I. Introduction to aortic coarctation Aortic coarctation is the gradual peeling and expansion of the intima due to a local tear in the intima, which is subjected to a strong blood shock, forming two lumens, true and false, within the artery. This leads to a number of manifestations including tear-like pain. The aorta is the main blood vessel of the body, which bears the pressure directly from the beating heart and has a huge blood flow. The occurrence of a tear in the intimal layer has a very high chance of rupture and a very high mortality rate if proper and timely treatment is not provided. The normal human arterial vasculature consists of 3 layers of structures, the intima, the mesentery and the epima, and the 3 layers fit closely together to carry the blood flow through. Arterial entrapment, on the other hand, is the gradual peeling and expansion of the intima due to a localized tear in the intima, which is subjected to a strong blood shock, creating two lumens, a true and a false, within the artery. This leads to a number of manifestations including tear-like pain. Depending on the site of the rupture and the location of the artery, the entrapment can involve various parts of the body. The most common and most dangerous is aortic entrapment, while others include superior mesenteric artery entrapment, carotid artery entrapment, etc. The manifestation varies depending on the location of the blood supply. The cause of aortic coarctation is the result of the interaction of abnormal mesenteric structure and abnormal hemodynamics of the aorta. Aortic dissection is prone to occur when the aortic structure is abnormal. Common factors include Marfan syndrome, congenital cardiovascular malformations, idiopathic degenerative changes in the aortic mesentery, hypertension, aortic atherosclerosis, inflammatory disease of the aorta, etc. We know the American female volleyball player Hyman and the male volleyball player Zhu Gang as these reasons, and collapsed on the sports field. Arterial wall damage is also easily caused when hemodynamic changes occur. The most common cause is hypertension, and almost all patients with aortic coarctation have poorly controlled hypertension. In other words, the control of hypertension has a comprehensive impact on the prevention, treatment, and prognosis of aortic coarctation, and is the most basic and least negligible means of treatment and prevention. Pregnancy is another high incidence factor, associated with altered hemodynamics during pregnancy. In women with onset before the age of 40, 50% of them occur during pregnancy. Another proportion of patients originate from trauma, especially car accidents. The ratio of male to female incidence of aortic coarctation is 2 to 5:1; the common age of onset is between 45 and 70 years, and the youngest patient reported so far was only 13 years old. There are two major medical classifications of aortic coarctation based on the location of the intimal fissure and the extent of coarctation involvement. The most widely used is the 3-type classification proposed by Professor DeBakey et al, in 1965. Type I: Aortic coarctation involving the ascending aorta to the descending aorta and even to the abdominal aorta. Type II: Aortic coarctation involving only the ascending aorta. Type III: Aortic coarctation involving the descending aorta, such as downward involvement of the abdominal aorta is type IIIA; downward involvement of the abdominal aorta is type IIIB. In 1970, Professor Daily of Stanford University and others proposed another classification method based mainly on the location of the proximal endothelial fissure: Stanford type A: equivalent to DeBakey type I and II, Stanford type B: equivalent to DeBakey type III. type: equivalent to DeBakey type III.