Viral myocarditis (VMC) is a focal or diffuse inflammation of the myocardium caused by a virus. The pathology is characterized by myocardial cell degeneration and necrosis, interstitial inflammatory cell infiltration, and fibrous exudate. It may be accompanied by pericardial or endocardial inflammatory lesions. The clinical presentation varies in severity. The prognosis is mostly good, but a few children may have heart failure, cardiogenic shock, or severe arrhythmias.
The detection rate of viral myocarditis confirmed by biopsy and autopsy is 1% to 31% in foreign data. According to a survey of pediatric viral myocarditis in 9 provinces and cities in China, there were significant regional differences in the estimated incidence and prevalence of myocarditis in children under 14 years of age, with an incidence of 29.15/100,000 and a prevalence of 41.86/100,000 in Harbin, and the lowest incidence of 6.88/100,000 and a prevalence of 8.03/100,000 in Fuzhou.
Etiology and pathogenesis
1, etiology: more than 30 kinds of viruses are known to cause myocarditis, the most common viruses are coxsackievirus (group B and A), adenovirus and echovirus, followed by cytomegalovirus, influenza and parainfluenza viruses, varicella virus, measles virus, herpes simplex virus, mumps virus, infectious hepatitis virus, human acquired immunodeficiency virus (HIV) and poliovirus. etc. Current studies have shown that microvirus B19 is the more common pathogen other than enterovirus and adenovirus. It is worth noting that coxsackievirus group B infection in the neonatal period can lead to a population epidemic, and its mortality rate can be as high as 50% or more.
2, pathogenesis: the pathogenesis of the disease is not fully understood. At present, it is believed that it is mainly related to the direct damage to myocardial cells caused by virus replication and myocardial damage caused by the virus triggering the body’s autoimmune response. In the acute phase, the virus invades cardiomyocytes through the relevant receptors of cardiomyocytes and replicates intracellularly, leading to cardiomyocyte degeneration, necrosis and lysis and apoptosis; the body is stimulated by the virus and activates cellular and humoral immune responses; studies have shown that cell-mediated cytotoxicity kills target cells mainly through two effects: one is through the action of perforin (PFP) and granzyme, specifically T cells , NK cells and target cells recognize and contact each other, the granule contents PFP and granzyme are released into the cell interstitial space, perforin punches holes in the target cell membrane, and granzyme enters the target cells to initiate apoptosis; secondly, apoptosis is induced by the action of Fas and Fas ligands. In addition, myocardial lipid peroxidation is enhanced after viral infection, and there is oxygen radical and lipid peroxidation damage. Persistent viral infection is thought to be one of the main mechanisms of chronic myocarditis and its evolution to dilated cardiomyopathy.
3. Pathological changes: cosmetically, the inflamed myocardial tissue is flabby, pale and scarred. In the microscopic view, clusters of plasma cells, lymphocytes and some eosinophilic erythrocyte infiltrates are seen in the acute stage, and giant cell infiltrates in the later stage.
Clinical manifestations] The clinical manifestations vary greatly in severity, depending on the age of onset and the acute or chronic course of the infection.
1, symptoms: newborns are often sudden onset, mostly secondary to systemic viremia, and involves multiple organ systems, including the heart. Older children have a history of upper respiratory tract infection or gastroenteritis within a month before the onset of the disease. In newborns, the disease is severe and progresses rapidly, with severe heart failure, fever, refusal to eat, vomiting, diarrhea and lethargy, respiratory distress, gray skin, pale extremities, rapid and weak pulse, swelling of the face and extremities, and often complicated by meningitis, pancreatitis and hepatitis. In older children, the onset of the disease is insidious, with symptoms of weakness, limited activity, palpitations, and chest pain. Some patients have a chronic process, evolving into inflammatory dilated cardiomyopathy.
2, signs: there may be apical region of the first heart sound low blunt, tachycardia, part of the gallop rhythm, can hear the pericardial friction sound, the heart boundary is mildly enlarged. In severe heart failure, shortness of breath and cyanosis, marked enlargement of the heart borders, wet rales in the lungs, hepatomegaly, and sunken swelling of the lower limbs. In severe cases, cardiogenic shock may occur suddenly, with a weak pulse and decreased blood pressure.
[Auxiliary examination
1. ECG examination: QRS low voltage, ST-T segment changes, prolonged Q-T interval, arrhythmias including various pre-term contractions, supraventricular and ventricular tachycardia, atrial fibrillation and ventricular fibrillation, and second- or third-degree atrioventricular block can be seen.
2.X-ray: The heart shadow is seen to be mildly to severely enlarged, and the heart beat is diminished.
3.Echocardiography: Cardiac ultrasound may show enlarged heart chambers, impaired left ventricular myocardial systolic function, occasional myocardial thinning and thrombus, and a small amount of pericardial effusion and mitral valve closure insufficiency.
4, laboratory tests myocardial damage blood biochemical indicators.
(1) Creatine phosphokinase (CPK) and its isoenzyme (CK-MB) can be elevated in 3-6 hours after the onset of disease, reaching a peak in 2-5 days and recovering within 2 weeks. Lactate dehydrogenase (LDH) and α-hydroxybutyrate dehydrogenase (α-HBDH) are elevated in the early diagnosis of myocarditis.
(2) Cardiac troponin (cTnI or cTnT) is usually elevated at 2-4 hours of onset and decreases to normal in 2-3 weeks. cTn is a non-enzymatic serum marker with high specificity (90%) and sensitivity for the evaluation of myocardial injury and is the preferred marker for the detection of myocardial injury.
5, cardiac magnetic resonance energy (CMR): CMR myocardial perfusion and myocardial activity examination has high sensitivity and specificity in identifying myocarditis, and has a certain diagnostic value for VMC.
6. Virological diagnosis: Virus isolation from pharyngeal swabs, pharyngeal washings, stool, blood, or viral nucleic acid testing and serum viral antibody assay from myocardium and blood in the early stage of the disease can help in pathogenic diagnosis. Serum virus antibody determination must be compared between the acute phase and the recovery phase.
7, myocardial biopsy: endomyocardial myocardial biopsy is still the gold standard for the diagnosis of myocarditis.
[Diagnosis] Diagnostic criteria for viral myocarditis (1999 revised draft, Kunming, China)
1, clinical diagnosis based on
(1) Cardiac insufficiency, cardiogenic shock or cardio-cerebral syndrome.
(2) Heart enlargement (X-ray and echocardiography have one of the manifestations).
(3) ECG changes: ST- in 2 or more major leads (I, II, aVF and V5) dominated by R waves
T changes lasting more than 4 days with dynamic changes, sinus and atrioventricular block, complete right or left bundle branch block, paired or parallel premature beats, ectopic tachycardia due to non-atrioventricular node and atrioventricular folding, low voltage (except in neonates) and abnormal Q waves.
(4) Elevated CK-MB or positive cardiac troponin (cTnI or cTnT).
2, pathogenetic diagnosis based on
(1) Confirmation index: The diagnosis can be confirmed by one of the following findings from endocardial, myocardial, or pericardial (biopsy, pathology) or pericardial puncture fluid examination. (1) isolation of virus; (2) detection of viral nucleic acid by viral nucleic acid probe; (3) positive specific viral antibody.
(2) Reference basis: Myocarditis can be considered to be caused by a virus if one of the following is present in combination with clinical manifestations Virus isolated from stool, pharyngeal specimen or blood, and the titer of serum isotype antibody in the recovery period is more than 4 times higher or lower than that of the first serum. The blood was positive for specific IgM antibodies early in the course of the disease. Viral nucleic acid was detected in the blood of the child with a viral nucleic acid probe.
Basis for diagnosis: Two clinical diagnostic bases are available for clinical diagnosis. Evidence of viral infection at the same time or 1 to 3 weeks before the onset of the disease supports the diagnosis. The diagnosis of viral myocarditis can be confirmed if one of the pathogenic confirmatory bases is also available, and the clinical diagnosis of viral myocarditis can be made if one of the pathogenic reference bases is available. If the diagnosis is not confirmed, the necessary treatment or follow-up should be given to confirm or exclude myocarditis according to the changes in the condition. Rheumatic myocarditis, toxic myocarditis, congenital heart disease, myocardial damage caused by rheumatic diseases and metabolic diseases (such as hyperthyroidism), primary cardiomyopathy, primary endocardial elastosis, congenital atrioventricular block, cardiac autonomic abnormalities, hyperreceptor function, and drug-induced electrocardiographic changes should be excluded.
Treatment】
1.Rest: Bed rest is required in the acute phase, and activity is restricted to reduce the cardiac load.
2, for the early stage of the disease is still in the viraemia stage, can be used to triazole nucleoside and other antiviral treatment.
3.Improve myocardial nutrition.
(1) High-dose VitC has the effect of eliminating oxygen free radicals. 100~200mg/kg.d, add 10% glucose solution 20~50ml, slowly push intravenously, the course of treatment is 3~4 weeks.
(2) Fructose 1,6 diphosphate (FDP) can improve myocardial energy metabolism, increase myocardial energy, and inhibit neutrophil oxygen radical generation. It can be administered as 100-250mg/kg intravenously for 1~3 weeks.
(3) Coenzyme Ql0 has the effect of protecting myocardium, 1 mg/kg.d, divided into two times, and used for 3 months.
(4) Astragalus has antiviral and myocardial protective effects, and can be taken orally for a long time.
(4) Astragalus has antiviral and myocardial protective effects, and can be given orally for a long time. Intravenous infusion of high-dose gammaglobulin increases cardiac preload, and heart failure should be closely observed for deterioration and allergic reactions during treatment.
5, adrenocorticotropic hormone and immunosuppressants: usually not used. For heavy patients combined with cardiogenic shock, lethal arrhythmias such as third-degree atrioventricular block or ventricular tachycardia, myocardial biopsy confirmed as chronic autoimmune myocardial inflammatory response, should be applied early and in adequate doses. Methylprednisolone 15-30 mg/kg for 1 to 3 days and then change to prednisone, or dexamethasone 0.5-1 mg/kg for 1 week and then gradually reduce the dose, or prednisone 2 mg/kg in three oral doses, and then gradually reduce the dose to 0.3 mg/kg after 1 to 2 weeks and maintain for 16 to 20 weeks. Immunosuppressant can be chosen from cycloheximide.
6.Anti-heart failure treatment.
(1) Fast-acting diuretics (tachyphylaxis 1mg/kg, 1 to 2 times a day)
(2) fast-acting positive inotropic drugs, such as dobutamine or dobutamine, are beneficial in seriously ill children.
(3) Oxygen and bed rest.
(4) Use digitalis with caution, especially in progressively deteriorating children, because the inflamed myocardium is very sensitive to digitalis, use only 1/2 of the usual dose, and ECG testing is required early in the application; and pay attention to potassium chloride supplementation to avoid digitalis toxicity. If serious arrhythmias or other signs of digitalis toxicity appear, stop using it.
7. Angiotensin II-converting enzyme inhibitors such as captopril are beneficial for children in the acute phase of the disease.