Peripheral vascular disease has a high rate of disability, and the effectiveness of medical treatment is minimal, and surgical treatment is invasive and limited. 1964, American physicians D Yuba and ludkil. pioneered a mediated treatment of peripheral vascular disease without surgery, and in 1972 Gnuntzig invented the double-lumen balloon catheter, making this technology mature. Since then, laser angioplasty, kinetic angioplasty (spin mill catheter), endovascular stenting, ultrasonic angioplasty, gene therapy and endovascular radiation therapy to prevent postoperative restenosis have been developed. The continuous progress of treatment methods, the indications are expanding, and the treatment effect is significantly improved. The devices will be compounded, bio-one drug, and the operation will be more simplified. At present, balloon catheters and endovascular stents will remain the main therapeutic tools. In the future, endovascular radiation therapy and gene therapy will be the main focus of treatment to prevent restenosis. Therefore, an increasing number of eclipse FM vascular diseases can be treated by percutaneous vascular interventions, the advantages of which cannot be replaced by drug and surgical treatments. The development of endovasculare clusion (EV E) or endovascular scent gifting has enriched the treatment of aortic coarctation and made the procedure less invasive and safer. 1.1 Diagnosis of aortic coarctation The staging of aortic coarctation: Stanford staging: regardless of the origin of the coarctation, as long as the ascending aorta is involved, it is called type A; if the coarctation originates in the thoracic descending aorta and does not involve the ascending aorta, it is called type B. Debakey staging: type 1 aortic coarctation originates in the ascending aorta and involves the abdominal aorta; type II aortic coarctation is limited to the ascending aorta; type III aortic coarctation originates in the thoracic descending aorta and does not involve the ascending aorta. Aortic coarctation originates in the thoracic descending aorta and does not involve the abdominal aorta downward is called ⅢA, and that involving the abdominal aorta is called ⅢB. Division of aortic coarctation: The division method of coarctation fissure (8 zones): Zone 0: fissure is located in the ascending aorta; Zone 1: fissure is located between the anomalous trunk and the opening of the left common carotid artery; Zone 2: fissure is located between the left common carotid artery and the opening of the left subclavian artery; Zone 3: fissure is located in the left subclavian Zone 3: the fissure is located in the aortic arch distal to the opening of the left subclavian artery; Zone 4: the fissure is located in the thoracic descending aorta; Zone 5: the fissure involves the abdominal visceral arteries; Zone 6: the fissure is located in the abdominal aortic segment below the renal artery; Zone 7: the fissure is located in the iliac artery. Staging of aortic coarctation: acute phase: within 3 d of the onset of aortic coarctation; subacute phase: 3 d-2 months; chronic phase: more than 2 months. 1.2 Interventional treatment of aortic coarctation Aortic coarctation should be treated internally first. The main purpose of medical treatment is to control blood pressure (blood pressure is controlled at the level of 120/70 mmHg) to prevent dilatation and rupture of aortic coarctation, as well as sedation and analgesia. The main advantages of endoluminal isolation as a new procedure for the treatment of aortic coarctation are focused on its minimally invasive nature. The preoperative management protocol includes fasting but not water and medications (especially antihypertensives) in the evening and morning before surgery, adequate hydration before induction of anesthesia (intravenous infusion of 1000 ml of crystalloid) and administration of agents to prevent and treat post-luminal isolation syndrome and prophylactic application of antibiotics. 1.2.1 Indications Acute and chronic B type 3-4 and 6-7 aortic coarctation with a diameter greater than 5 cm or with complications are currently the preferred indications for endoluminal isolation; endoluminal isolation of A type 0-2 and B type 5 aortic coarctation is controversial, but endoluminal isolation with additional surgery can be performed conditionally. 1.2.2 Contraindications Acute and chronic phase A type 0-2 zone aortic coarctation and B type 5 zone aortic coarctation are not suitable for conventional endoluminal isolation; coexisting other diseases with life expectancy of less than 1 year are not suitable for endoluminal isolation. 1.2.3 Preoperative imaging assessment of aortic coarctation can be performed by MRA or CTA, combined with intraoperative DSA for comprehensive and accurate assessment and measurement. The main parameters to be evaluated are: the length and internal diameter of the proximal aneurysm neck (the thoracic aorta between the opening of the left subclavian artery and the clamping fissure); the degree of aortic tortuosity; the patency of the branch arteries; and, most importantly, the precise localization of the fissure and the identification of the true and false lumen of the clamping. When closure of the left subclavian artery is required, the vertebral arteries should also be carefully evaluated bilaterally to determine if reconstruction of the left vertebral artery is required prior to or concurrent with isolation of the aortic coarctation. In addition, ultrasound should be routinely performed to assess the bilateral femoral and skeletal artery diameters in order to select the introducer arteries according to the caliber of the introducer system. 1.2.4 Selection of endoluminal grafts Currently, the endoluminal grafts used for the treatment of aortic coarctation consist mainly of straight stainless steel or memory alloy stents together with artificial vessels. The selected graft needs to meet two requirements: first, it needs to have sufficient circumferential support to ensure a close fit between the graft and the aorta, which is mainly achieved by selecting a graft diameter 10%-20% larger than the diameter of the aneurysm neck; second, in order to adapt to the curvature of the aortic arch after graft release without damaging the aortic intima, the graft must maintain good axial suppleness. This is mainly achieved by the segmental stent design plus the longitudinal fixation wire placed on the major curvature side of the aortic arch. 1.2.5 The routine procedure for type B aortic coarctation is performed in a DSA-equipped catheterization laboratory under general anesthesia. The patient is placed in a flat position, and according to the preoperative evaluation. The side of the iliac artery that is not involved is selected and the common femoral artery (or iliac artery) is dissected out as the introducer artery. A 5-6F pigtail catheter with a ruler is placed through the left adipose artery (or flexural artery) for thoracic aortography (LA0 45°) to the ascending aorta. The opening of the left subclavian artery and the rupture of the coarctation are marked on the monitor screen, and the length and diameter of the aneurysmal neck and the maximum diameter and length of the aortic coarctation are measured, according to which a graft of appropriate caliber and length is selected. After systemic heparinization (heparin lmg/kg, intravenous push), a superrigid guidewire (0.038in x 26 0cm, I in II 2.54cm.) was introduced into the true lumen through the guiding artery puncture and directly into the ascending aorta, and then the graft was introduced along this superrigid guidewire, and after positioning, the graft was released by controlled hypotension to a systolic pressure of 70 mmHg, with the proximal end fixed to the normal thoracic artery distal to the opening of the left subclavian artery. The proximal end of the graft is fixed to the normal thoracic aorta distal to the opening of the left subclavian artery and the distal end is fixed distal to the cleft of the entrapment. In the chronic phase, a low-pressure balloon can be used to moderately dilate the graft to make it adhere tightly. In the acute phase, because the aortic endothelium is prone to rupture, it is not advisable to use a balloon to dilate the graft after releasing it to avoid forming a new rupture. The aortogram is performed again via the left brachial artery (or flexor artery) with a pigtail catheter preplaced, and attention is paid to the patency of the left subclavian artery, the patency of the graft, the presence of twisting and displacement, and the presence of endoleaks at the proximal or distal end of the graft. If the angiogram confirms that the aortic coarctation has been completely isolated and the false lumen is no longer visible, withdraw the catheter and suture the introducer artery and incision. 1,2.6 Complications after endoluminal isolation: Endoleaks are the continued regurgitation of blood from various sources into the aneurysmal cavity after endoluminal isolation. The risk of endoleaks is that they can lead to continued enlargement or even rupture of the aortic coarctation. There are four types of endoleaks: Type 1 endoleak refers to the phenomenon that blood flows into the aneurysm cavity through the fissure between the proximal end of the intraluminal graft and the autologous artery. Type II endoleaks can be left untreated if the backflow is not large and can be self-closed during the follow-up observation; if the backflow is large, another section of intraluminal graft should be added to isolate and close the endoleak; Type III endoleak refers to the phenomenon of backflow from the intercostal artery into the intercalated pseudocavity, generally the backflow is small and can be self-closed during the follow-up observation after surgery; Type IV endoleak refers to the phenomenon of blood flowing into the intercalated pseudocavity from the pinhole of the intraluminal graft or even from the breakage. The treatment of type IV endoleaks is usually to select a shorter and appropriate sized endoluminal graft to isolate and close the original breach. The postoperative syndrome of endoluminal isolation is a clinical syndrome that occurs after surgery and is usually characterized by “three highs and two lows”, i.e., elevated body temperature (usually not exceeding 38.5°C), elevated white blood cell count (108/L higher than the preoperative average), and elevated C-reactive protein; at the same time, red blood cells and platelets are reduced to varying degrees. The syndrome was initially considered to be caused by a combination of foreign body reaction to the graft, resorption of thrombus formation in the tumor cavity, mechanical destruction of blood cells by the graft, and the effects of contrast agents and x-ray radiation. Patients with mild symptoms can gradually recover within two weeks after intraoperative and postoperative symptomatic treatment with small doses of adrenal glucocorticoids and anti-inflammatory and analgesic drugs. For patients with more severe symptoms, hemoglobin below 80 g/L and platelet count below 60 x 109/L should be supplemented in a timely manner.