Coronary artery disease, or coronary atherosclerotic heart disease, is the most common and important type of atherosclerosis (AS). It is characterized by local lipid and complex sugar accumulation, fibrous tissue hyperplasia and calcium deposition, and arterial mid-layer degeneration, starting from the intima, and secondary lesions such as intraplaque hemorrhage, plaque rupture and local thrombosis. Because of the yellow atheromatous appearance of the lipid accumulation in the arterial intima, it is called atherosclerosis. At present, it is widely believed that coronary atherosclerosis is the result of multifactorial and multi-pathway interactions. 1, the traditional understanding of the pathogenesis of coronary atherosclerosis is called risk factor or susceptibility factor. It has been proved that atherosclerosis is related to the following factors, including gender, age, hypertension, dyslipidemia, diabetes and abnormal glucose tolerance, smoking, obesity, family history, as well as lack of exercise, poor dietary habits, excessive alcohol consumption, psychosocial factors, etc. The atherosclerosis mechanism once considered mainly includes the lipid infiltration theory, thrombosis theory, smooth muscle cell cloning theory, etc. 2, the pathogenesis of coronary artery atherosclerotic heart disease research progress In recent years, with the continuous research, the risk factors and pathogenesis of coronary heart disease have made a lot of progress. The newly discovered risk factors for atherosclerosis mainly include: viral and chlamydial infections; increased homocysteine in blood; increased insulin resistance; increased fibrinogen and some coagulation factors in blood, etc. Regarding the mechanism of coronary artery atherosclerosis, a new viewpoint has been proposed, namely, the “endothelial damage response” theory. This theory suggests that all risk factors of the disease eventually damage the intima, and the formation of atherosclerotic lesions is the result of an inflammatory-fibroproliferative response to intima damage, which includes the autoimmune response mechanism. 2.1 Infections and atherosclerosis It has been established that infections such as Chlamydia pneumoniae, Helicobacter pylori, periodontal disease, and viruses such as cytomegalovirus, herpes virus, and hepatitis A virus are major factors in the development of coronary atherosclerosis. The possible mechanisms of infection leading to atherosclerosis are: damage to arteries by immune complexes after infection; inflammatory response; promotion of smooth muscle cell migration and proliferation; reduction of plaque stability; and promotion of thrombosis. 2.2 Inflammatory response Several studies have shown that AS is an inflammatory response, and this view has been recognized. early lesions of AS contain only monocyte-derived macrophages and T lymphocytes, indicating the presence of inflammatory damage; when the lesions evolve to form atherosclerotic plaques, they are found to contain not only a large amount of lipids, but also inflammatory cells such as monocytes and lymphocytes infiltration. Therefore, the inflammatory response plays a role in all stages of the onset and progression of AS to the final rupture of the plaque surface and concurrent thrombosis. In addition, studies in gene regulation have further confirmed that the inflammatory response is present throughout the course of AS. Recent studies suggest that extra-arterial inflammation is associated with the formation and stenosis of AS and may also be a contributing factor to AS. In conclusion, the proposed inflammatory theory of atherosclerosis has advanced the understanding of the pathogenesis of AS. 2.3 Autoimmune response Studies have shown that an autoimmune response corresponding to heat shock protein (HSP60) exists at the initial stage of AS injury. It is believed that when intimal cells are subjected to adverse stimuli such as hypertension, smoking, oxygen free radicals, and infection, the anti-microbial HSP60 response will select autochthonous HSP60 as a marker, leading to phase 1 inflammation of AS, followed by severe injury such as plaque, foam cell formation, extracellular matrix and extracellular lipid deposition, ulceration, and calcification. 2.4 Increased insulin resistance Insulin resistance (IR) is a phenomenon in which the biological response of the body to a certain amount of insulin is lower than the expected normal level. the mechanism of IR leading to AS may be: causing disorders of lipid metabolism; inducing hypertension; causing blood hypercoagulation; pro-adhesive molecule expression; causing endothelial cell dysfunction; etc. 2.5 High serum homocysteine (HHcy) A large number of facts show that homocysteine serum concentrations ≥12 μmol/L and ≤l00 μmol/L are the most widespread and strongest independent causative factors of atherosclerosis-induced cardiovascular disease. Even a slight increase in serum Hcy levels will increase the incidence of cardiovascular disease 2- to 3-fold. Currently, the mechanism by which Hhcy causes AS has not been determined and may be related to endothelial damage and diminished anticoagulant activity, including induction of endoplasmic reticulum stress, induction of altered cell signaling pathways; induction of activation of inflammatory factors; and induction of reactive oxygen radical production. 2.6 Imbalance of serum-related components 2.6.1 Imbalance of serum proteins Relevant studies have shown that intermediates of serum protein metabolism, such as glycoprotein α antitrypsin, α-enzyme hypoglycoprotein, macroglobulin, ketocyanin, and transferrin, are significantly associated with coronary atherosclerosis. Elevated lipoprotein α and β100 and decreased AⅠ-Ⅱ are also significantly associated with coronary atherosclerosis. 2.6.2 Imbalance of trace elements in blood Studies have shown that HDL-C in blood decreases significantly with increased zinc intake, and HDL-C returns to normal after termination of zinc intake, and massive zinc supplementation can promote coronary atherosclerosis. Insufficient copper can lead to elevated blood cholesterol, and cholesterol returns to normal after copper supplementation. The atherosclerotic process is accelerated when blood chromium is reduced [10]. Low blood manganese can cause degeneration of pancreatic islet B-cells, resulting in decreased glucose tolerance. Low blood selenium can cause a decrease in glutathione peroxidase and a decrease in prostaglandin synthesis, which increases the risk of thrombosis. Low magnesium is one of the pathological bases for the formation of coronary heart disease. Decreased iron is closely associated with an increased risk of coronary heart disease. 2.6.3 Blood vitamin imbalance It has long been established that vitamin B1 deficiency is associated with the development of cardiovascular disease. Recently, low plasma folate and vitamin B6 have been found to be independently associated with elevated blood cysteine and as an independent risk factor for coronary atherosclerosis. Low plasma vitamin C has a reduced antioxidant effect and has a reduced role in preventing or delaying coronary atherosclerosis. Vitamin D plays a role in vascular calcification, and its deficiency is most likely an important risk factor for those with vascular calcification in osteoporosis. 2.6.4 Blood fiber imbalance The results of a large study showed that higher fiber intake was associated with lower cardiovascular events and overall mortality. When the fiber products of intestinal digestion of fiber-rich foods enter the bloodstream, they are converted primarily into serum enterolactone. Enterolactone plays an important role in the prevention of atherosclerosis. In addition, progress has been made on the role of genetic polymorphisms in the pathogenesis of coronary heart disease. Studies have confirmed that fibrinogen activator inhibitor I (PAI-1) , apolipoprotein E (APOE), plasma coagulation factor VII and plasminogen, G protein β3 suballele and α-endocannabinoid gene (ADDI) polymorphisms, and angiotensinogen gene T235 polymorphism are risk factors for coronary heart disease.