Myocarditis refers to a diffuse or focal infiltration of inflammatory cells in the interstitial myocardium and its adjacent myocardial fibers that are necrotic or degenerative due to infection or other causes. The main pathogen is a virus, but others such as bacteria, mycoplasma, protozoa, fungi, chlamydia, and poisoning and allergies can cause the disease. The pathological changes of myocarditis caused by various pathogens are non-specific, with enlargement of the heart chambers, especially in the left ventricle; focal or diffuse mononuclear cell infiltration can be seen in the acute phase, and diffuse myocardial necrosis and loss of myocardial fiber transverse striations can be seen in heavy cases.
Diagnostic points
1.Clinical manifestations
1/3~1/2 children have prodromal symptoms a few days or 1-3 weeks before the onset of the disease, manifested as respiratory infection or gastrointestinal symptoms. In mild cases, there may be no conscious symptoms and only ECG abnormalities. In infants and young children, the symptoms are depression, crying, pallor, fatigue, excessive sweating and loss of appetite, etc. Crying and pallor with episodic changes have important diagnostic value. Older children may complain of dizziness, fatigue, chest tightness, palpitations and precordial discomfort or even pain. In a few cases, cardiac insufficiency or sudden onset of cardiogenic shock may occur within 1 to 3 days, which may be life-threatening. Physical examination may show pallor, cyanosis around the lips, and cold hands and feet. The first heart sound in the apical region is diminished or depressed. Increased heart rate is common, and some may have bradycardia, often with arrhythmias, usually without murmurs. There are signs of cardiac insufficiency.
2.Auxiliary tests
Laboratory tests Serum creatine phosphate isoenzyme (CK-MB), lactate dehydrogenase (LDH), alpha-hydroxybutyrate dehydrogenase (alpha-HBDH) and portal aminotransferase (AST) are increased. elevated CK-MB can be used as a basis for early diagnosis; LDH has poor specificity, but LDH1 is higher than LDH2 or LDH1 is higher than 40% is significant for the diagnosis of myocarditis. Increased serum troponin (cTnT, cTnI) reflects higher sensitivity and specificity of myocardial injury.
ECG: flat or inverted T waves, reduced ST segment, low voltage, arrhythmias: may include premature beats, ectopic tachycardia, conduction block, prolonged Q-T interval, etc.
Echocardiography Left ventricular enlargement, decreased septal and posterior left ventricular wall motion, decreased left ventricular ejection fraction and shortening fraction may be seen. There may be a small amount of pericardial effusion and mitral valve incomplete closure.
Diagnostic criteria] (1999 national revised draft)
1. Clinical diagnosis based on.
(1) Cardiac insufficiency, cardiogenic shock or cardio-cerebral syndrome.
(2) Heart enlargement.
(3) EKG changes: ST-T changes in 2 or more major leads (Ⅰ,Ⅱ,aVF,V5) dominated by R waves for more than 4 days with dynamic changes, sinus atrial and atrioventricular block, complete right or left bundle branch block, paired or parallel premature beats, ectopic tachycardia caused by non-atrioventricular node and atrioventricular folding, low voltage (except in neonates) and abnormal Q waves.
(4) Elevated CK-MB or positive cTnI/cTnT.
2. Pathogenetic basis.
(1) Confirmation indicator Positive evidence of virology in endocardium, myocardium, pericardium or pericardial fluid.
(2) Reference basis Positive evidence of virological examination in stool, pharyngeal swab or blood.
3. Confirmation of diagnosis based on.
(1) With 2 clinical diagnostic bases, myocarditis can be clinically diagnosed. Evidence of viral infection at the same time or 1 to 3 weeks before the onset of disease supports the diagnosis.
(2) With one of the pathogenic confirmation basis, the diagnosis of viral myocarditis can be confirmed, with one of the pathogenic reference basis, the clinical diagnosis of viral myocarditis.
(3) Where no confirmatory basis is available, the necessary treatment or follow-up should be given to confirm or exclude myocarditis according to changes in the condition.
Differential diagnosis
1. β-receptor hyperfunction: ECG manifestation with tachycardia and non-specific ST segment and T wave changes, mostly seen in school-age girls. Propranolol test is positive, heart rate slows down after oral metoprolol, ST segment and T wave return to normal, and myocardial enzyme examination is in normal range.
2. Acute rheumatic allocarditis: In addition to symptoms similar to viral myocarditis, murmurs can be heard in the apical region, and some of them can be heard as gallop rhythm. The electrocardiogram shows first-degree AV block, increased ASO titer, moderate to severe increase in blood sedimentation, and obvious relief of symptoms and signs with anti-rheumatic treatment.
3. dilated cardiomyopathy: some dilated cardiomyopathies can be developed from viral myocarditis, generally viral myocarditis with acute onset, ECG with ST-T changes, QRS wave low voltage and arrhythmias are common, and heart enlargement is not as obvious as dilated heart disease, but sometimes myocardial biopsy is still needed to confirm the diagnosis.
Treatment points]
1.Basic treatment: In the acute stage, bed rest should be taken to keep as quiet as possible to reduce the heart load.
2, antiviral treatment: acute people are still in the stage of viraemia, antiviral treatment should be carried out, often choose triazolyl nucleoside, etc., severe myocarditis choose alpha interferon.
3.Treatment for myocardial damage.
(1) High-dose vitamin C: 100-200mg/kg each time, 10% glucose in 10-12.5% solution, intravenous infusion, once a day.
(2) Glucocorticosteroids: Not recommended for the common type. In severe myocarditis, progressive increase of CK-MB, combined heart failure, cardiogenic shock and lethal arrhythmia, glucocorticoids should be applied early, in sufficient amount and for a short period. Hydrocortisone 10mg/(kg.d) is often used as an intravenous drip, and the dose is reduced once the symptoms are relieved, or prednisone is used orally for 2 to 4 weeks. Intravenous gammaglobulin can be tried.
(3) Promote myocardial metabolism: fructose 1,6-diphosphate (FDP), ATP, coenzyme A, coenzyme Q10, etc.
(4) Other medications: Chinese herbal medicine Shengve drink, Huangqi, etc.
(5) Heart failure treatment: Those with heart failure should be corrected, and the dose of digitalis should be small, and attention should be paid to potassium supplementation.
(6) Arrhythmia treatment: Relevant medications can be administered according to the type of arrhythmia.