Pediatric viral myocarditis

Introduction to viral myocarditis in children Viral myocarditis is a viral localized focal or diffuse interstitial inflammation and fibrosis, lysis or necrosis. Its clinical manifestations are diverse, versatile and variability. Causes of the disease Many viruses can cause human myocarditis, of which enterovirus is the most common virus, especially Coxsackie virus B1 ~ 6 type (CVB1 ~ 6 type) is more common, recent research data show that adenovirus is viral myocarditis One of the main causes. basic knowledge The proportion of the disease: the disease is more common in children with a history of rotavirus diarrhea, the incidence rate is about 0.5% -1% Susceptible people: young children Mode of infection: non-infectious Complications: arrhythmia, bradycardia, heart failure, cardiogenic shock, A-S syndrome

Causes of viral myocarditis in children

Virus infection (95%)

Many viruses can cause human myocarditis. Among them, enterovirus is the most common virus, especially Coxsackie virus type B1~6 (CVB1~6 type), among which Coxsack B1~B5 type is the most common; secondly; There are Coxsackie A4, A16 type; Ecovirus 9, 11, 22 virus infection, whether the disease and severity of the disease are related to the virulence of the virus and the susceptibility of the child. Recent research data indicate that adenovirus is one of the major causes of viral myocarditis.

Pathogenesis

Whether the disease and severity of the disease are related to the virulence of the infected virus and the susceptibility of the child, the current research on the pathogenesis mainly focuses on two aspects:

Immune mechanism

Some scholars in the United States and Japan have confirmed that the cellular immunity of viral myocarditis plays a leading role, followed by the local action of the virus. After infection with the coke-type Coxsackie B virus, the spleen is stimulated to produce home-reactive, cytolytic T lymphocytes. Cells, which have autoimmune effects on cardiomyocytes as antigens, have a lysis effect on infected and uninfected cardiomyocytes, cause extensive lesions, severe cell necrosis, and can produce virus-specific cytolytic T After lymphocytes and virus infection, there are myocardial antigens on the surface of cardiomyocytes that are altered by viruses. Since T lymphocytes can recognize this antigen and cause the infected cardiomyocytes to dissolve and cause inflammation, the above two T cells are all thymus-dependent T cells. After resection of the thymus, the virus does not re-infect the above reaction, the study also shows that the same pro-cardiac virus infection, different individuals have different degrees of disease, and some do not even have lesions, may be related to the genetic and physical status of the recipient, in addition to Scholars have shown that in addition to T cells, natural killer cells are also involved in the dissolution of cardiomyocytes, 1987 In the biochemical immunization laboratory of the Institute of Pediatrics, the mouse cardiomyocytes cultured in vitro were infected with Coxsackie virus. The mechanism of virus and T cell damage to the myocardium was found to be different. After the virus infects the cells, it is released after replication, resulting in autolysis of the cells. And the spread of infection; and T cells are killing cardiomyocytes, destroying the site of viral replication, and finally leading to the termination of viral infection. When the disease develops clinically, most of the infected myocardium is isolated from the virus, so scholars believe that myocarditis Myocardial injury is mainly a T cell-mediated autoimmune mechanism, and viral infection is the initiator of the immune response.

2. Research on free radicals

Oxygen free radicals refer to atoms and atomic groups with odd electrons. Oxygen is the most important electron acceptor in the body. In the process of oxidative metabolism, a variety of free radicals can be produced, which are extremely active and highly destructive to tissues. The three most common types are superoxide anion (O2-), hydrogen peroxide (H2O2), and hydroxyl radical (-OH). Normal myocardium contains many enzymes that can be removed at any time, mainly superoxide dismutase. (SOD), glutathione peroxidase, peroxidase, etc., oxygen free radicals lose the integrity of the cell membrane by affecting the metabolism of cellular lipids, proteins, sugars and nucleic acids, resulting in increased permeability, subcellular organelles And the destruction of proteins, enzymes and nucleic acids in the nucleus, impaired cell function, cell destruction, and death.

Pediatric viral myocarditis prevention

On weekdays, exercise should be strengthened, physical fitness should be enhanced, vaccination against various viral infections should be carried out, and adverse factors such as cold and fever should be reduced. In the course of treatment, it is necessary to prevent repeated colds. Prevention of neonatal period must prevent viral infection of pregnant women and do a good job. Disinfection and isolation of the baby room and maternal and child room in the maternity hospital.

Pediatric viral myocarditis complications Complications arrhythmia bradycardia heart failure cardiogenic shock A-S syndrome

A variety of arrhythmia, pre-contraction more common, bradycardia (atrioventricular block), tachycardia (ventricular tachycardia, atrial tachycardia) may also have atrial fibrillation, atrial flutter, and heart Failure, cardiogenic shock, multiple organ failure, A-S syndrome, neonatal myocarditis often complicated by jaundice, multiple organ dysfunction, DIC, heart-brain-hepatic syndrome.

Viral myocarditis symptoms in children Common symptoms Electrocardiogram abnormal shortness of breath shortness of breath, comfortable chest tightness, fatigue, diastolic, galloping, systolic murmur, pale, dizziness, inflammatory cell infiltration

It is reported that 40% to 80% of patients with viral myocarditis have a history of infection with pioneering viruses such as upper respiratory tract infection or diarrhea. The clinical manifestations of viral myocarditis often depend on the extent and severity of the disease, and the severity of the symptoms varies greatly. The light type may have no symptoms. Or manifested as fatigue, sweating, palpitations, shortness of breath, chest tightness, dizziness, pale, signs: tachycardia (or slow), the first heart sound is low blunt, when there is diastolic galloping and 3, 4 heart sounds, Mild systolic murmurs in the apical region and various arrhythmias (pre-contraction are more common), severe onset is more urgent, can be manifested as heart failure and/or cardiogenic shock, severe arrhythmia, sudden death, severe Available in the following types (can appear overlapping):

Heart failure type caused by acute pump failure

This type of sudden congestive heart failure and / or cardiogenic shock, and then can develop liver, pancreas, kidney and brain and other organ failure, this type of emergency echocardiography can sometimes see ventricular septum Ventricular hypertrophy, ventricular hypertrophy with heart function is also reduced in parallel, cardiac function and cardiac hypertrophy return to normal time for weeks or years, acute ventricular hypertrophy may be caused by myocardial cell swelling and interstitial edema, long duration of hypertrophy It is speculated that it is related to factors such as cell infiltration.

2. A-Syst Syndrome

This type of sudden onset, extremely rapid, clinical manifestations of sudden syncope, severe loss of consciousness, pale, often accompanied by convulsions and incontinence, auscultation of bradycardia (complete atrioventricular block) or tachycardia ( Ventricular tachycardia), the former is more common, ECG can identify the type of arrhythmia, this type has many prodromal symptoms such as respiratory infection or intestinal infection, to the time of cardiac symptoms (average 1.5 days), acute phase (After temporary pacing or termination of ventricular tachycardia), more can return to normal, such as correct and timely treatment, the prognosis is better.

3. tachycardia

This type can express atrial tachycardia and ventricular tachycardia. The former has a longer duration of prodromal symptoms to cardiac symptoms (average 10 days, ie atrial myocarditis), mostly transient, and the prognosis is generally good. Atrial flutter, atrial fibrillation or shifting behavior of chronic atrial tachycardia, ventricular tachycardia (especially hemodynamic disorder) are often critically ill, can also occur sudden death, but mostly transient, acute phase After the tachycardia disappeared, the prognosis is later, and the residual ventricular contraction should be closely observed.

4. Neonatal myocarditis

Neonatal viral myocarditis can have diarrhea, pre-existing symptoms such as eating less or sudden onset of symptoms, clinical manifestations are mostly non-specific symptoms and involve multiple organs or similar severe sepsis, according to Cherry statistics 45 cases, feeding Difficulties accounted for 84%, cardiac symptoms 81%, shortness of breath 75%, cyanosis 72%, fever 70%, pharyngitis 64%, liver spleen 53%, bimodal type 35%, central nervous system symptoms 27%, hemorrhage or jaundice 13%, 8% of diarrhea, according to Rozkovec, neonatal Coxsackie viral myocarditis echocardiographic findings may be similar to dilated cardiomyopathy, or ventricular wall tumor-like changes, neonatal myocarditis progresses rapidly, high mortality The prognosis is poor and prone to prevalence. Since Javertt (1956) first reported the prevalence of neonatal myocarditis caused by Coxsackie B virus (in a baby hospital in a South African hospital, there were 10 neonates in a month or so). Of the 10 cases, 5 died and 3 cases were autopsied. The myocardium was mainly inflammation and necrosis, accompanied by multiple organ damage. Later, in Rhodesia, the Netherlands and the United States, there were several outbreaks. In recent years, there are also newborns in China. Viral myocardium According to reports of epidemic outbreaks, 38 cases of neonatal Coxsackie virus infection occurred in a hospital in a hospital in Northeast China (1993), and 14 cases (36.8%) were complicated with myocarditis, 8 of which were involved in multiple organ involvement in addition to myocardial injury ( There were 4 cases of liver damage, 4 cases of disseminated intravascular coagulation, and 2 cases of meningitis. There were clinical manifestations of severe sepsis, and 8 cases died. The pathogen was confirmed to be Coxsackie B3 and B5 viruses.

Examination of viral myocarditis in children

1. Myocardial enzymology changes

When the myocardium is damaged, the activity of more than 10 enzymes in the serum can be increased. Currently, it is mainly used for the diagnosis of viral myocarditis, creatine kinase (CK) and its isoenzyme CK-MB, lactate dehydrogenase (LDH) and its Isozyme LDH1, LDH2.

(1) Creatine kinase and its isoenzyme: Creatine kinase (CK) is mainly found in skeletal muscle, myocardium and brain tissue, so in many cases, myocarditis, muscular dystrophy, dermatomyositis, central nervous system Diseases (brain trauma, Reye syndrome, meningitis), neonatal asphyxia, myocardial infarction, etc. can increase CK, myocardial damage, usually rise in 3 to 6 hours after onset, 2 to 5 days At the peak, most cases return to normal within 2 weeks. It is known that CK has four isoenzymes, namely CK-MB (skeletal muscle type), CK-MB myocardium type, CK-BB (brain type) and mitochondrial isoenzyme. ASTm, isoenzyme (CK-MB) is mainly derived from myocardium, and is of great value for early diagnosis of myocarditis. The normal human serum has CK-MB of less than 5% (ie, MB accounts for less than 5% of total CK activity). Serum CK-MB activity 6% is an indicator of myocardial damage.

(2) Lactate dehydrogenase and its isoenzymes LDHl, LDH2: Lactate dehydrogenase (LDH) is a widely distributed enzyme, which is contained in the myocardium, skeletal muscle, liver, kidney and blood. In the case of disease, it can be elevated, but the specificity is poor. When the heart muscle is damaged, it starts to rise in the onset of 24 to 48 hours, reaches the peak in 3 to 6 days, gradually recovers in 8 to 14 days, and the elders recover in about 2 months. Because LDH isoenzymes have organ-specificity, LDH1 is mainly present in the myocardium, and LDH1 and LDH2 are increased in viral myocarditis. In particular, LDHl is mainly increased, resulting in LDHl>LDH2. Evaluation of serum myocardial enzyme activity: The normal values of serum myocardial enzyme activity are different in children at different ages, such as CK, CK-MB, LDH and -HBDH (-hydroxybutane dehydrogenase). The normal value of children can be higher than that of adults. See Table 2, 3 (Japanese Pediatric Normal Standard Value Research Group, 1997). The total CK activity value varies with age: the neonatal value is high, reaching the highest point in 6 to 7 months, and gradually decreasing after 1 year old, reaching the adult level at 15 years old. Xiang Yuexiang et al. determined the activity of CK-MB by immunosuppression in different age groups. The results showed that children of different age groups (n=1284) and healthy adults (n=411, age 17-65 years old) There were significant differences. The CK-MB activity in children of different age groups was significantly higher than that in the adult group; there were differences among different age groups, and gradually decreased with age and adults; there was no difference between men and women. The quality analysis of CK-MB (CK-MB mass in ng/ml) is more accurate than the viability assay (in U/ml). There is data showing that the normal reference value of CK-MB quality children is not affected by age, and is >4.0 ng/ml (immunochemiluminescence).

2. Cardiac troponin

Cardiac troponin (cTn) is a regulatory protein in myocardial contraction and relaxation. It consists of three subunits (cTnT, cTnI and cTnC), and cTnT is a subunit that binds to tropomyosin. Unit, cTnI is an inhibitory subunit of myofibril ATPase, cTnC is a calcium ion binding subunit. When cardiomyocytes are damaged, cTnT (or cTnI) is easily released into the blood through the cell membrane, making cTnT in the blood. Significantly elevated, the normal human serum cTnT content is very small, the upper limit of the normal reference value measured by different methods are also different, commonly used detection methods are radioimmunoassay (RIA), enzyme immunoassay, enzyme immunochemiluminescence (CLIA) cTn is a non-enzymatic protein serum marker with high specificity and high sensitivity for evaluating myocardial injury. It is characterized by early appearance and long duration. Kühl et al. (1997) studied 80 cases of clinically diagnosed myocarditis. cTnT, the results showed that the sensitivity of the diagnosis was 53%, specificity was 94%, and patients with clinically diagnosed myocarditis, if cTnT increased, highly suggestive of myocarditis.

Auxiliary inspection

1. ECG changes

There are many abnormal changes in the electrocardiogram in the acute phase, such as ST-T changes, pre-systolic and atrioventricular block.

(1) ST segment and T wave change, visible ST segment offset, T wave flat, bidirectional or inverted.

(2) all kinds of tachyarrhythmia, in the pre-systolic contraction, the most common ventricular premature contraction, mostly frequent, can be two or three law or pair, can be multi-source; Sexual and ventricular tachycardia, atrial flutter and tremors.

(3) conduction block: can be sinus block, atrioventricular block, left or right bundle branch block, double bundle branch block or even three bundle branch block, of which the third degree atrioventricular block Important, (4) QRS complex low voltage (except neonatal), QT interval prolongation and abnormal Q wave (pseudo myocardial infarction) are still visible.

2. X-ray performance

The heart size is normal or increased to varying degrees. In the case of heart failure, the heart is significantly enlarged and the pulmonary veins are congested. Under fluoroscopy, the heart beat is weakened.

3. Myocarditis radionuclide myocardial imaging

Radionuclide myocardial imaging can show changes in the characteristics of myocarditis: inflammation or necrosis imaging.

(1) Inflammation imaging: 67Ga myocardial imaging: 90% after 67Ga intravenous injection combined with transferrin, ferritin and lactoferrin in vivo. Leukocytes are rich in lactoferrin, 67Ga has the property of being taken up by myocardial inflammatory cells (T lymphocytes and macrophages, etc.), and 67Ga is easily aggregated into the inflammation site by ion or transferrin binding (enhanced vascular permeability) And development. 67Ga myocardial imaging has a higher diagnostic value for myocarditis. 67Ga-decanoic acid was injected intravenously, and imaging was performed at 24h and 72h after injection ( camera). According to the qualitative test of myocardial imaging, semi-quantitative diagnosis was made according to the ratio of heart and lung radioactivity distribution (H/L). The ratio of H/L concentration > 1.2 is positive. H/L 1.2 to 1.3 is mild, 1.3 to 1.4 is moderate, and >1.4 is severe.

(2) Necrosis imaging: 99mTc-PYP myocardial necrosis imaging: myocardial necrosis, calcium ions in the cardiomyocytes rapidly enter, forming hydroxyapatite crystal, 99mTc-PYP (pyrophosphate) is a bone imaging agent 2 to 3 hours after intravenous injection, it is adsorbed on the hydroxyapatite crystal of the myocardium, so that the myocardial necrosis is developed (normal myocardial tissue is not developed). The degree of concentration is related to the following factors: 1 blood flow; 2 necrosis time; 3 necrotic tissue number (tomographic imaging > 1g easy to detect), myocardial necrosis imaging in myocarditis, but less sensitive, 111ln-anti Myosin antibody myocardial necrosis imaging: when myocardial necrosis, myosin light chain is released into the blood circulation, while the heavy chain remains in the cardiomyocytes, and the 111In-labeled monoclonal anti-myosin antibody can specifically bind to the heavy chain. The myocardial necrosis was imaged, and the amount of binding was proportional to the size and extent of necrosis. It was inversely proportional to the local myocardial blood flow. Planar SPECT imaging was performed 24 hours after intravenous injection of 111In-anti-myosin antibody. Visible myocarditis was seen in myocardium. There is diffuse 111In-anti-myosin antibody uptake, Kühl et al (1997) reported 65 patients with suspected myocarditis, 48 cases of myocarditis and 17 cases of no myocarditis by endocardial biopsy immunohistochemistry; Antimyosin scintigraphy (AMS) showed that the specificity of AMS detection for immunohistochemical diagnosis of myocarditis was 86% and the sensitivity was 66%.

(3) myocardial perfusion imaging: currently 99mTc-MIBI (methoxyisobutyl isocyanide) is most commonly used, 99mTc-MIBI can be taken up by normal cardiomyocytes after intravenous injection, the amount of myocardial aggregation of radiopharmaceuticals and the crown of this area Arterial blood perfusion is positively correlated. In myocarditis, due to inflammatory cell infiltration, interstitial fibrous tissue hyperplasia, degeneration, etc., resulting in myocardial ischemia, normal myocardial cells are reduced, so radionuclide myocardial imaging normal and lightening The phase-to-phase radioactivity distribution (spotted changes) can make a prognostic diagnosis of myocarditis, but the specificity is poor.

4. Endomyocardial biopsy

(1) Histopathological diagnosis: Dallas histopathological diagnosis criteria The definition of myocarditis morphology is myocardial inflammatory cell infiltration, accompanied by adjacent myocardial cell necrosis and/or degenerative lesions, which can be divided into the following.

1 active myocarditis: active myocarditis must have inflammatory cell infiltration, and must also have adjacent degrees of damage and necrosis of myocardial cells.

2 critical myocarditis: critical myocarditis (borderline myocarditis) with inflammatory cell infiltration, but no myocardial cell damage or necrosis, need to confirm the endocardial myocardial biopsy.

3 no myocarditis: no myocarditis (no myocarditis) histology is normal, Hahn and other 31 centers of the diagnosis of myocarditis 2233 cases of endocardial myocardial biopsy (according to Dallas histopathological diagnostic criteria) confirmed active myocarditis in 214 cases (accounting for 9.6 %), 12 cases of critical myocarditis (0.5%), and no signs of myocarditis in 2007 (89.9%),

(2) Immunohistological diagnosis: In recent years, immunohistochemical examination has been successfully applied to the diagnosis of myocardial inflammatory process. Immunohistochemical features: activation of immune cells and expression of major histocompatibility complex antigens and adhesion molecules by various markers Enhanced, specific monoclonal antibodies (such as anti-CD2, anti-CD3, anti-CD4, and anti-CD8 antibodies) directly combined with human lymphocyte cell surface antigen for quantitative analysis of myocardial infiltration of inflammatory cells, specific monoclonal The number of antibody-binding lymphocytes was >2.0/high power field (x400). That is, the specific monoclonal antibody binding lymphocyte number is >7.0/mm2 positive, the major histocompatibility complex (MHC), and the human MHC is called HLA (human leukocyte antigen, HLA) gene or HLA gene complex, HLA gene mainly includes HLA-I and HLA-II genes, cell adhesion molecules (CAM), according to structural characteristics can be separated into the adhesion family, the selectin family, the immunoglobulin superfamily, etc. The anti-MHC or CAM monoclonal antibody is combined with myocardial MHC or CAM antigen to analyze the expression of MHC and CAM, which can display immunologically activated tissue markers, and there are abnormalities in the expression and quantity of MHC and CAM in viral myocarditis. (Schultheiss and Kühl) Clinical diagnosis of suspected myocarditis (359 cases) for histological and immunohistological analysis of endomyocardial biopsy.

Diagnosis and diagnosis of viral myocarditis in children

diagnosis

The clinical and virological basis of the 9-provincial myocarditis collaboration group proposed in China in 1978 has been widely used in clinical practice. The diagnostic criteria are:

Diagnose based on

Pathogenic diagnosis

(1) Separation of the pericardial puncture fluid, pericardium, myocardial or endocardium from the patient, or positive for specific fluorescent antibodies.

(2) The virus is isolated from the stool of the child, throat swab or blood, and the titer of the homologous virus neutralizing antibody in the serum of the recovery period is increased or decreased by more than 4 times compared with the first serum. 2. Clinical diagnosis basis (1) Main indicators: 1 acute and chronic cardiac insufficiency or cardio-cerebral syndrome, 2 with galloping and pericarditis, 3 heart enlargement, 4 electrocardiogram showing obvious arrhythmia (except for sporadic and frequent pre-systolic contraction) Ectopic rhythm, sinus arrest, second degree of atrioventricular, sinus, complete left or right and double, three bundle branch block), or significant ST-T wave changes (except for standard III leads) ST-T changes for more than 3 consecutive days), or positive for exercise test.

(2) Secondary indicators: 1 At the same time or 1 to 3 weeks before, there was a history of upper respiratory tract infection, diarrhea and other viral infections, 2 with obvious weakness, pale, sweaty, palpitations, chest tightness, dizziness, pain in the anterior region. Cold hands and feet, muscle pain and other symptoms, or at least two, infants may have antifeedant, cyanosis, limbs cold, binocular gaze, etc., newborns can be combined with maternal epidemiological history to make a diagnosis, 3 pre-cardiac area can be heard and the first heart sound is obvious Low blunt or quiet tachycardia, 4 electrocardiogram with mild abnormalities (referring to abnormal electrocardiogram abnormalities other than the above-mentioned obvious arrhythmia), 5 early stage may have serum creatine phosphokinase (CPK), aspartate aminotransferase (AST) or lactic acid Dehydrogenase (LDH) is increased, and anti-myocardial antibodies are increased in the course of the disease.

3. Diagnosis conditions

(1) There are 2 main indicators, or 1 main indicator and 2 secondary indicators (both ECG indicators are required).

(2) At the same time, one of the first to second items of pathogens is diagnosed as viral myocarditis. In the case of myocarditis, other systems in the body have obvious viral infections, and no virus should be virologically examined, combined with medical history. Clinically, it can be considered that myocarditis is also caused by a virus.

(3) Where all of the above conditions are not met, but clinically suspected to be myocarditis, long-term follow-up may be performed as "suspected myocarditis". If there is a systematic dynamic change, it may be considered as myocarditis or in the follow-up.

(4) When considering the above conditions, the following diseases should be excluded: rheumatic myocarditis, toxic myocarditis, tuberculous pericarditis, congenital heart disease, collagen disease and metabolic disease, myocardial damage, primary cardiomyopathy, Congenital atrioventricular block, Keshan disease, high altitude heart disease, neurological or electrolyte disorder, skin mucosal lymph node syndrome, benign premature contraction, and drug-induced ECG changes, etc.

4. The clinical stage is mainly based on the condition of the disease, and the length of the disease is only for reference.

(1) Acute phase: The symptoms are obvious and variable, and the course of the disease is more than 6 months.

(2) Recovery period: clinical symptoms and ECG changes gradually improved, but have not recovered, the course of disease is generally more than 6 months.

(3) prolongation period: clinical symptoms appear repeatedly, electrocardiogram and X-ray changes are not healed, and laboratory tests have symptoms of disease activity, and the course of disease is more than 1 year.

(4) Chronic phase: progressive heart enlargement or repeated heart failure, the course of disease is more than 1 year. In 1994, the National Pediatric Cardiovascular Conference revised the original diagnosis basis, and increased the number of children from the pathogen diagnosis basis. Myocardium or blood was detected by PCR method for enterovirus-specific nucleic acid protein; in the main indicators, the condition of positive nuclear test was increased, and some people were asked to diagnose acute myocarditis: see Table 7, score: 30 points for diagnosis, possible diagnosis 20 Points, less than 20 points can not be diagnosed.

5. Evaluation of Endocardial Myocardial Biopsy The endocardial myocardial biopsy has been carried out abroad since the 1980s, providing a basis for the diagnosis of myocarditis. Foreign countries advocate this as the only diagnostic basis. The pathological change of biopsy is The diagnosis is well-founded. In 1984, cardiac pathologists in some countries proposed the Dallas Criteria for the diagnosis of myocarditis in Dallas. It has been recognized by many scholars. (1) Diagnosis of pathological changes:

1 active myocarditis (with or without fibrosis): requires inflammatory cell infiltration and nearby cell damage including clear cell necrosis, vacuoles, cell shape, cell disintegration and extracellular lymphocytes, unaffected cells It is normal.

2 clinical myocarditis (non-diagnostic need for biopsy review): inflammatory infiltration sparse, no cell damage in the light microscope, such as the original biopsy specimens and then biopsy, found active myocarditis changes, can be exempted from biopsy.

3 no signs of myocarditis.

(2) Review biopsy results after treatment: divided into 3 categories:

1 (continuous) myocarditis: the degree of lesion is the same as or worse than the original test results.

2 dissipative myocarditis: inflammatory infiltration is less than before, and there are obvious repair changes.

3 Dissipated myocarditis: no inflammatory infiltration or cell necrosis left.

(3) Clinical manifestation combined with biopsy: In 1983, Fenoglio was based on 34 cases of myocarditis with a history of viral infection. The clinical manifestations combined with biopsy also classified myocarditis into three categories:

1 acute myocarditis: clinical manifestations of acute onset, heart failure, heart condition gradually deteriorated, most died within 6 months, a few improved or cured, autopsy and biopsy showed enlarged heart, extensive distribution of necrotic foci, myocardial necrosis , interstitial inflammatory exudation and edema.

2 rapid progressive myocarditis: clinical manifestations of acute heart failure, the heart condition gradually deteriorated, improved and worsened, heart failure repeated attacks, more than 6 months to 3 years of death, autopsy myocardial lesions extensive, scattered distribution of myocardial necrosis, It is accompanied by a repair process and local fibrosis, and a few have endocardial thickening and perivascular fibrosis.

3 chronic myocarditis: a long history of clinical disease, a slower condition, examination of cardiac insufficiency, heart failure often repeated many times, biopsy see scattered localized lesions, myocardial damage and interstitial fibrous exudation and inflammatory cells Infiltration, fibrosis is more obvious, the endocardial myocardial biopsy mortality of catheter method is 0.04% 0.07%, biopsy can provide 70%80% exact pathological basis, 1985~1994, GP and Armed Police General Hospital of PLA General Hospital The Hospital Pediatric Cardiovascular Research Center conducted a total of 103 endocardial myocardial biopsies, with no deaths, with a success rate of 96.9%, and a pathological diagnosis basis of 99.1%.

6. The problem that viral myocarditis should pay attention to in diagnosis

(1) Understanding of some electrocardiograms:

1 clinical can see the premature contraction or non-paroxysmal tachycardia, generally should be added as a standing body surface electrocardiogram, if the stereocardiogram is normal, it is caused by imbalance of neuromodulation, but if the stereocardiogram is still abnormal Suspected organic changes, combined with enzymatic examination and clinical manifestations to further confirm the diagnosis.

The identification of 2T wave changes, on the conventional body surface electrocardiogram, the volatility of T wave is very large, can be morphological, polarity change or amplitude anomaly, but also all three, so in the children or youth multi-lead T wave changes May be pathological, may also be non-pathological, so the necessary identification, A. half-past-two syndrome: "two and a half syndrome" II, III, aVF lead The T wave is inverted, so the child is easily misdiagnosed as myocarditis. The electrocardiogram is characterized by a frontal QRS axis of 90° and a T axis of -30°. The T-QRS axis is similar to the watch at 2:30, normal person T-QRS. The electric axis is in the warrior's heart. When the breath is at rest, the T wave returns to normal. C. The upright T wave changes: the polarity and shape of the T wave change with the change of the body position. When the erect position, the TI wave is inverted, or when lying down, TI Shallow inversion and deepening when deep or deep inhalation, more common in cardiovascular neurosis or elongated body type, obesity, pregnancy, ascites and other squat elevation, V5 ~ V6 T wave can also be low, even inverted, Lol can correct, D. T wave changes after hyperventilation: normal people can see the pre-cardiac lead T wave vibration after hyperventilation Decrease or invert, mostly occurs about 20s after hyperventilation, so each time an electrocardiogram is recorded during hyperventilation and calmness, if the T wave returns to normal after hyperventilation, it can be considered as a continuous "naive" T wave, and vice versa. The T wave returns to normal when breathing calmly, indicating that the T wave abnormality is caused by excessive ventilation.

3 ventricular premature contraction recognition: premature ventricular contraction accounted for 67.2% of all kinds of pre-contraction in children, often the QRS, ST-T wave malformation is not obvious, originated from the right ventricle and ventricular stage without obvious symptoms Pre-contraction is called "benign pre-contraction" or "functional pre-contraction", but according to our 45 patients with "benign pre-contraction" endocardial biopsy, except for 2 cases of histopathology, regardless of optical microscope and Electron microscopy showed different degrees of organic changes in the endocardium and myocardium, and 4 of them were endocardial, myocardial tissue polymerase chain reaction (PCR), confirmed by DNA specific fragment amplification Coxsackie The virus indicates the relationship between myocardial damage and viral infection, so it is considered that "benign pre-contraction" should be carefully observed and further examined.

(2) Enzymatic changes: When the virus is myocarditis, the myocardial cells are damaged, the cell membrane is destroyed, and the intracellular enzyme can be released into the blood. When the factors affecting the enzymatic changes are excluded, the enzymatic examination for the diagnosis of myocarditis, the degree of damage, Estimated efficacy is very helpful.

1CK, CK-MB: When the myocardium is damaged, it can rise in 3~6h, reach the peak in 2~5 days, return to normal in 2 weeks, CK-MB rises faster than the total activity of CK, but it fades quickly, so it is worthy of early diagnosis. Big.

2LDH and its isoenzymes LDH1, LDH2: when the myocardial damage, 24 to 48h began to rise, reached a peak at 3 to 6 days, returned to normal after 8 to 14 days, and increased LDH1 and LDH2 in myocarditis, LDH1/LDH2>1 If LDH is elevated, LDH1 does not increase, LDH1/LDH2.

3 Aspartate aminotransferase (AST): the general onset of 6 to 8h began to rise, reached the peak in the second week, more than 4 weeks to return to normal, its sensitivity and specificity is not as good as CPK, LDH and its isoenzyme, three myocardial enzyme sensitivity CK-MB is the best, the specificity is LDH1, CPK and isoenzyme appear early, and the regression is fast; LDH is the opposite; AST appears early, and the regression is late, and the disease duration is less than 2 months.

Differential diagnosis

Viral myocarditis should be identified primarily with the following diseases:

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 involve the pericardium and endocardium, clinical fever, large joint swelling and pain, ring erythema and subcutaneous nodules, physical examination of heart enlargement , sinus tachycardia, systolic reflux murmur can be heard in the anterior region, even the pericardial friction sound can be heard, the anti-chain "O" is increased, the throat swab cultures the group A streptococcus, the erythrocyte sedimentation rate increases, and the electrocardiogram can be There was a degree of atrioventricular block.

2. -receptor hyperfunction

More common in girls aged 6 to 14 years old, the onset and exacerbation of the disease are often associated with emotional changes (such as anger) and mental stress (such as pre-examination), symptom diversity, but similar to the performance of sympathetic excitability, physical examination heart sounds Enhanced, ECG has T wave low level inversion and ST changes, propranolol test positive, dobutamine stress echocardiography test cardiac beta receptor hyperfunction.

3. Congenital atrioventricular block

Mostly three-degree block, there may be syncope and Adams-Stokes syndrome in the child's medical history, but most of the children are well tolerated, generally no chest tightness, palpitations, pale, etc., ECG suggests third degree atrioventricular block The QRS wave is narrow and there is 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, ESR, C-reactive protein Increased, leukocytosis, anemia and related organ damage, involving the heart can have myocardial myocardial enzymes increased, abnormal ECG, effective for antibiotic treatment and effective for hormones and aspirin drugs, lupus erythematosus is more common in school-age girls, may have fever , rash, white blood cells, red blood cells and platelets are reduced, lupus cells can be found in the blood, and antinuclear antibodies are positive.

5. Skin mucosal lymph node syndrome

More common in children 2 to 4 years old, fever, conjunctival hyperemia, diffuse hyperemia of the oral mucosa, cleft palate, bayberry tongue, superficial lymph nodes, hard edema at the extremities, echocardiographic coronary artery lesions, need to pay attention to In severe cases of severe mucocutaneous lymph node syndrome complicated with 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.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.