Myocarditis in children

Introduction to Pediatric Myocarditis Myocarditis is a focal or diffuse inflammatory infiltration of the myocardium with necrosis and/or degeneration of adjacent cardiomyocytes, which is characterized by myocardial ischemic damage associated with coronary lesions. Myocarditis is associated with a variety of causes and pathogenic factors. Infectious myocarditis includes viruses, bacteria, rickettsia, spirochetes, fungi and parasitic infections, of which viral myocarditis is most common. Chagasdisease is caused by Trypanosomacruzi infection, which occurs in South America and Brazil. It can be caused by acute myocarditis in the acute phase. Most of them are latent and the symptoms are not obvious. The dilated heart muscle is formed in the chronic phase. The disease began to show that the heart was significantly enlarged, heart failure and arrhythmia occurred, leading to death. Immune-mediated diseases, both chemical and physical factors can cause myocarditis, which is often part of a systemic disease. basic knowledge Sickness ratio: 2% Susceptible people: children Mode of infection: non-infectious Complications: arrhythmia, bradycardia, atrial fibrillation, atrial flutter, heart failure, cardiogenic shock

Causes of pediatric myocarditis

Common causes (45%):

Common causes of myocarditis, viruses that cause viral myocarditis are adenoviruses (especially serotypes 2 and 5) and enteroviruses (coxsackieviruses A and B, echovirus, poliovirus), among which Coxsackievirus B group (CVB) is the most common.

Other causes (35%):

Other viruses that cause viral myocarditis include: herpes simplex virus, varicella and herpes zoster virus, giant cell inclusion body virus, rubella virus, mumps virus, hepatitis C virus, dengue virus, yellow fever virus, rabies Virus, respiratory enterovirus, etc.

In recent years, the application of polymerase chain reaction (PCR) technology to detect viral gene sequences has improved the etiology of myocarditis. It has been reported that 58 cases of viral myocarditis have been reported. The age of children is 2 days to 13 years old. Small RNA virus, the positive rate was 48%, of which 4 cases were spotted and identified as Coxsackie B3 virus. In the past, the cause of the disease was unknown. The so-called idiopathic myocarditis or interstitial myocarditis, some of which may be viral myocarditis .

Pathogenesis

Pathogenesis

The pathogenesis of myocarditis has not yet been fully elucidated. According to recent research results, Canadian scholars Liu and Mason have divided the pathogenesis of myocarditis into three stages, namely, the stage of viral infection, the stage of autoimmune and the stage of dilated cardiomyopathy.

Recent studies have shown that mammals have Coxsackie virus and adenovirus co-receptors (CAR). CAR can facilitate the entry of these viruses into cells after contact with cells, which is a key step in viral infection, complement flexin attenuation acceleration factor. (DAF) and integrin V3 and V5 have the role of assisting CAR. The immune response is produced after viral infection. Once the immune system is activated, it enters the autoimmune phase. At this stage, T cells use host cells as molecular similarities. Target attack, some cytokines and cross-reactive autoantibodies can accelerate this process. The activation of T cells is related to viral peptides. The related cytokines include tumor necrosis factor alpha, interleukin-1 and interleukin-6. In the stage of dilated cardiomyopathy, myocardial remodeling, Badorff and Knowlton and other studies show that Coxsackie virus protease is involved in myocardial remodeling, and other related factors include matrix metalloproteinase, gelatinase, collagenase and elastase. The application of the agent can significantly reduce the degree of dilated cardiomyopathy. In addition, the virus can directly cause myocardial fineness. Apoptosis.

2. Pathological changes

The heart shows different degrees of enlargement. The myocardium is very soft in appearance. Under the microscope, there are monocytes in the connective tissue between the myocardial fibers and around the blood vessels, lymphocytes and neutrophils infiltrating, and the myocardial fibers are denatured to varying degrees. The horizontal stripes disappear, the sarcoplasm is coagulated and/or dissolved, and it is small focal, speckled or large necrosis, myocardial dissolution, nucleus and cytoplasm can disappear, residual cell membrane, heart disease distribution is often left ventricular and interventricular septum Heavy, followed by the right ventricle, the left and right atrium are the lightest, viral myocarditis is often accompanied by serous fibrinous pericarditis, the amount of exudate is small, and some have endocarditis, in chronic cases, in addition to myocardial fibrosis, Visible fibroblast proliferation and scar formation, endocardial elastic fiber hyperplasia and ventricular wall thrombosis, wall thrombus can cause brain, kidney, lung and other infarction, electron microscopy can see broken myocardial cells, myofilament loss, muscle fiber Protein structure destruction, mitochondrial degeneration and calcification, viruses can be isolated from the pericardium, myocardial or endocardium of death cases, and PCR can also be applied to the myocardium. Endocardium or the pericardium find specific viral nucleic acids, electron microscopy examination showed viral particles.

Pediatric myocarditis prevention

On weekdays, exercise should be strengthened to enhance physical fitness, prevent injections of various viral infections, and reduce adverse factors such as cold and fever. Prevent repeated colds during the treatment. Prevention of neonatal period must prevent viral infection in pregnant women, and do a good job of disinfection and isolation of the maternal and maternal and child rooms. Eat more fruits and vegetables to improve your personal resistance and moderate exercise.

Pediatric myocarditis complications Complications arrhythmia bradycardia atrial fibrillation atrial flutter heart failure cardiogenic shock

A variety of arrhythmia, pre-contraction more common, bradycardia (atrioventricular block) tachycardia (ventricular tachycardia, atrial tachycardia) may also have atrial fibrillation, atrial flutter. Concurrent heart failure, cardiogenic shock, multiple organ failure, Aspen syndrome, etc. Neonatal myocarditis often complicated by jaundice, multiple organ damage, DIC and so on.

Pediatric Myocarditis Symptoms Common Symptoms Systolic murmurs, convulsions, horses, heart sounds, edema, chest tightness, heart palpitations, arrhythmia, skin, cold, cold, sweat, fatigue

The clinical features are the severity of the disease, and the symptoms are lighter than those seen in the examination. Most of them have a history of viral infections such as upper respiratory tract infection or digestive tract infection within 2 or 3 weeks before the onset of cardiac symptoms.

Acute phase

New onset, clinical symptoms are obvious and changeable, the course of disease is no more than 6 months, mild symptoms, mainly fatigue, followed by sweating, pale, palpitations, shortness of breath, chest tightness, dizziness, lack of energy, etc., the examination can be pale, There may be bun around the mouth, and the first heart sound of the apex is low and blunt, and the soft squeaky systolic murmur is seen. Sometimes there is premature contraction, medium-sized contraction, and the onset is more urgent. In addition to the aforementioned symptoms, the fatigue is prominent, and the elderly often complain. Pain in the anterior area, the onset of acute illness may be accompanied by nausea, vomiting, check the heart rate is too fast or too slow, or the arrhythmia, the child is irritated, the hair may appear in the mouth, cold hands and feet, cold sweat, the heart may be slightly larger, The heart sound is blunt, the apex of the apex is shrinking, there may be galloping and/or various arrhythmia, low blood pressure, low pulse pressure difference, liver enlargement, some lungs have a voice, heavy weight is rare, and it is fulminant. Rapid onset, cardiac dysfunction or sudden cardiogenic shock within 1 or 2 days, the child is extremely weak, dizziness, irritability, vomiting, pain or pressure in the precordial area, some breathing difficulties, sweating, cold skin , small babies refuse to eat, array Trouble, weakness, cold hands and feet, difficulty breathing, check to see gray, lips, cold limbs, fingertips cyanosis, weak or untouchable, low blood pressure or not measured, heart sounds blunt, the first heart sound of the apex almost Can not hear, there may be systolic murmur, often galloping, tachycardia, slow or severe arrhythmia, lungs have voice, liver can rapidly increase, and some have acute left heart failure, pulmonary edema, condition Rapid development, such as rescue is not timely, life-threatening.

2. Deferred period

After the acute phase, clinical symptoms recurred, ECG and X-ray changes were delayed, and laboratory tests showed signs of disease activity, and the course of disease was more than half a year.

3. Chronic phase

Progressive heart enlargement, or repeated heart failure, the course of disease lasts for more than 1 year, the chronic phase is more common in children, some of the onset is hidden, and it is chronic when found; some are insufficient in the acute phase or the treatment is not timely and repeated many times. Caused by chronic phase, often delayed for several years and died of infection, arrhythmia or heart failure.

Examination of pediatric myocarditis

Laboratory inspection

1. General inspection

Leukocytes are slightly elevated, neutrophils are increased, and blood sedimentation is slightly increased.

2. Myocardial enzyme

Serum aspartate aminotransferase (GOT), creatine phosphokinase (CPK), creatine phosphokinase isoenzyme (CPK-MB), lactate dehydrogenase (LDH), and alpha-hydroxybutyrate dehydrogenase (HBDH) in the acute phase Both can be elevated, but the increase in CPK-MB is more meaningful for the diagnosis of myocardial injury.

(1) CPK-MB: CK in normal human serum is almost all CK-MM, accounting for 94% to 96%, and CK-MB is less than 5%. CPK-MB is a myocardial-specific cytoplasmic isoenzyme. The normal serum contains a small amount. If the serum CK-MB is significantly increased, it is more likely to be involved in myocardial involvement. Compared with the total activity of CK, it has a higher specificity for judging myocardial injury. Sensitivity. Serum CK-MB 6% (ie, MB accounts for more than 6% of total CK activity) is considered to be a specific indicator of myocardial damage. Therefore, its level can be used as an early diagnosis basis for myocarditis.

(2) LDH: It is widely distributed in the body and has poor specificity, while LDH isoenzyme serum has diagnostic significance. For example, LDH1>LDH2 or LDH1>40% is more meaningful for the diagnosis of myocarditis. Since the increase in enzyme activity may have non-cardiac factors, comprehensive analysis should be performed in combination with clinical practice.

Troponin

Cardiac troponin T (cTnT) and cardiac troponin I (cTnI) are characteristic of myocardium and therefore have higher specificity than CK-MB. Recent studies have suggested that cardiac troponin has a higher diagnostic value for heart disease such as myocardial infarction and myocarditis. Troponin (Tn) is a regulatory protein of muscle tissue involved in the regulation of calcium activation in muscle contraction. It has three subunits: TnT, TnI and TnC. Tn is present in the myocardium and skeletal muscle, but the regulatory genes of the two are different and are easily distinguished by immunological methods. The current clinical application is to detect serum myocardial TnT (cTnT). Increased serum cTnT is a specific marker of myocardial injury, and 0.2 ng/ml is abnormal. cTnT is distributed in the cytoplasm of cardiomyocytes at 5%, and 95% binds to structural proteins of cardiomyocytes. In the early stage of myocardial injury, cTnT is first released into the bloodstream and the serum concentration is increased. Serum cTnT increased in patients with acute myocardial infarction within 3 hours after onset, which was higher than CK-MB and lasted for a long time. The sensitivity and specificity of serum cTnT in detecting myocardial injury in children with myocarditis were higher than those in CK-MB and LDH1. Serum cTnT is significantly elevated in mild myocardial injury and CK-MB activity is still normal, so its sensitivity to detecting myocardial minimal lesions is higher than CK-MB, which is important for the diagnosis of myocarditis. In addition, cTnT and cTnI last longer than CK-MB. There is a "long-term diagnostic window."

4. Virological examination

In the early stage, a specific virus can be isolated from the pericardial effusion, throat swab, and stool. Viral RNA can be detected by polymerase chain reaction. In the convalescent serum, the homologous virus neutralizing antibody or hemagglutination inhibitory antibody was increased or decreased four-fold compared with the earlier first serum, or the specific IgM was positive. In the case of death, the virus can be isolated from the pericardium, myocardium or endocardium, or the specific fluorescent antibody is positive. Electron microscopy can detect viral particles near myocardial necrosis. There are a few children with positive anti-cardiac antibodies. The titer of serum virus antibody in the recovery period was more than 4 times higher than that in the acute phase. Serum anti-myocardial antibodies are often elevated during the course of the disease.

Film degree exam

Electrocardiogram

There are many sinus tachycardia in the acute phase. Arrhythmia such as pre-systolic contraction, ectopic tachycardia, etc. are occasionally seen, but myocarditis can not be diagnosed by pre-systolic contraction. The most common ECG changes are T wave flatness or inversion and QRS low voltage, T wave changes may be caused by repolarization of myocardial cells in the lesion, and low voltage may be related to myocardial edema. If the subendocardial myocardium is extensively damaged, there may be ST-segment depression; in severe cases, there may be myocardial infarction-like ST elevation. A new Q wave appears on the ECG, or the original Q wave deepens, reflecting necrosis and scar formation in the area. The QT interval can be extended, and various degrees of conduction block are not uncommon.

2. Chest X-ray examination

In the acute phase, the heart beat is weakened, the left ventricle is extended, and the heart shadow is in a flask shape when the myocardial tension is poor, or the normal bow is lost. The heart shadow of a long-term person can be lightly and severely enlarged, showing a large size and a left ventricle. Pulmonary congestion or edema can be seen in heart failure. A few have pericardial effusion.

3. Echocardiography

In the case of heart failure, the left ventricular end-diastolic and end-systolic diameters increase, the shortening fraction and ejection fraction decrease, and the left atrial diameter increases. Sometimes the left ventricular free wall movement is inconsistent. The left ventricle does not increase in the light, but it may be seen that there is local abnormality in the free wall.

4. Radionuclide imaging examination

Positive myocardial imaging of 67Ga suggests myocarditis. Myocardial imaging with 111In monoclonal anti-myosin antibody can detect myocardial necrosis and contribute to the diagnosis of myocarditis.

Diagnosis and diagnosis of pediatric myocarditis

diagnosis

In September 1999, the National Symposium on Pediatric Myocarditis and Heart Disease was held in Kunming. The participants discussed the Diagnostic Criteria for Pediatric Viral Myocarditis at the Weihai Conference in Shandong in May 1994. The revised Diagnostic Standards are now published. For the reference of clinicians, this diagnostic criteria can not be used mechanically. Some patients with mild or occult susceptibility are easily missed. Only a comprehensive analysis of clinical data can make a correct diagnosis.

1. Clinical diagnosis basis

(1) cardiac dysfunction, cardiogenic shock or cardio-cerebral syndrome.

(2) Heart enlargement (X-ray, one of the manifestations of echocardiography).

(3) ECG changes: ST-T changes of two or more main leads (I, II, aVF, V5) with R waves mainly lasted for more than 4 days with dynamic changes, sinus conduction block, room Ventricular block, complete right or left bundle branch block, syndrome, polymorphism, multiple sources, paired or parallel pre-contraction, atrial tachycardia caused by non-compartmental node and atrioventricular reentry , low voltage (except newborn) and abnormal Q wave,

(4) CK-MB elevation or positive cardiac troponin (cTnI or cTnT).

2. Pathogen diagnosis basis

(1) Confirmation indicators: self-contained endocardial, myocardium, pericardium (biopsy, pathology) or pericardial puncture examination, found that one of the following can be diagnosed with myocarditis caused by the virus.

1 separate the virus,

2 using viral nucleic acid probe to detect viral nucleic acid,

3 specific virus antibody positive.

(2) Reference basis: One of the following may be combined with clinical manifestations to consider the myocarditis virus,

1 The virus was isolated from the stool of the child, throat swab or blood, and the titer of serum isotype antibody in the recovery period was increased or decreased by more than 4 times compared with the first serum.

2 In the early stage of the disease, the blood-specific IgM antibody is positive.

3 Virus nucleic acid probe was used to detect viral nucleic acid from the blood of the child.

3. Basis for diagnosis

(1) It has 2 clinical diagnosis basis, which can be diagnosed as myocarditis, and the evidence of viral infection at the same time or 1 to 3 weeks before the onset of the disease supports the diagnosis.

(2) At the same time, it has one of the evidences for the diagnosis of pathogens. It can be diagnosed as viral myocarditis and has one of the pathogens. It can be diagnosed as viral myocarditis.

(3) Where there is no basis for diagnosis, the necessary treatment or follow-up should be given, and the myocarditis should be diagnosed or excluded according to the change of the condition.

(4) should exclude rheumatic myocarditis, toxic myocarditis, congenital heart disease, connective tissue disease and myocardial damage of metabolic diseases, hyperthyroidism, primary cardiomyopathy, primary endocardial fibroelastosis , congenital atrioventricular block, cardiac autonomic dysfunction, beta receptor hyperfunction and drug-induced ECG changes.

4. Staging

(1) Acute phase: new onset, symptoms and positive test findings are obviously variable, and the general course of disease is within half a year.

(2) Prolongation period: clinical symptoms appear repeatedly, objective examination indicators are delayed, and the course of disease is more than half a year.

(3) Chronic phase: progressive heart enlargement, repeated heart failure or arrhythmia, mild and severe when the condition is over, the course of disease is more than 1 year.

Differential diagnosis

1. Rheumatic myocarditis: more common in preschool and school age children after 5 years old, with a history of pre-infection, in addition to myocardial damage, lesions often involving the pericardium and endocardium, clinical fever, large joint swelling and pain, ring erythema and subcutaneous Summary, physical examination of the heart enlargement, sinus tachycardia, systolic reflux murmurs can be heard in the anterior region, and pericardial friction can be heard. The anti-chain "O" increased, the throat swab cultured the group A streptococcus, the erythrocyte sedimentation rate increased, and the ECG showed a atrioventricular block.

2. -receptor hyperactivity: more common in girls aged 6 to 14 years old, the onset and exacerbation of the disease are often related to emotional changes (such as anger) and mental stress (such as pre-examination), symptom diversity, but similar to sympathetic The performance of increased neurogenic excitability. The heart sound of the physical examination was enhanced. The electrocardiogram showed T wave low level inversion and ST change, the propranolol test was positive, and the dobutamine stress echocardiography test showed that the heart receptor function was hyperactive.

3. Congenital atrioventricular block: mostly third-degree block, there may be syncope and Adams-Stokes syndrome in the history of the child, but most children are well tolerated, generally no chest tightness, palpitations, pale complexion, etc. . The electrocardiogram showed a third degree atrioventricular block, the QRS wave was narrow, and there was no dynamic change in the atrioventricular block.

4. Autoimmune diseases: more common systemic juvenile rheumatoid arthritis and lupus erythematosus. The main clinical features of systemic juvenile rheumatoid arthritis are fever, joint pain, lymph nodes, hepatosplenomegaly, congestive rash, increased erythrocyte sedimentation rate, increased C-reactive protein, leukocytosis, anemia and related organ damage. Involved in the heart, there may be an increase in myocardial zymogram and an abnormal electrocardiogram. It is not effective for antibiotic treatment and is effective for the treatment of drugs such as hormones and aspirin. Lupus erythematosus is more common in school-age girls, may have fever, rash, blood white blood cells, red blood cells and platelets reduced, lupus cells can be found in the blood, anti-nuclear antibodies positive.

5. Skin mucosal lymph node syndrome: more common in children 2 to 4 years old, fever, conjunctival hyperemia, diffuse hyperemia of oral mucosa, cleft palate, bayberry tongue, superficial lymphadenopathy, hard edema at the extremities, echocardiographic coronary artery There are many lesions. It should be noted that when severe skin mucosal lymph node syndrome is complicated by coronary artery damage, myocardial ischemia can occur in coronary artery infarction. At this time, abnormal Q wave can appear on the electrocardiogram. At this time, differential diagnosis should be made according to clinical condition and echocardiography.

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