Pediatric myocardial damage is currently the most common clinical diagnosis in the cardiovascular specialty and includes myocardial involvement from a variety of causes and cannot be diagnosed clinically as myocarditis, cardiomyopathy, precordial disease, or heart valve disease, which are collectively referred to clinically as myocardial damage. Mostly caused by or complicated by infection, arrhythmia, coronary artery disease, lack of oxygen, poisoning (drugs and toxins), metabolic diseases, neuromuscular diseases, hematological diseases, etc. Symptoms The main symptoms are long sigh, shortness of breath and slightly pale face; some older children may complain of precordial discomfort, chest tightness and fatigue after activity; or no symptoms. There are no obvious positive signs, no obvious abnormalities in cardiac examination, normal heart borders, strong heart sounds, some may have tachycardia or bradycardia, premature beats. Serum cardiac enzymes (GOT, CPK, CK-MB, LDH) can be elevated in the acute phase, but the elevation of CPK and CK-MB is more significant for the diagnosis of myocardial injury. Measurement of serum troponin (Tn) is often negative. ECG: ECG changes in myocardial damage are nonspecific and can present with various types of ECG abnormalities, but they are not sufficient for the ECG changes of myocarditis: minor T-wave changes, ST-segment shifts (limb conduction <0,05 mV< span="">, chest conduction <0,1 mV), QRS low voltage, and arrhythmias such as occasional premature beats, type I0 or II0I atrioventricular block The ECG changes may be milder, such as occasional premature beats, I0 or II0I AV block, intraventricular block, etc. (ECG diagnostic criteria for myocarditis are: 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 block, AV block, complete right or left bundle branch block, premature beats in association, polymorphic, multiple sources, paired or parallel, ectopic tachycardia due to non-atrial node and atrioventricular folding, low voltage (except in neonates) and abnormalities. except in newborns) and abnormal Q waves.) Echocardiography reveals normal cardiac structure and systolic function. Very small amount of pericardial effusion may be seen IV. Differential diagnosis Infectious myocarditis, rheumatic heart disease, congenital heart disease, primary cardiomyopathy, primary endocardial elastosis, congenital AV block, cardiac autonomic abnormalities, ion channelopathies (e.g., Brugada syndrome, long Q-T syndrome, catecholamine-sensitive ventricular tachycardia), β-receptor hyperfunction, and drug-induced Electrocardiographic changes. V. Treatment: 1. General treatment For those with symptoms, appropriate oxygen can be administered; pay attention to rest and sleep; avoid repeated infections; minimize activities, exempt school-age children from sports activities, and avoid violent crying in infants and children; 2. Anti-infective treatment For children with infections, active symptomatic anti-infective (bacterial, viral, mycoplasma, etc.) treatment is required. 3.Cardioprotective therapy Provide myocardial energy and promote myocardial cell repair; the course of treatment usually lasts 3-6 months. 4.Follow-up observation After 6 months of treatment, if the child still has electrocardiogram changes that do not recover, cardiac enzymes continue to rise, etc. (remove infection and other causative factors), it is necessary to improve the electrocardiogram, Holter, echocardiography, plate motion test, spiral CT of the heart, cardiac nuclear magnetic examination, etc., as appropriate, to re-evaluate the child's condition, clarify myocardial disease and whether there is coronary artery disease, and further adjust the treatment.