The heart is one of the most active organs in the human body, and there are a large number of cellular enzymes in the heart to accomplish various physiological activities. After an acute infarction (AMI), because of myocardial ischemia and necrosis or increased cell membrane permeability, the cellular enzymes in the myocardium are released into the blood. Therefore, changes in serum enzymes can be used to reflect the occurrence of AMI and the size of the lesion. At the same time, due to the different physiological characteristics of various enzymes, such as: different intracellular localization, different molecular weight, different biological half-life, etc., resulting in the time of entry of various enzymes into the blood, the speed of entry into the blood and the duration of different in the serum, which provides the basis for clinical use as a judgment of the course of disease and healing. Cardiac enzymes are a group of enzymes related to myocardial injury and have been used for decades. In the past, most hospitals in China examined myocardial enzymes including LDH, CK, CK-MB, a-HBDH and GOT, which have some auxiliary effect on the diagnosis of myocardial injury, but now the diagnostic value of myocardial enzyme profile has lagged behind due to the emergence of myocardial markers. The disadvantage of myocardial enzyme profile is that it lacks tissue specificity, and many other tissue injuries can also lead to increased activity of various enzymes, in addition, the time of elevation is late, for example, AST ↑ at 6-12h in acute infarction, peaks at 48h, and returns to normal at 3-5d. Relying only on myocardial enzyme profile to assist in the diagnosis of myocardial disease is likely to delay the timely diagnosis of myocardial injury, or even miss the diagnosis, which is a great medical risk. For this reason, the combination of troponin and cardiac enzyme profile compensates for the deficiencies of cardiac enzyme profile to assist in the diagnosis of cardiomyopathy. Troponin exists only in cardiomyocytes and is considered the most specific biochemical marker for AMI diagnosis. cTnI, due to its small molecular weight, is rapidly released from the cardiomyocyte plasma after onset and the blood concentration rises rapidly; they appear early, as early as 2 h after the onset of symptoms; the degradation process of troponin from myogenic fibers lasts for a long time and can remain elevated in the blood for a longer period of time. Therefore, it has the advantages of early elevation of CK-MB and long diagnostic time window of LD1. In AMI patients, it rises 3-6 hours after the onset of the disease, and the sensitivity of the test reaches 100% within 10-120 hours after the onset of the disease. The increase can last for 2-3 weeks in patients with late or high peaks. It is more relevant in patients with non-Q-wave MI, subacute MI, or in patients whose prognosis cannot be determined with CK-MB. It has a wide diagnostic window (4-10 days) and is the non-enzymatic marker with the longest maintenance time. In addition, the magnitude of cTn increase in myocardial injury is large, 5 to 10 times higher than that of CK-MB. Therefore, it can also be used for the diagnosis of micro-myocardial injury (MMD), which is difficult to do with previous enzymatic markers. cTn also has prognostic value and should be considered high risk in any patient with coronary artery disease, even if ECG or other tests (e.g. exercise test) are negative, as long as cTn is elevated. It is the best marker for early diagnosis of AMI. For pediatric patients, the normal reference value of cardiac troponin spectrum is mostly the adult standard, while the normal reference value for pediatric patients is higher than that for adults, and the majority of children have a cardiac troponin spectrum that is 2-3 times higher than the normal reference value, so do not assume that a pediatric patient with an increased value of cardiac troponin spectrum is suffering from myocarditis, but should use the determination of cardiac troponin to aid in the diagnosis of myocarditis.