, it can be characterized by regional wall motion abnormality, which is characterized by decreased exercise, loss of movement or even contradictory movement. In middle-aged and elderly patients, it is necessary to distinguish it from coronary heart disease.

(2) may have left ventricular contraction and/or diastolic dysfunction, manifested as decreased cardiac output, decreased ejection fraction, decreased short-axis shortening score, decreased wall motion, end-systolic and/or end-diastolic left ventricle The inner diameter increased, the mitral E peak decreased, the A peak increased, the A/E ratio increased, the left ventricular peak filling rate decreased during diastole, the peak filling time prolonged, and the atrial systolic filling increased.

(3) Due to myocardial necrosis, fibrosis and inflammatory cell infiltration, myocardial echogenicity is different from normal myocardium, which can be manifested as enhanced echogenicity and heterogeneity of myocardial echo, but lacks specificity. The above changes are also seen in various myocardium. disease.

(4) Other changes include temporary thickening of the wall, associated with temporary interstitial edema, and sometimes wall thrombus.

5, nuclear examination

2/3 patients can see a decrease in left ventricular ejection fraction. The use of 201 (201Tl) and 99m(99mTc)-MIBI myocardial perfusion imaging is valuable for understanding whether viral myocarditis is focal or diffuse myocardial necrosis. Recently, 111In (indium)-labeled monoclonal anti-myosin antibody imaging was performed to examine myocardial necrosis, with high sensitivity (100%), but lack of specificity (58%), and radionuclide 67Ga (gallium) development diagnosis Viral myocarditis also has high sensitivity. In addition, cardiac function status and degree of injury can be assessed by radionuclide gate angiography. Radionuclide myocardial imaging is a non-invasive test that is easily accepted by patients and has high sensitivity. In the future, research on the specificity of myocarditis must be strengthened.

6, virological examination

The clinical significance of pharyngeal and anal swab virus isolation is not significant, because most myocarditis is caused by immune allergic reaction. When the clinical symptoms appear, no virus can be isolated from the throat swab or feces. Even if the virus is isolated, it is difficult to determine the myocarditis virus. If the virus is isolated from the myocardial biopsy by myocardial biopsy, or by immunofluorescence, enzyme staining and other immunohistochemical techniques to detect viral gene fragments or viral protein antigens, although the specificity is high, most patients have obvious cardiac symptoms. The intramyocardial virus is no longer present. It is only suitable for early stage and infants. It has little practical value in clinical application and has certain risks. At present, it is widely used to confirm the specific virus antibody in duplicate serum. Viral myocarditis, commonly used in clinical practice are:

(1) Determination of virus neutralizing antibody: Take the serum of the acute phase and the second serum after 2 to 4 weeks, and determine the titer of the homologous virus neutralizing antibody. If the second serum titer is 4 times higher than the first time. Or once 1:640, it can be used as a positive standard. If the serum reaches 1:320 as a suspected positive, if it is based on 1:32, it should be 256 positive and 128 is suspected positive.

(2) Hemagglutination inhibition test: In the influenza epidemic, in order to clarify the relationship between influenza virus and myocarditis, the hemagglutination inhibition test can be used to detect the antibody titer of the two serum influenza viruses in the acute phase and the recovery phase, if the recovery serum is earlier Antibody titers 4 times, or 1 1: 640 positive, in addition, the use of enzyme-labeled immunosorbent assay (ELISA) to detect specific IgM and IgG may also be helpful.

(3) Virus-specific IgM: positive for 1:320, if there is a blood-borne enterovirus nucleic acid-positive person, it is more supportive of recent viral infection.

Diagnosis and diagnosis of viral myocarditis

diagnosis

Diagnosis can be based on medical history, clinical symptoms, and laboratory tests.

Differential diagnosis

1, rheumatic myocarditis

Rheumatic myocarditis is one of the important manifestations of rheumatic fever, and its incidence is related to streptococcal infection. Therefore, children with rheumatic myocarditis have a history of streptococcal infection before the onset, such as tonsillitis, pharyngitis, scarlet fever, etc. Yes:

(1) It is more common in school-age children and adolescence, infants and young children are rare, and viral myocarditis can occur in any age group, including newborns, infants and even adults.

(2) cardiac involvement including endocardium, myocardium and pericardium, so called whole heart inflammation, the most common endocardial involvement, especially the mitral valve and aortic valve, and viral myocarditis mainly invades the myocardium. It can also involve the pericardium. This is called viral myocardial pericarditis, and it is rare to involve heart valves.

(3) Rheumatic myocarditis is mainly manifested as galloping. Electrocardiogram is mainly caused by P2R interval prolongation (É degree atrioventricular block), severe arrhythmia is rare, and viral myocarditis has various types of premature beats, but also different degrees of sinus block, atrioventricular block And tachycardia, etc., in addition, rheumatic myocarditis caused by sudden death is rare, and viral myocarditis can cause sudden death in sick children.

(4) Laboratory tests for rheumatic myocarditis may have evidence of streptococcal infection, such as high anti-"O", positive C-reactive protein, etc., and viral myocarditis mainly manifests as abnormalities in myocardial zymogram or antibodies related to viral infection. The titer is elevated and the immunoglobulin is abnormal.

2, endocardial fibroelastosis

Endocardial fibroelastosis (EFE) and myocarditis have similarities. The pathological changes are mainly endocardial elastic fiber thickening, lesions may involve the valve, and subendocardial myocardium may also undergo degeneration or necrosis. In the infants that occur in about 6 months, the clinical manifestations are enlarged heart (mainly left ventricular) and congestive heart failure, which can be induced by upper respiratory tract infection. The electrocardiogram shows high voltage, suggesting that the atrium or ventricle is large (left ventricle) Most of the viral myocarditis is low voltage and ST2T wave abnormalities. EFE echocardiography is mainly characterized by enhanced endocardial reflection, thickening, and myocardial contraction. Most of the viral myocarditis is normal. When there is heart failure, the heart chamber is enlarged, the myocardial contraction is weak, and a few of the pericardial effusion signs are visible.

3, primary cardiomyopathy

Primary cardiomyopathy in children may have a family history, prolonged onset, long course of disease, mostly dilated (congestive) cardiomyopathy, arterial embolism, negative virus isolation, no short-term serum virus neutralizing antibody titer Internal increase, electrocardiogram often has a variety of arrhythmia, more serious than viral myocarditis, pathological Q wave, etc., its clinical features are significantly enlarged heart, X-ray manifestations of the heart is generally enlarged or spherical, weak heart beat, echocardiography Tuduo shows that the left atrium of the left atrium is large, the heart function is reduced, and the ventricular wall hypertrophy can also be displayed. The electrocardiogram can have high voltage, various arrhythmia and non-specific ST and T wave changes, but more recent data indicate that some viruses Myocarditis can evolve into clinically dilated cardiomyopathy, and some so-called primary cardiomyopathy may be a late manifestation of chronic viral myocarditis or myocarditis, making it difficult to identify.

4. Kawasaki disease

This disease is also known as skin and mucous membrane lymph node syndrome, the cause of which is still unclear, mainly involving skin, mucous membranes and lymph nodes. It is more common in infants and young children under 5 years old. Its clinical manifestations are fever (mostly high fever, lasting more than 5 days, antibiotic treatment is invalid) ), rash, combined with membranous inflammation, erythema of the lips, dry mouth mucosal inflammation, non-suppurative lymphadenitis, 10% to 40% of children with heart involvement, mainly coronary arteritis, may have myocardial ischemia, myocardial infarction or aneurysm rupture Sudden death, the disease needs to be differentiated from myocarditis when the heart is involved, but myocarditis usually does not have persistent fever, does not affect the skin mucosa and lymph nodes, echocardiography can sometimes find coronary dilatation and aneurysm.

5, non-viral myocarditis

(1) toxic myocarditis caused by diphtheria in children with myocarditis is prone to atrioventricular block, bundle branch block and premature beat, heart failure occurs quickly, and easy to cause cardiogenic shock, according to epidemiology of the disease Diagnostics and differential diagnosis have been made. In recent years, due to the widespread use of triple vaccines, the incidence of diphtheria has been greatly reduced, and myocarditis caused by diphtheria has become rare.

(2) Rocky Mountain spot heat (RM SF) is caused by rickettsial infection, mainly in the United States, Canada, Mexico, Central America and South Africa. Its clinical features are headache, fever and rash triad, RMSF due to Transmission, can be caused by rickettsial vasculitis and thrombosis caused by myocarditis, central nervous system damage, renal dysfunction, vascular collapse, pulmonary edema and ligament of the fingers and fingers, laboratory tests can have thrombocytopenia, low blood sodium, immunohistology The RMSF can be confirmed by examining the rickettsia or by PCR to find a rickettsial nucleic acid sequence in the bloodstream.

6, other diseases that cause myocardial damage

(1) autoimmune diseases including rheumatoid, systemic lupus erythematosus, nodular polyarteritis, dermatomyositis, scleroderma, etc., can cause myocardial damage, but the common feature of such diseases is often involving multiple Organs, therefore, in addition to myocardial damage, such patients can still see joints, skin, kidney, liver and spleen and other damage, laboratory tests showed rapid blood sedimentation, rheumatoid factor, anti-nuclear antibody positive, lupus cell positive.

(2) The glycogen accumulation disease is mainly sputum glycogen accumulation disease, which may have heart enlargement and heart murmur is not obvious. The electrocardiogram characteristic of PC is P wave high tip, P2R interval is shortened, QRS wave voltage is increased, and this disease is often violated. Skeletal muscle, so children often have low muscle tone.

7, beta receptor hyperfunction syndrome

Intrinsic is more common in young women, often with certain mental factors as incentives, complaints are more variable, and objective signs are less, no fever, elevated erythrocyte sedimentation rate and other evidence of inflammation, mainly manifested as ST segment of ECG, T wave changes and sinus tachycardia Speed, oral propranolol 20 ~ 30mg after half an hour can make ST segment, T wave changes back to normal; and ST-T changes caused by viral myocarditis caused by myocardial damage, can not recover after oral propranolol Normal, in addition, beta-receptor hyperfunction syndrome has no evidence of cardiac enlargement, cardiac dysfunction and other structural heart disease.

8, pericardial effusion

Viral myocarditis can sometimes involve the pericardium, or pericardial effusion, called viral myocardial pericarditis. At this time, it should be differentiated from pericarditis caused by other causes. Rheumatic pericarditis is often a part of rheumatic whole heart disease. Other manifestations of rheumatic fever, the two identify more difficult, suppurative pericarditis often have purulent infection, systemic poisoning symptoms, blood culture or pericardial culture is easy to be positive, antibiotic treatment is effective, tuberculous pericarditis more tuberculosis History and tuberculosis symptoms, less involving the myocardium, rarely cause arrhythmia, low pericardial sugar content, sometimes bloody, anti-tuberculosis treatment effective, if treated improperly can become constrictive pericarditis, and viral myocardium Pericarditis generally does not have a large amount of effusion, and there is little sign of cardiac tamponade. The pericardial culture is negative, only a few may form constrictive pericarditis. As for tumor, urinary pericarditis, each has its clinical characteristics. Identification with viral myocarditis, no further details.

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