The aorta is the “backbone” of the heart to each organ. We all know that oil plants continuously send power to each processing plant through pipelines, and in the human body, if the heart is compared to an oil plant, then the aorta is the “oil pipeline” that delivers nutrients to each organ in the body. “, this pipe once ruptured what will happen? It will lead to instant hemorrhage and all organs will lose their blood supply, the consequences are unimaginable! Aortic coarctation is a “catastrophic disease” caused by the separation of the inner lining of the aortic wall from the middle layer, and its degree of danger can be imagined. The shape of the aorta is like an inverted umbrella handle The aorta starts from the upper end of the heart and turns downward to supply blood to the whole body; the straight part of the handle of the umbrella handle is called the “ascending aorta”, the curved part of the handle is called the “aortic arch”, and the straight part of the umbrella bone is the “descending aorta” that continues to supply blood to the whole body. The straight portion of the handle is called the “ascending aorta”, the curved handle is called the “aortic arch”, and the straight portion of the umbilicus is the “descending aorta”, which is responsible for the systemic blood supply. Aortic coarctation is called type A aortic coarctation when it occurs in the entire artery, and type B aortic coarctation when it occurs only in the descending aorta. ”Aortic coarctation” is medically known as a vicious, dangerous and acute malignant life-killer of which acute type A aortic coarctation is a very dangerous surgical emergency, with a prevalent age of 45 to 60 years old in China and a male to female incidence ratio of 3:1. According to foreign literature, about 50% of patients with aortic coarctation without surgical treatment die within 48 hours after the onset of the disease (within the first 48 hours, the mortality rate increases at the rate of one percent per hour), that is, the mortality rate is about 50% within the first 48 to 72 hours after the onset of the disease, up to 70% within one week, and 90% within one month. This means that the mortality rate is about 50% within the first 48 to 72 hours, 70% within one week, and 90% within one month. The typical symptoms of aortic coarctation are sudden, persistent, severe tearing pain that is usually increasing and can occur in the back, lower back, or abdomen, and is often unbearable and easily confused with other diseases. Aortic coarctation is the rupture of the aortic intima and the separation of the intima from the middle layer of the aortic wall. The structure of the aorta is divided into three layers from the inside to the outside, namely the intima, the middle layer, and the outer layer, and when the pressure in the lumen of the vessel rises to a certain level, the weak point of the intima will suddenly tear and a large amount of blood will rush in between the intima and the middle layer, separating the intima from the middle layer of the aortic wall and forming a “false lumen” between the intima and the middle layer relative to the original lumen (true lumen). This condition is called aortic coarctation. The normal adult aortic wall is quite resistant to pressure, and a pressure of 66.7 kPa (500 mmHg) or more is required to make the wall split, while the blood pressure of normal people is usually 100-130 mmHg. Therefore, the prerequisites for the formation of aortic coarctation are arterial wall defects, especially defects of the middle layer, and various causes of aortic wall degeneration or lesions of the middle elastic fibers and smooth muscle are the internal causes of aortic coarctation. Aortic luminal hemodynamic changes (e.g., hypertension) are the exogenous cause of formation. Most of the endothelial tears occur in the wall of the aortic lumen where the pressure of blood flow is greatest or most variable, i.e., the right lateral wall of the ascending aorta or the proximal end of the descending aorta, and the blood in the aortic lumen separates the middle layer through the endothelial tear to form the interstitial layer, which extends longitudinally and circumferentially along the aortic wall and can be limited or extensive, from the ascending aorta to the abdominal aorta in extensive cases. Continuous expansion of the pseudolumen and narrowing or collapse of the true lumen by compression are the most important and fundamental pathophysiological changes of aortic coarctation. The compression and narrowing or collapse of the true lumen of the aorta involves all branches of the aorta, leading to ischemic or necrotic changes in the organs, especially the coronary p-spinal arteries and the abdominal organ vessels and both iliac arteries. If there is no rupture in other parts of the “false cavity”, thus blood accumulates in the “false cavity”, and the relatively high pressure of blood in the lumen of the vessel keeps pouring into the “false cavity”, which in turn causes blood vessels to After rupture, rapid bleeding and pericardial tamponade will lead to clinical death, and the success rate of resuscitation is very low.