Coronary artery disease is a series of pathological changes caused by the narrowing and occlusion of the coronary artery lumen due to atherosclerotic lesions. The clinical manifestations of coronary artery disease (angina pectoris, myocardial infarction, arrhythmia, heart failure and sudden death) vary depending on the degree, location, extent, speed and frequency of occlusion. A normal coronary artery has a moderate caliber, elastic walls, regular lumen, and an intact and smooth lining, and the lumen undergoes corresponding adaptive changes in response to the physiological and pathological state of the body and the composition of the blood contained in the lumen. From a normal coronary vessel to a severely stenosed or completely occluded vessel mostly undergoes two different progression phases: the slow progression phase and the rapid progression phase. Slow progression phase: In the early stage of coronary atherosclerosis, atherosclerotic plaques rich in inflammatory cells and lipids are deposited and accumulate in the vessel wall, causing progressive narrowing or even occlusion of the coronary lumen, a process that begins in childhood and takes mostly 30 to 40 years to develop to the extent that it causes clinical symptoms. Therefore, the vast majority of coronary atherosclerosis develops symptoms and draws attention only after the age of 30-40. Of course in recent years there has been a trend toward younger onset of coronary heart disease, and some patients with coronary heart disease in their 20s or even younger have been reported. Because the lipid-rich atheromatous plaques of these patients exist under the intima of coronary vessels and are covered by intact endothelial cells with antithrombotic effect on the surface, the blood vessels are not prone to thrombus formation despite progressive stenosis. When the lesion progresses slowly enough to significantly affect coronary blood flow, patients exhibit symptoms of angina during exercise or at rest while having ample time to form collateral blood flow from other vessels to that ischemic region – the collateral circulation. These patients may be clinically asymptomatic or may present with stable angina (exertional angina), which is relatively uneventful and has a relatively good prognosis. Aggressive, standardized drug therapy is usually sufficient and does not require interventional or bypass therapy. Rapidly progressive stage: When the atherosclerotic plaque accumulated in the wall of coronary artery reaches a certain volume, in the state of local vascular inflammation, corrosion, ulceration, stress, wall diastolic reaction and intravascular bleeding, it will lead to plaque rupture, so that the integrity of local vascular endothelial cells on the surface of plaque is damaged, and the lipids in the atherosclerotic plaque overflow into the vascular lumen, and distal vascular lipid embolism occurs; more serious is that Plaque rupture can cause local intravascular thrombosis, causing further severe narrowing and occlusion of the lumen within a short period of time (within minutes to days) – the rapid progressive phase. The rapid progressive phase mostly occurs on top of the slow progressive phase and, therefore, mostly occurs in people over 30-40 years of age. Due to the sudden onset of the rapid progression phase, about half of the patients will have a complete occlusion of the vessel within a short period of time, causing sudden death or acute myocardial infarction; about less than 50% of the patients will have a non-occlusive severe stenosis of the coronary vessels within a short period of time, which will lead to a new onset of angina symptoms or a sudden aggravation of the existing stable exertional angina, however, the thrombotic nature of the coronary vessels in these patients alterations have a tendency to worsen in the short term leading to more severe stenosis or occlusion of the vessel, and are therefore called unstable angina, which, if not treated promptly, can rapidly progress to occlusive lesions and cause sudden death or acute myocardial infarction. Patients with rapid progressive changes are too late to form collateral circulation, and they are not prepared for this and lack proper understanding of the disease, so the prognosis is more dangerous. These patients should receive aggressive coronary angiography and revascularization therapy including interventional and bypass therapy. As can be seen, the slow progression phase begins in childhood with progressive lumen narrowing and an intact endothelial cell layer in the lumen. Since only slowly increasing lipid-based atherosclerotic plaque components are present at the lesion site and there are no thrombotic components in the lumen, the lesion progresses slowly and the prognosis is relatively good. After the slow progression reaches a certain level, it can rapidly progress to the rapid progression stage under specific triggers. Rapid progression stage, which occurs after slow progression reaches a certain stage, is mainly characterized by the destruction of the integrity of the intima and the presence of secondary thrombotic components in the lesion site. Since the thrombus can elongate within a short period of time, it is an unstable lesion, and if it increases rapidly within a short period of time, it can cause significant narrowing or even occlusion of the lumen, which has a poor prognosis and requires active intervention.