Aortic coarctation is the rupture of the intima and middle layers of the aorta, and blood flow enters the aortic wall, stripping the aorta into two inner and outer layers, called aortic coarctation. Acute aortic coarctation is an extremely dangerous cardiovascular emergency with acute chest pain as the main manifestation, and its consequences can be catastrophic if not accurately diagnosed and treated. Recent literature has reported that the incidence of acute coarctation can be as high as 3 per 100,000 per year, and there is a trend to increase year by year. Patients who are not diagnosed and treated in a timely manner die about half of the time two days after the onset of the disease, and 70% die one week after the onset of the disease. In recent years, advances in diagnostic techniques, improved surgical techniques, and effective perioperative management have led to significant improvements in treatment outcomes and prognosis. Understanding the etiology, anatomical and pathological changes, and clinical manifestations of aortic coarctation is extremely important for accurate and timely diagnosis and effective treatment. The main causes of aortic coarctation formation are: hypertension, atherosclerosis, cystic necrosis of the middle layer of the artery, aortic constriction, aortitis, trauma and syphilis. In clinical cases, domestic cases are mostly congenital mid-layer dysplasia in young adults, etc., but the proportion of atherosclerosis and hypertension in patients with the disease has gradually increased in recent years. The pathological basis is the lesion of the middle layer and smooth muscle of the aorta, which leads to intimal tearing, arterial wall peeling and hematoma spreading in the middle of the arterial wall and expanding to the whole layer. Once the intima is torn, the extent of the peeling gradually increases due to the downward and reverse impact of the blood flow, and the wall tear can be as deep as the middle layer. In hypertensive patients, the rupture of the wall can often break into the thoracic cavity or pericardium, resulting in sudden death due to pericardial tamponade, or into the aorta to form a second opening, creating a pseudo-luminal flow path in the aorta, resulting in obstruction of important branch arteries and, in severe cases, ischemic necrosis of vital organs. Tears of the intima are most commonly seen in the proximal end of the ascending aorta and the beginning of the descending aorta. There are two common classifications of endothelial tears depending on the site of the tear: DeBakey classifies them into three types. type I endothelial tears are located in the ascending aorta or arch, and the dissection extends to the arch and descending aorta up to the iliac artery. type II endothelial tears are the same as type I, but the dissection is limited to the ascending aorta and arch. type III is located in the aortic isthmus, distal to the left subclavian artery. Another commonly used classification classifies the entrapment into Stanford types A and B. Type A includes DeBekay I and II, and type B is the same as DeBekay type III. The onset of the disease within 2 weeks is called acute entrapment, while those without a history of acute disease or those with an onset of more than 2 weeks are classified as chronic entrapment. In the early years, due to the lack of knowledge about aortic coarctation and the lack of corresponding tests, the diagnosis rate was not high, and it was often confused with acute infarction and delayed the diagnosis and treatment. With the increasing level of understanding of acute entrapment and the development of non-invasive examination techniques, the detection rate has improved and most patients can be diagnosed early. Sudden and severe chest and back pain is the most common symptom at the onset. About 90% of patients in the acute phase of entrapment exhibit persistent chest and back pain, which is tearing or knife-like and unbearable. Patients exhibit irritability, anxiety, fear, and near-death feelings that are not relieved by analgesic medications. When the dissection involves a large branch of the aorta or when the aneurysm compresses the surrounding tissues, it can cause corresponding manifestations in various organs. Diastolic or systolic murmurs in the aortic valve area may occur when the aortic valve is involved in the dissection. When the clammy dissection involves the coronary artery, it may cause acute myocardial ischemia or myocardial infarction, and when the clammy dissection breaks into the pericardium, it may cause rapid pericardial tamponade, leading to sudden death. When peripheral artery obstruction occurs, weak pulsation of carotid artery or limb artery may occur, and in severe cases, ischemic necrosis of limb may occur. In cases where the interposition involves the cephalobrachial artery in the aortic arch, it may cause cerebral blood supply deficiency and even coma and hemiparesis. Intercostal artery involvement in the descending aorta may affect spinal cord blood supply and cause paraplegia. Involvement of the abdominal organ branches may cause inadequate blood supply to the liver, impaired liver function, abdominal manifestations such as acute abdomen or gastrointestinal bleeding, renal function impairment and renal hypertension. Echocardiography is a non-invasive test commonly used in clinical practice, which can show the location and extent of the aneurysm and whether the aortic valve is involved, but the detection rate of distal ascending aorta and descending aortic coarctation is reduced. Transesophageal echocardiography can quickly differentiate ascending aortic aneurysms from coarctation, but has the concern of invasive manipulation leading to increased blood pressure for coarctation extension. MRI is currently an important test for the rapid diagnosis of entrapment and is more beneficial for the dynamic display of aortic disease, especially the observation of aortic intimal tears and their pseudolumina. In recent years, rapid CT has been used to diagnose thoracic aortic aneurysms, and two- and three-dimensional reconstruction can show the relationship between the entrapment and the arch vessels, the true and false lumen, and the extent of the lesion; its main disadvantage is that it is unfavorable to the determination of the location of the tear and the condition of the arterial branch vessels. In recent years, CT angiography (CTA) technology has overcome the above disadvantages and can show the true and false luminal flow in the aorta through the difference of contrast concentration, especially the aortic intimal laceration and its false lumen can be clearly shown, thus it is the gold standard for the diagnosis of aortic coarctation at this stage. For acute aortic coarctation, once diagnosed, monitoring treatment should be carried out immediately to take effective interventions to stabilize the vital signs. The main therapeutic measures include analgesia, sedation and blood pressure lowering. Blood pressure is generally controlled at a systolic pressure of 100 ~ 120 mmHg and a mean pressure of 60 ~ 70 mmHg. After stabilization, ultrasound, CT, and MRI are reviewed to clarify the site and extent of the aortic wall dissection lesion to determine the need for surgical treatment and the surgical approach. In cases of Stanford type A or DeBakey type I and II, surgical treatment should be performed, based on the principles of excision of the intimal torn portion of the aorta, repair of the detached intima at both ends, and connection of the aortic conduit with an artificial vessel graft. In Stanford type B or DeBakey type III cases, the pain is not controlled by medical treatment, the aortic wall peeling lesion continues to enlarge, the aortic head and arm branches show murmurs and weak pulsations or aortic valve murmurs, or coma, stroke, cold limb pain, decreased urine output or absence of urine suggest compression or obstruction of the main branches of the aorta. Surgical treatment should be performed if there is obstruction. Surgical procedures can be performed by descending aortic prosthetic vascular grafting, but due to the improvement of noninvasive diagnostic techniques in recent years, the endothelium can be accurately located for type III entrapment stripping, and laminated stent endoluminal isolation has been widely used for the treatment of descending aortic entrapment. This method can reduce the trauma of surgery, anesthesia, and extracorporeal circulation to patients with good results.