The cause of the disease is still unknown and may be a combination of factors leading to its onset. 1, class metabolic disorders The application of high cholesterol and animal fat diet to animals such as rabbits to form atherosclerotic plaques, the results are similar to humans, which put forward the view that lipid metabolism is related to the disease, how hyperlipidemia violates the blood vessel wall? Experiments with angiotensin and other vasoconstrictors suggest that it may be through vasoconstrictors that increase cellular contraction and cellular relaxation, which increases cellular lacunae and facilitates lipid entry. It is not clear how many hyperlipidemic individuals develop atherosclerosis in humans, but atherosclerosis is seen to occur frequently in diabetics and to start early. At the same time, hyperlipidemia may not always suffer from atherosclerosis, which has been confirmed in recent years, and may be related to the high content of HDL, the ratio is not seen to be out of whack, or the ratio of apolipoproteins is out of whack, etc. 2, thrombogenesis Some people believe that atherosclerotic plaque is the mistake of blood clots, and no lipid retention in the vessel wall, but although this statement is difficult to confirm, however, can see thrombosis, fibrin accumulation and fibrin dissolution, in the pathogenesis of the disease is to play a role. 3.Altered blood supply to the arterial wall The normal sources of nutrients to the arterial vasculature are: ① Vascular trophoblast branches through the outer membrane but not into the inner membrane; ② Nutrients in the lumen of the vessel directly supply the inner membrane. Once the artery is diseased, capillaries form and penetrate into the endothelium, anastomosing with vascular trophoblast branches and reaching into the vascular lumen. If the pressure changes or the supporting tissue is necrotic, these vessels will rupture, causing small bleeding under the endothelium, and the result will cause fatty degeneration and lead to atherosclerotic plaque. 4, abnormal load on the arterial wall Atherosclerosis in hypertensive patients, the incidence of which is 2 to 3 times higher than normal, and the high and low blood pressure is proportional to the degree of atherosclerosis and histological changes, high pressure blood flow produces tension mechanical damage to the arterial wall, prompting local thrombosis, and fatty degenerative deposits promote the formation of atherosclerosis. 5, genetic factors such as the same family or siblings the incidence of the disease is higher than others. It should be paid attention to. 6, infection In recent years, the role of infection factors in the development of atherosclerosis has attracted the attention of many scholars. Infection can cause changes in the function of cells in the vessel wall, changes in vascular permeability, as well as the formation of immune complexes deposited in the vessel wall and activation of complement to further damage the intima, all of which can contribute to thrombosis. In addition, infection affects lipid metabolism can also contribute to atherosclerosis. 7.Other factors such as obesity, diabetes, vitamin deficiency and imbalance of trace elements are all related to atherosclerosis.