Myocardial infarction is the old name for myocardial infarction. Myocardial infarction is a necrosis of myocardial cells, which is irreversible. The process of structural and energy metabolic changes (myocardial remodeling) of the myocardium after myocardial infarction is also unstoppable, but its progression can be slowed down on the basis of reasonable medication. We use medication, or stenting or bypass to recanalize the originally narrowed coronary artery and restore myocardial perfusion, which may save the ischemic but surviving myocardium, but cannot restore the necrotic myocardium, and myocardial cell death is irreversible. Does that mean that since the necrotic myocardium is irreversible and since myocardial infarction has already occurred, it is futile to treat it again? Actually, it is not. Here, we need to add two concepts to our cognition, one is depressed myocardium, that is, the myocardial cells have temporarily lost their function due to the momentary lack of blood supply, if it is restored to the blood supply, this part of the myocardium can still restore its function; the other is hibernating myocardium, that is, due to the long-term insufficient blood supply, this part of the myocardium is like an animal hibernation, or a kind of adaptive pseudo-death, with the restoration of blood supply to improve, this part of the With the restoration of blood supply, the function of this part of myocardium can be gradually restored. Therefore, for these myocardium in the infarcted area, we need to identify whether it is truly dead, or whether it has temporarily lost function or is hibernating because of a chronic “food” deficit. In another analogy, when the water flow of an irrigation canal is reduced, the seedlings farthest away from the canal may be necrotic, but there are many seedlings close to the canal that will recover if the water supply is restored as soon as possible, so “time is myocardium” and the reason for doing interventions or bypasses to open blood vessels as soon as possible is to save more dying myocardium. The reason for going to interventional surgery or bypass to open the vessel as soon as possible is to save more dying myocardium and minimize myocardial necrosis. After the opening of the vessel, we will use beta-blockers and angiotensin-converting enzyme receptor antagonists to delay the process of structural and energy metabolic remodeling of the myocardium and slow down the development of heart failure as much as possible on the basis of conventional secondary prevention medication for coronary artery disease, provided that the patient’s blood pressure and heart rate are tolerable. That part of the necrotic myocardial cells in myocardial infarction is irreversible, and this part of the myocardium does not regenerate. We use myocardial reperfusion (percutaneous coronary intervention, thrombolysis or coronary artery bypass grafting) and drug therapy to save more dying myocardium, prevent infarct expansion, and delay the process of myocardial remodeling.