Recently a medical background hit drama has such an episode: an elderly man after the onset of the emergency room, the doctor’s initial diagnosis of acute myocardial infarction and recommended interventional treatment, the patient’s son inquired on the phone that myocardial enzymes have not been elevated when questioned “myocardial enzymes are not high how do you diagnose acute heart attack”? So, what exactly do doctors base their diagnosis of acute heart attack on? Acute myocardial infarction is an ischemic myocardial necrosis that occurs when the coronary artery blood supply is suddenly interrupted, resulting in severe ischemia and hypoxia of the myocardium. After the interruption of coronary blood flow, local diastolic dysfunction of the myocardium first appears, which is manifested as stiff and uncoordinated myocardial movement, followed by systolic dysfunction manifested as reduced or even no local movement, followed by ischemic chest pain and abnormal changes in ECG. If not treated, chest pain caused by heart attack usually gradually relieves after several hours to more than ten hours (at this time, the affected myocardium is necrotic). In the early stage of myocardial infarction, the ECG shows T-wave hyperacusis (called the super-acute stage, which can be fully recovered without leaving traces of infarction if treated in time, but most patients have not been seen at this time and the diagnosis cannot be determined by T-wave hyperacusis alone), after which ST-segment elevation and T-wave fusion show the typical pattern of acute infarction, and within a few hours to a day, the ST-segment gradually falls back while the T-wave decreases, and within a day to a few days Most patients are permanently left with Q waves and inverted T waves, while a few can recover or partially recover. Myoglobin levels in the blood begin to rise about 2 hours after the onset of infarction, but myoglobin is also contained in skeletal muscle, so myoglobin elevation cannot be used as a basis for confirming the diagnosis of myocardial infarction. Troponin (cTnT or cTnI) begins to rise about 6 hours after the onset of the attack, and creatine kinase and its isoenzymes (so-called “cardiac enzymes”) rise 6-12 hours after the onset of the attack. Timely and effective restoration of coronary blood flow after the onset of acute infarction is the key to saving the patient, and it is no exaggeration to say that “time is myocardium and time is life”. If treated within 3 hours of onset, a significant number of patients can make a basic recovery; within 6 hours, most patients can retain relatively normal heart function; after 12 hours of onset, the benefits of treatment are minimal. From another perspective, the acute phase of myocardial infarction is easily combined with fatal malignant arrhythmias, and the risk of arrhythmia increases accordingly with longer delay after onset, and the patient may have lost the opportunity for treatment before the family finally makes up its mind to receive intervention. At the same time, the longer the time, the more thrombus load in the blocked coronary artery, and the effectiveness and success of the treatment will be affected. Clinically, in order to start effective treatment as early as possible, to save the dying myocardium, protect cardiac function and improve prognosis, for patients with sudden chest discomfort, as soon as the electrocardiogram shows changes in ST-segment elevation, the doctor can give a working diagnosis of acute myocardial infarction (of course, it may be denied as the disease progresses and the examination indexes accumulate) and start emergency treatment procedures accordingly without waiting for the myocardial enzyme The results of myocardial enzyme tests are not required. The cost is that individual patients may not be in acute infarction, such as stress cardiomyopathy and some patients with acute myocarditis, whose clinical manifestations, ECG changes, and laboratory parameters resemble acute infarction and are treated as acute infarction in the early stage of the disease and undergo coronary angiography, but this is after all an isolated phenomenon, and the cost is definitely worth it. As a result, once ischemic chest pain lasts for more than ten minutes or is not relieved after taking nitroglycerin for more than five minutes, you should immediately go to a large hospital that can carry out emergency interventional treatment, and if the electrocardiogram shows signs of acute heart attack, you should follow the doctor’s advice and decisively undergo interventional examination. If you wait until the myocardial enzymes (or troponin) are elevated and the diagnosis of acute infarction is confirmed before starting treatment, the treatment effect obtained by the patient will be greatly reduced.