Acute coronary syndrome (ACS) is a group of clinical syndromes caused by acute myocardial ischemia, including acute myocardial infarction (AMI) and unstable angina (UA). Acute myocardial infarction is further divided into ST-segment elevation myocardial infarction and non-ST-segment elevation myocardial infarction according to the characteristics of ST-segment changes on the electrocardiogram. What is the reason for grouping these diseases in coronary artery disease? The pathophysiological basis of ACS is that coronary atherosclerotic plaques are extremely unstable and prone to rupture and secondary complete or incomplete occlusive thrombosis, leading to a variety of serious cardiovascular events in the clinical setting. There are different types of thrombi in patients with ACS, with ST-segment elevation myocardial infarction often being a “red thrombus” formed by fibrin network blood cells, while non-ST-segment elevation ACS is a “white thrombus” formed by platelet aggregation. “white thrombus”. Therefore, for patients with ST-segment elevation myocardial infarction, fibrinolytic drugs, i.e., thrombolytic therapy, can be applied within the prescribed time window, but if the time window has passed and the myocardium in the infarcted area is completely necrotic, thrombolytic therapy not only cannot play a role in saving the myocardium, but may lead to serious bleeding complications. In contrast, non-ST-segment elevation ACS can only be treated with antiplatelet therapy, and thrombolytic therapy is not only unhelpful, but harmful.