As one of the most deadly diseases of the cardiovascular system, aortic coarctation is still defined by the vascular surgery community as a challenging aortic lesion. For a long time, resection of the proximal entrapment segment with an artificial vessel graft has been the standard surgical procedure for Stanford type B entrapment. These procedures are highly invasive and have a high perioperative mortality rate; especially in patients of advanced age or with comorbid systemic disease, the risks associated with surgery alone have outweighed the risks associated with the entrapment itself. It has been ten years since Dake and Nienaber reported the endoluminal treatment of acute and chronic aortic coarctation. With the increasing maturity of endoluminal vascular surgery techniques and the continuous improvement of stent materials, thoracic endovascular aneurysm repair (TEVAR) has shown great potential in the treatment of Stanford type B coarctation. In many vascular surgery centers, it has replaced conventional surgery as the procedure of choice for the treatment of type B clips. Autopsies show that 74% of deaths occur within 2 weeks of entrapment formation. Aortic coarctation within 14 days of onset is usually defined as acute coarctation, while those who survive the acute phase are defined as chronic coarctation regardless of treatment. 1/3 of patients with type B coarctation have no obvious spontaneous symptoms at onset and are already in the chronic phase when the diagnosis is obtained; the remaining patients have a clear history of onset and are admitted to the hospital in the acute phase for treatment. 1. Treatment strategies for aortic coarctation Stanford type B coarctation can safely survive the acute phase in approximately 85% to 90% of patients with aggressive medical treatment [1]. Surgical intervention in the acute phase is limited to those cases with disabling or fatal complications. The traditional treatment for chronic type B entrapment is pharmacological control of blood pressure and close follow-up, but in recent years, with the increasing awareness of the long-term prognosis of the disease and the maturation of TEVAR technology, it has become a hot topic of debate whether TEVAR treatment should be performed for chronic type B entrapment. To date, there is no unified standard for the indication of surgical intervention for chronic type B entrapment. Surgical intervention should be performed in cases of oversized interstitial aneurysm and rapidly enlarging pseudolumen; however, a risk/benefit analysis should also be performed on patients by integrating many factors such as their age, degree of blood pressure control, compliance with follow-up, and the presence of congenital connective tissue disease. In fact, approximately 60% of aortic coarctations are Stanford type A. TEVAR for type A coarctation has only been attempted experimentally in patients with limited lesions that cannot tolerate conventional surgery. DeBakey type II coarctation involving only the ascending aorta can be corrected by emergency surgery, but this group of patients accounts for only 1/3 of type A. The remaining 2/3 of DeBakey type I coarctations have persistent pseudo-luminal flow in the residual distal coarctation due to concomitant involvement of the descending aorta in approximately 63% of patients, but this does not increase the long-term mortality in this group of patients [2],[3] and their survival is comparable to that of chronic Stanford type B entrapment. Therefore, TEVAR is also worth considering in this group of patients, and its follow-up and surgical indications are consistent with those of chronic type B entrapment. The surgical goal of either conventional surgery or TEVAR is to reduce the rate of death and disability associated with the entrapment. The principles of TEVAR for aortic coarctation are to cover the proximal primary intimal rupture, isolate the aneurysmal lesion and ensure blood supply to the distal organs and major branches of the aorta, while pursuing complete thrombosis of the false lumen. As an emerging technology in its first decade, it is necessary to repeatedly examine its impact on the survival rate and quality of life of patients with coarctation in order to reasonably evaluate the status of TEVAR in the treatment of aortic coarctation and to standardize its surgical indications. With the widespread use of this technique in numerous vascular surgery centers worldwide, the literature on its efficacy and prognosis has been increasing year by year in recent years. Although preliminary observations are satisfactory, reliable long-term follow-up conclusions (>3 years) and persistent analysis of aortic remodeling are lacking because there are no uniform standards for surgical indications, stent materials, follow-up protocols, and image measurement means available in each center. 2. Prognosis of TEVAR in the acute phase About 73% of patients with acute Standford type B coarctation have no serious complications at the initial stage of the disease, and these patients are treated satisfactorily with pharmacological therapy, and TEVAR in the acute phase is generally not advocated for these patients [4]. Furthermore, the arterial wall in the acute phase of edema is less supportive, and stent placement is prone to loosening and displacement, and the weak septum is also vulnerable to stent injury. The incidence of various complications after acute TEVAR has been reported to be up to 76%, and the mortality rate within 30 days can be as high as 21% [5]. Therefore, it has been accepted by most scholars that the acute TEVAR is indicated for those with severe complications (distal organ “hypoperfusion”, rupture or tendency to rupture of the coarctation aneurysm, irresistible pain, and uncontrollable hypertension). TEVAR within 48 hours of onset, and its follow-up showed an early postoperative mortality rate of 25% ± 11%, no distant deaths, no neurological complications, complete thrombosis in the false lumen in 25% of patients and partial thrombosis in 38% of patients; and a postoperative survival rate of 73% ± 11% at 1 and 5 years [6]. Fattori et al. compared 59 conventional procedures and 66 TEVAR Fattori et al. compared the data of 59 conventional and 66 TEVAR procedures for acute type B entrapment, with an in-hospital mortality rate of 33.9% in the former and only 10.6% in the latter [7]. Parker summarized 942 cases of acute type B entrapment treated with TEVAR, with an in-hospital mortality rate of only 9% and a serious complication rate of only 8.1%; the rate of re-lumpectomy within 20 months after surgery was 10.4% and the rupture rate was only 0.8% [8]. The main causes of early postoperative death are rupture, distal organ hypoperfusion, and multiorgan failure. Therefore, many scholars, represented by researchers at Stanford University, believe that TEVAR in type B (or retrograde type A) entrapment with lethal complications in the acute phase is not aimed at eliminating intracavitary flow, but only at covering the primary rupture, restoring superior flow in the true lumen, relieving distal hypoperfusion and preventing rupture, thus providing the opportunity for further resuscitation and follow-up, and ultimately improving the salvage success rate. Based on the extension of this concept, the PETTICOAT concept was proposed, i.e., when the overlying stent covers the proximal rupture, if the distal true lumen is still hypoperfused, a bare stent can be used in the distal true lumen to assist the true lumen in restoring superior blood flow [9]. The introduction of this concept even gradually eliminated open-window and branch endovascular stenting.Dialetto et al. summarized 28 cases each of type B entrapment with and without complications, treated with TEVAR and medication, respectively, with no difference in early and intermediate mortality between the two groups; postoperative CT follow-up revealed that those who received TEVAR had a significantly higher proportion of pseudoluminal thrombosis and a lower incidence of late tumor-like dilatation [ 10]. This suggests, at least, that TEVAR is no less effective than drug therapy for acute type B entrapment. 3. prognosis of TEVAR in the chronic phase Although pharmacological treatment improves survival during hospitalization in acute type B entrapment without complications, it does not improve the long-term survival of patients with chronic entrapment [11]. Between 20% and 50% of these patients will later develop neoplastic degeneration, new entrapment formation, and pseudolumen enlargement leading to rupture. The 5-year survival rate with drug therapy alone is approximately 50%. Therefore, there are conflicting views as to whether chronic type B entrapment should be treated with prophylactic TEVAR. It has been found that in the natural course of chronic type B entrapment, those with spontaneous thrombosis in the false lumen have a better long-term prognosis than those with perfusion in the false lumen present, but the former only occurs in <4% of patients [12]. Based on these concepts, the aim of TEVAR for chronic entrapment is not focused on improving distal organ hypoperfusion, but rather on promoting intra-pseudoluminal thrombosis and preventing rupture due to pseudoluminal aneurysmal expansion. It has been reported that the success rate of TEVAR technique in the chronic phase is 96%, with a 30-day mortality rate of 3.2% ± 1.4%, a serious complication rate of 9% ± 2%, and an incidence of cerebral infarction and spinal cord ischemia of approximately 1.2% and 0.5% [13], [14]. A retrospective study showed a 1-year mortality rate of 27.5% for chronic type B entrapment treated with drugs alone compared with 5.1% for elective TEVAR [15].Kato et al. found that postoperative mortality and recent complication rates were significantly lower for TEVAR in the chronic phase than for TEVAR in the acute phase [16]. These results suggest that TEVAR performed in the chronic phase has a lower perioperative risk and a better intermediate prognosis, but there is a lack of strong evidence on the impact on the long-term prognosis. The INSTEAD study, started in Europe in 2004, is the only multicenter prospective randomized clinical study comparing the efficacy of pharmacotherapy and TEVAR in chronic type B entrapment [15]. Its preliminary results showed a 1-year mortality rate of 3% and 10% in the drug treatment and TEVAR groups, respectively [14]. This result negates the advantage of prophylactic TEVAR in stable chronic type B entrapment. Therefore, the application of TEVAR is currently advocated in the high-risk chronic entrapment population, including entrapment aneurysm diameter of 5.5-6 cm, aortic diameter dilatation of more than 1 cm per year, uncontrollable hypertension due to true luminal stenosis or renal hypoperfusion, and recurrent chest and back pain that cannot be eliminated; the patient's age, coexisting diseases, and compliance with follow-up are also taken into account. 4. Postoperative complications of TEVAR Compared with conventional surgery, postoperative complications of TEVAR for aortic coarctation have been significantly reduced. However, common complications still include endoleaks, cerebral infarction, paraplegia, retrograde type A entrapment, intestinal ischemia and limb ischemia. The incidence of endoleaks after TEVAR for aortic coarctation is less than 6% [17], which is significantly lower than that of true aortic aneurysms. Smaller type I endoleaks will close on their own, and larger type I endoleaks are mostly detected intraoperatively and can be corrected by balloon dilation, but this operation is not required routinely in patients without endoleaks to avoid increasing the incidence of retrograde type A entrapment. type II endoleaks are mostly from retrograde flow from the subclavian or intercostal arteries and are mostly self-closing, but require further management if complicated by an expanding false lumen. Other forms of endoleaks or stent displacement have been reported occasionally. Cerebral infarction is probably the most common neurological complication, with an incidence of approximately 3% [18]. It is thought to be mainly associated with excessive intraoperative aortic arch manipulation and combined carotid/vertebral artery system disease. Although it is currently believed that the left subclavian artery can be covered if necessary without triggering serious consequences, a study from EUROSTAR showed that the incidence of postoperative cerebral infarction after TEVAR with coverage of the left subclavian artery without reconstruction was significantly higher than in the reconstruction group (8.3% versus 0%) [19]. Previously, it was thought that spinal cord ischemia after TEVAR was mainly related to the obscured root maximal artery. After years of practice, it was found that the incidence of paraplegia due to spinal cord ischemia after TEVAR was only 0.8% [20] and was associated with long segmental coverage of the thoracic aorta, history of previous aortic surgery, hypotension, and coverage of the left subclavian artery. Zhongshan Hospital of Fudan University summarized 102 cases of type B entrapment with TEVAR, and no postoperative paraplegia was seen [21]. It is now believed that intraoperative maintenance of cerebrospinal fluid pressure <10 mmHg has a role in preventing its occurrence. Retrograde type A entrapment has received sufficient attention in recent years, and its etiology is still unclear, and it is thought that it may be related to weakness of the aortic wall and medical factors (excessive balloon dilation, catheter injury, or stent anchorage area trauma), with an incidence of 4% to 20%. Zhongshan Hospital of Fudan University summarized 443 cases of type B entrapment with TEVAR and 11 cases (2.48%) of retrograde type A entrapment, of which 8 cases were treated with reopening surgery and 2 cases were treated conservatively, 1 case died 2 hours after TEVAR and 2 cases died within 1 week after opening surgery, with an overall mortality rate of 27.3% [22]. 5. postoperative follow-up and the prognostic impact of pseudocavity perfusion Regardless of the treatment measures, residual pseudocavity will be at lifetime risk of distant tumor-like changes and rupture, and patients must adhere to pharmacological antihypertensive therapy, close blood pressure monitoring, and regular imaging follow-up. Systemic hypertension, advanced age, aortic dilatation, and continuous flow within the false lumen are all high risk factors for the development of distant adverse events. Aortic coarctation with poorly controlled blood pressure will have a 10-fold increased rupture rate [4]. It is estimated that approximately 1/3 of patients experience pseudolumen expansion, entrapment aneurysm formation, or rupture within 5 years after TEVAR [18]. Residual rupture and persistent pseudolumen perfusion are the underlying causes of continued postoperative pressure elevation within the pseudolumen. The proportion of pseudolumen thrombosis in the covered segment of the thoracic aorta after acute phase TEVAR is approximately 80% to 90%, and 50% to 60% of pseudolumen perfusion can exist in the distal unstented area to the level of the iliac artery with only 20% of pseudolumen thrombosis [23]. Studies have shown that the number of residual ruptures after TEVAR for chronic entrapment is much higher than for those with TEVAR in the acute phase; together with the hardening of the septal scar, it is more difficult to obtain complete pseudoluminal thrombosis and to restore the true lumen volume to the pre-entrapment level in TEVAR in the chronic phase.Huptas et al. found by imaging follow-up that recovery of true lumen volume and reduction of pseudolumina occurred early after TEVAR for type B entrapment, with a mean At 14 months of follow-up, the true lumen volume would further recover to near normal aorta, while the false lumen further shrank, but similar true and false lumen volume remodeling was not observed in the drug-treated group [24]. Therefore, not all patients with postoperative pseudoluminal perfusion require early management; Resch et al. found that only 12% of those with pseudoluminal perfusion after acute TEVAR developed aneurysmal expansion in the intermediate and distal stages, and this percentage was only 23% after chronic TEVAR [25]. Surgical treatment, whether conventional surgical treatment or TEVAR, is limited to slowing the progression of the disease and increasing life expectancy, and is not likely to reverse its natural course. As with TEVAR for other types of aortic disease, the prognosis of TEVAR for aortic coarctation is more dependent on the mastery of surgical indications and operator experience than advances in stent materials.TEVAR has delivered unprecedented and relatively favorable early and intermediate outcomes for patients with aortic coarctation. We look forward to the emergence of more and more high-level evidence-based medicine to assess its long-term prognosis and ultimately establish the place of TEVAR in the treatment of aortic coarctation.