The etiology is still unknown; more than 80% of patients with aortic coarctation have hypertension, and many have cystic middle lamina necrosis. Hypertension is not the cause of cystic middle lamina necrosis, but can contribute to its development. Clinical and animal experiments have found that it is not the height of blood pressure but the magnitude of blood pressure fluctuations that is associated with aortic coarctation splitting. In animal experiments, feeding pigs with sallow beans can cause aortic coarctation, and the beta-aminopropionitrile in sallow beans acts on the stroma of the artery, the muscle and elastic tissue of the middle layer, making the artery vulnerable. Feeding rats with aminoacetonitrile and deoxycorticosterone can also cause aortic coarctation; the lack of copper in the feed makes the animal synthesize elastic scleroprotein disorder, which can also produce similar results. Other genetic disorders such as Turner syndrome and Ehlers-Danlos syndrome also have a tendency to develop aortic coarctation. Aortic coarctation also tends to occur during pregnancy for unknown reasons, and it is assumed that endocrine changes during pregnancy cause structural changes in the aorta and make it easy to split. Jiang Xionggang, Department of Cardiac Surgery, Wuhan Union Medical College Hospital The aortic wall of a normal adult is quite resistant to pressure, and it takes more than 66.7 kPa (500 mmHg) for the wall to rupture. Therefore, the prerequisite for causing a clamping fracture is a defect in the arterial wall, especially in the middle layer. In general, degenerative changes of the middle layer muscles predominate in older individuals, while in younger individuals, the lack of elastic fibers predominates. In the rare cases of aortic coarctation without intimal fissures, it may be due to intramural hemorrhage caused by rupture of the trophoblastic vessels within the lesion of mesodegeneration. The coexistence of atherosclerosis contributes to the development of aortic coarctation.