Mr. Han came to the follow-up clinic and everything was normal, with no signs of what had happened. Seven years ago, thirty-five-year-old Mr. Han had a week of intermittent sinking in the precordial region, which occurred at work and rest, usually for no more than ten minutes. On the eighth night, while drinking with friends, this feeling reappeared, and the degree was significantly increased, and the crushing pain was unbearable and did not ease for half an hour. Mr. Han called 120 in a panic, and it was this call that saved his life. If he hadn’t been in the emergency vehicle when the sudden ventricular fibrillation occurred, it is estimated that Mr. Han would have crossed the threshold of death. Mr. Han arrived at the resuscitation room about 3 hours before the chest pain occurred, and the doctor diagnosed acute extensive anterior wall myocardial infarction and gave the recommendation of emergency coronary angiography + stent implantation. Mr. Han, who had experienced a life-or-death situation, did not hesitate to sign immediately. After some thrombus aspiration, intracoronary injection of anti-platelet drugs, balloon dilation and stent implantation, the blood flow in the anterior descending branch returned to normal. Mr. Han gave up his life of smoking and drinking, and started to lead a healthy lifestyle with regular work and rest, a rationed diet, less salt and oil, smoking and alcohol cessation, regular follow-up, medication compliance, and moderate exercise. Seven years have passed since then, and Mr. Han is no different from a normal person. Mr. Han’s experience is more than usual among many myocardial infarction patients, but the simple story is never as simple as it seems. First, why did young Mr. Han suffer from myocardial infarction? Young Mr. Han was not as healthy as he thought he was. He had a number of cardiovascular risk factors: long smoking age, heavy smoking, alcohol consumption, elevated LDL, and a family history. Body image is inherited and so are diseases, and his family history indicates that Mr. Han’s blood vessels are more susceptible to damage than the average person. Vessels that are susceptible to damage are corroded by smoking, alcohol, and high blood lipids with lipid deposition, inflammatory response, and plaque formation. Under the stimulation of alcohol and emotion, the edge of the plaque ruptures and bleeds secondary to thrombus formation blocking the vessel, leading to ischemic necrosis of the heart muscle. The anterior descending branch is the largest vessel in the heart, supplying the entire anterior wall of the heart, and proximal blockage will lead to myocardial necrosis of the entire anterior wall. To prevent myocardial infarction, we must prevent coronary atherosclerosis, and to prevent plaque rupture and bleeding in coronary arteries that are already hardened. To do so, we must strictly control the effects of various adverse factors, including tobacco and alcohol stimulation, poor diet, little movement, overweight and obesity, violent mood swings, as well as hypertension, diabetes, hyperlipidemia, chronic kidney disease, hyperhomocysteinemia, and hyperuricemia. The earlier control can protect the blood vessels from damage, do not be delayed by the propaganda that taking drugs is harmful to treatment (see is a drug is three times more toxic, it should be used). Second, why are the ECG and ultrasound still normal after the heart attack? Because of the extensive anterior wall myocardial infarction, even if stents are implanted, most of them will leave myocardial necrosis and complications such as heart enlargement, myocardial hypokinesis and heart failure, which can often be seen on ECG and echocardiography. Han’s normal ECG and echocardiogram were related to his correct emergency response, not to his youth. Mr. Han’s first call for an ambulance won him precious time to save his life. Imagine what would have been the end if the cardiac arrest had not occurred in an emergency vehicle, with no medical care around and no defibrillator waiting for him. Second, the first decisive signature provided the possibility of timely implementation of surgery. After the doctor gave his advice, he did not dwell on the possible complications that delayed the decision but signed decisively. His full trust and understanding minimized the delay. For a heart attack, time is the heart muscle, the earlier the opening the more the heart muscle can be saved, the later the opening, the greater the extent of myocardial necrosis. A complete opening of the blocked vessel within 3 hours of onset is likely to save most of the myocardium on the verge of necrosis; within 3 to 12 hours, only part of the ischemic myocardium can be saved; beyond 12 hours, the chance of emergency opening is basically lost, except for a few cases. In addition, the angina attack one week before the infarction also plays a role in protecting the myocardium to a certain extent, that is, the phenomenon of “ischemic pre-adaptation”. Why is there no “left ventricular remodeling” after infarction? Reconstruction, as the name implies, is the structural deformation of the heart in response to myocardial necrosis, thereby alleviating the effects of myocardial necrosis on function, and can play a compensatory role for a period of time. Signs of LV remodeling include enlargement of the heart, thinning and loss of motion in the necrotic zone, thickening and increased motion in the non-necrotic zone, and valvular regurgitation. Once left ventricular remodeling is initiated, it is difficult to terminate, and as the degree of deformation increases, function decreases and eventually fails to compensate for heart failure. The extent of myocardial necrosis is a major factor in initiating remodeling, and the most effective means to avoid remodeling is to reduce the extent of myocardial necrosis. First-time myocardial salvage after acute myocardial infarction can minimize the risk of remodeling and is a key step in the prevention and treatment of heart failure. Mr. Han’s complete opening of the vessel within three hours of onset prevented the “left ventricular remodeling” caused by myocardial necrosis and prevented the occurrence of heart failure. Seizing the key point of the event chain can not only win at the time, but also win the future. Fourth, can myocardial infarction be avoided? Mr. Han had a prognosis a week before the infarction, but his lack of vigilance led to acute extensive anterior wall myocardial infarction due to failure to seek timely medical attention. If early diagnosis and treatment are possible, avoiding acute myocardial infarction is not a dream. The sinking a week before is a manifestation of unstable angina pectoris. Unstable angina and myocardial infarction are completely similar in their pathogenesis: both are caused by rupture and bleeding of unstable atherosclerotic plaques in blood vessels and secondary thrombosis. Depending on the degree of vessel occlusion by thrombus, the clinical manifestations are unstable angina, non-ST-segment elevation myocardial infarction, and ST-segment elevation myocardial infarction. The clinical manifestations are unstable angina pectoris when the blockage of blood vessel is mild, the blood flow is little affected, and there is myocardial ischemia but not yet myocardial necrosis; when the blockage of blood vessel is aggravated and some blood flow still passes through, a small part of myocardial necrosis can occur, which is called non-ST-segment elevation myocardial infarction; when the blood vessel is completely blocked, it leads to ST-segment elevation myocardial infarction. Of the three, ST-segment elevation myocardial infarction has the most rapid onset and is the most severe, and is prone to cardiac arrest and the greatest extent of myocardial necrosis. If aggressive antiplatelet therapy and anti-ischemic therapy are given before thrombus formation or early thrombus formation, it is possible to inhibit the expansion of thrombus to the point of complete blockage of blood vessels. Important insights from Mr. Han’s experience: 1. See a doctor promptly when heart disease symptoms appear; call for help promptly when the condition worsens; trust professionals and don’t delay the time. 2.Adhere to a healthy lifestyle and regular follow-up after the acute phase to avoid re-damage of blood vessels. 3.Youngness is not a guarantee of vascular health; vascular health requires moderation and effort at all times.