An aneurysm is defined as a permanent restrictive dilatation of the arterial vessel wall exceeding 50% of the normal vessel diameter. Therefore, a precise definition of abdominal aortic aneurysm (AAA) would require calculation of the ratio of normal to dilated abdominal aorta in the same individual, with correction for influencing factors such as age, sex, race and body surface area. Usually, AAA can be diagnosed with an abdominal aortic diameter of more than 3 cm. 1. Incidence The occurrence of AAA is related to many epidemiological factors, such as age, gender, race, family history, and smoking. The incidence of AAA is correspondingly higher in people of advanced age, males, Caucasians, positive family history, and long-term smokers. The Malma Hospital in Sweden has performed autopsies on all patients who died during hospitalization and found that the incidence of AAA gradually increases with age in people over 50 years of age and can reach 5.9% in male patients over 80 years of age [1]. 2. Etiology The biological mechanisms of aneurysm development are complex, and genetic susceptibility, atherosclerosis and various proteases have been shown to be directly related to its occurrence. All etiologies ultimately manifest as degenerative changes in the middle layer of the aorta, followed by dilatation under blood flow pressure to form aneurysms. 2.1 Genetic susceptibility Several studies have shown that the occurrence of aneurysms is closely related to genetics. A 9-year follow-up of foreign patients with AAA found that aneurysms at all sites also occurred in 15% of the immediate family members of AAA patients, compared with 2% of controls, P<0.001 [2]. Other studies have shown that familial AAA generally develops at an earlier age than sporadic AAA, but there is no evidence that the former is more likely to rupture than the latter; AAA occurrence is strongly associated with polycystic kidney, which has been shown to be an autosomal dominant disorder. 2.2 Atherosclerotic factors AAA and peripheral atherosclerotic occlusive disease, although presenting differently, one as vasodilatation and the other as stenosis occlusion, are often concomitant and share common risk factors, such as smoking, hypertension, hyperlipidemia, diabetes mellitus and cardiovascular disease. This is all strong evidence that atherosclerosis is inextricably linked to the development of aneurysms. 2.3 Role of various proteases A notable histological manifestation of aneurysms is degeneration of the middle elastic membrane, where collagen and elastin in the tissue are destroyed by the corresponding proteases; increased local metalloproteinases (MMP), which contribute to the translocation of smooth muscle cells and lead to structural destruction of the vascular middle layer; and increased local macrophage and cytokine concentrations, suggesting the presence of an inflammatory response. All three of these points may lead to aneurysm wall disruption and dilation and aneurysm formation. 2.4 Congenital aneurysms Some congenital disorders are often associated with cystic changes in the middle layer of the aorta, which can lead to congenital aneurysm formation. The most common of these is Marfan syndrome. This is an autosomal dominant disorder with clinical manifestations such as skeletal malformations, ligamentous laxity, lens prolapse, aortic dilatation, and cardiac valve insufficiency. Other rare congenital disorders include Ehlers-Danlos syndrome. Although some congenital disorders have been shown to be caused by single gene lesions, most are formed by a combination of polygenic lesions. 2.5 Inflammatory AAA Inflammatory AAA is a specific type of aneurysm with an unusually thick, shiny white, hard wall that is highly susceptible to fibrotic adhesions to intra-abdominal organs (e.g., ureter, duodenum). Inflammatory AAA was first described in 1972 by Walker et al. Further studies found an abnormally increased distribution of macrophages and cytokines within the wall of inflammatory aneurysms compared to normal AAA. Therefore, it is now generally accepted that inflammatory AAA is an extreme manifestation of aneurysmal inflammation. Epidemiological studies have shown that the incidence of inflammatory AAA accounts for about 5% of all AAAs. There are no significant differences between inflammatory AAA and common AAA in terms of risk factors, treatment options and prognosis. In terms of clinical manifestations, inflammatory AAA is more likely to present with symptoms such as back or abdominal pain, and is usually accompanied by increased blood sedimentation. Chronic abdominal pain, weight loss, and increased blood sedimentation are the triad of diagnosing inflammatory AAA. 2.6 Infectious AAA Infectious AAA is a rare disease. In recent years, with the continuous development of antibiotics, its incidence is even decreasing. Primary infections of the aortic wall resulting in aneurysms are rare, and most infectious AAAs are caused by secondary infections. Staphylococcus and Salmonella are the most common infectious AAA causative agents, while Mycobacterium tuberculosis and syphilis can also cause aortic aneurysms to occur. 3. Natural course The natural course of AAA is the gradual enlargement of the aneurysm and the formation of an appendage thrombus due to continuous turbulent flow of blood in the aneurysmal cavity. Therefore, the most common complications of AAA are aneurysm rupture, distal organ embolism and adjacent organ compression. 3.1 Natural course of AAA Epidemiological data show that when the AAA is less than 4 cm in diameter, the annual growth rate is around 1 mm to 4 mm; when the tumor is 4 cm to 5 cm in diameter, the annual growth rate is around 4 mm to 5 mm; when the tumor is more than 5 cm in diameter, the annual growth rate is greater than 5 mm, and the tumor eventually ruptures at a rate of 20%; if the tumor is greater than 6 cm in diameter, the tumor annual growth rate is between 7mm and 8mm, and the eventual rupture rate of the tumor increases to 40%. The risk of ruptured AAA is extremely high, with a mortality rate of 90% [3]. Therefore, it is now generally accepted that surgical treatment is required when the AAA aneurysm is greater than 5 cm in diameter. In women, due to the thin diameter of the abdominal aorta, surgical treatment should be considered if the aneurysm is greater than 4.5 cm [4]. In addition, if the AAA aneurysm diameter grows too fast and is greater than the aforementioned average value, early surgical treatment should also be considered.Factors associated with AAA rupture, in addition to aneurysm diameter, include hypertension, chronic obstructive pulmonary disease, long-term smoking, female and positive family history, all of which increase the risk of AAA rupture. 3.2 Natural course of common iliac artery aneurysms Isolated common iliac artery aneurysms without concomitant AAA are rare, and therefore epidemiological data on this subject are scarce. Approximately 1/2 to 1/3 of common iliac aneurysms are bilateral, and most patients are asymptomatic at the time of diagnosis. Common iliac artery aneurysms larger than 5 cm in diameter are prone to rupture and require surgical treatment. There are few reports of rupture of common iliac artery aneurysms less than 3 cm in diameter. Therefore, it is generally believed that common iliac artery aneurysms less than 3 cm in diameter only require close monitoring and regular review. 3.3 Local compression or erosion of AAA aneurysms When AAA aneurysms are large, they can compress the duodenum and cause symptoms of upper gastrointestinal obstruction such as difficulty in eating, and in severe cases, they can invade the duodenum to form duodenal fistula and cause gastrointestinal hemorrhage, which is one of the most fatal complications of AAA. In addition, AAA can also compress the inferior vena cava or renal vein, and even occur as abdominal aorta-inferior vena cava or abdominal aorta-renal vein fistula, leading to acute heart failure and death. 4. Diagnosis 4.1 Symptomatic AAA Pain is the most common complaint of AAA. The site of pain is usually located in the middle abdomen or low back, and the nature of pain is usually dull and can last for hours or even days. This pain is characterized by the fact that it usually does not change with body position or movement, which is different from the common low back pain in the elderly and needs to be differentiated. When the pain suddenly increases, it is often indicative of an impending AAA rupture. Blood is often confined to the posterior peritoneum after rupture of the aneurysm, so blood pressure does not drop too rapidly and bruising of the abdominal wall (Grey-Turner sign) can occur bilaterally, spreading further to the perineum. The tumor may also rupture into the abdominal cavity, which is associated with abdominal muscle tension and hypotension due to massive blood loss; rupture into the duodenum may result in upper gastrointestinal hemorrhage and death due to rapid onset of hypovolemic shock. 4.2 Asymptomatic AAA Most AAAs are asymptomatic, and patients find pulsatile abdominal masses unintentionally or during physical examination. Since AAA and peripheral arterial occlusive disease share the same high-risk factors, regular aortic and peripheral arterial examinations should be performed in this high-risk group to achieve early detection and diagnosis and to reduce AAA rupture rate and mortality. 4.3 Physical examination When examining the above high-risk group, pay attention to the examination of the abdominal aorta and peripheral arteries. If a widened pulsatile area in the abdomen is found, the occurrence of AAA should be alerted. In general, most AAAs larger than 4 cm in diameter can be detected by meticulous physical examination, and factors such as obesity may affect the sensitivity of the examination. There is no evidence-based medical evidence to confirm that inspection increases the risk of AAA rupture. 4.4 Imaging 4.4.1 Color Doppler ultrasound Ultrasound is characterized by being noninvasive, inexpensive, radiation-free, and has reliable data. Color Doppler ultrasound has been widely used to screen AAA for more than 90% of the brine in the outfitting line. However, its shortcomings are that it is operator-dependent, and different cut lines of the probe will yield different data, which affects the objectivity of the result measurement; for AAA and iliac artery aneurysm in deeper locations, its diagnostic accuracy is also reduced due to intestinal gas interference. 4.4.2 Plain abdominal X-ray A significant proportion of AAAs are found when abdominal X-ray is performed, and the images show an arcuate calcification with expansion in the aortic region; they can also show a large soft tissue shadow in the abdomen, making the contours of the psoas major muscle poorly displayed, all of which suggest the presence of AAA. 4.4.3 CT angiography CT angiography is less invasive, less expensive, and can accurately measure various data of AAA, which has basically replaced transcatheter angiography. Especially, multi-detector CT emerged in recent years, which can obtain more high-quality images in a shorter time, and further improve the accuracy of CT diagnosis. In some medical centers, CT angiography has gradually become the gold standard for preoperative examination and postoperative follow-up of AAA. preoperative CT evaluation of AAA includes: the maximum diameter of the aneurysm; the relationship between the aneurysm and the renal artery; the length, diameter, and angulation and calcification of the normal aorta under the renal artery (i.e., the neck of the aneurysm); the diameter and tortuosity of the iliac artery; it also requires careful analysis of any vascular variants, such as the collateral renal artery , bilateral inferior vena cava, or left renal vein behind the aorta, etc. All these data can be clearly understood by a single high-quality CT angiogram. 4.4.4 Magnetic resonance angiography Compared with CT angiography, magnetic resonance angiography has the advantage of being able to show severely calcified vessels, with a small amount of contrast and little impact on cardiac and renal function. Therefore, MR angiography is the preferred diagnostic imaging tool for patients with renal insufficiency. The disadvantage is that the scan time is long, it is not suitable for patients with metal grafts placed in the body and claustrophobia, and there is still a gap in imaging quality compared with CT. 5.Conservative treatment 5.1 Close monitoring If the tumor is less than 4cm in diameter, color Doppler ultrasound examination is recommended every 2 to 3 years; if the tumor is larger than 4cm but less than 5cm in diameter, close monitoring is needed, and color Doppler ultrasound or CT angiography is recommended at least once a year. Once the tumor is found to be more than 5 cm, or the tumor grows too fast during the monitoring period, early surgery is needed. 5.2 Medication After the diagnosis of AAA is confirmed, smoking should be strictly abstained during the observation period, and attention should be paid to controlling blood pressure and heart rate. It has been found that oral β-blockers can reduce the rate of expansion of atherosclerosis-induced AAA, effectively reducing the rupture rate and mortality due to perioperative adverse cardiac events, which is the only drug proven to be effective in the conservative treatment of AAA [5]. The rationale may be that by slowing down the heart rate, the intra-aortic pressure is reduced, thus reducing the impact of blood flow on the aortic wall and slowing down the rate of aneurysm expansion. 6, AAA open surgery The earliest AAA resection and artificial vessel grafting originated in the 1960s. After more than 40 years of development, it has evolved and matured, and has become one of the classic surgeries. Although, in recent years, EVAR has developed rapidly, causing a great impact on the dominance of open surgery. However, for AAA patients with low risk factors who are in good general condition and can tolerate surgery, open surgery is still the standard procedure for treatment because of its definite immediate and long-term results. 6.1 Incision choice The classical open surgical incision for AAA is chosen as a median abdominal incision to enter the abdominal cavity layer by layer and open the retroperitoneum to expose the AAA. a left-sided extraperitoneal incision approach has also been attempted and is considered suitable for patients who have had multiple abdominal surgeries with heavy abdominal adhesions. However, there is no definitive evidence-based medical evidence to suggest a significant difference between the two approaches in terms of perioperative surgical complications and long-term treatment outcomes. 6.2 Preoperative evaluation AAA patients are also at high risk for cardiovascular disease; therefore, preoperative cardiac evaluation is particularly important. Studies have demonstrated that perioperative mortality in open AAA surgery is significantly correlated with preoperative patient cardiac function, and mortality is significantly increased if patients have poor preoperative cardiac function. Therefore, a detailed preoperative cardiac evaluation with electrocardiogram and cardiac ultrasound and, if necessary, coronary angiography is required to adequately assess the degree of coronary stenosis. In addition to this, careful evaluation of pulmonary function and liver and kidney function should be performed preoperatively. 6.3 Perioperative Outcomes Comprehensive literature reports that the mortality rate for elective open surgery for AAA ranges from 2% to 8%, with results varying from center to center due to differences in experience. The mortality rate for ruptured AAA surgery is much higher, ranging from 40% to 70% in all centers [6-9]. The higher the age of the patient, the higher the perioperative mortality; female patients have a significantly higher mortality rate than males. Preoperative patient cardiac function, pulmonary function, and renal function were all independent factors influencing perioperative mortality. 6.4 Long-term survival and complications The 5-year survival rate for elective AAA surgery ranges from 60% to 75%, and the 10-year survival rate ranges from 40% to 50% [10, 11]. AAA involving the renal artery has a lower prognosis and long-term survival rate than common infrarenal AAA due to the need for renal artery grafting, with a 5-year survival rate of less than 50% [12]. complications of open AAA surgery include: anastomotic bleeding, pseudoaneurysm; colonic ischemia; graft occlusion; graft infection, combined with duodenal fistula, with incidence rates ranging from 0.5% to 5%. 7. Endovascular aneurysm repair (EVAR) 7.1 Introduction Parodi et al. first used trans-femoral AAA EVAR in an attempt to apply it to high-risk patients who were not suitable for open surgery. Over the next decade, interventional devices and related surgical techniques have rapidly evolved and improved and matured. Because EVAR avoids long abdominal incisions, it greatly reduces surgical trauma; it can be performed with regional block anesthesia or local anesthesia, and is particularly suitable for patients with severe combined cardiopulmonary insufficiency and other high-risk factors. Due to the minimally invasive nature of EVAR, its indications are rapidly expanding in some countries and medical centers, and it has even begun to replace traditional open surgery in AAA patients with low risk factors. The stent grafts currently used in EVAR are made by suturing and fixing the artificial vessel inside a metal stent to prevent twisting and ectasia of the artificial vessel and to maintain stability. To accommodate aortic bifurcation structures and to increase the stability of the stented vessel, most current stent graft products use a patterned design in which the main body and one iliac branch are placed through one femoral artery and the other iliac branch is placed through the contralateral femoral artery and positioned for docking. An important prerequisite for the implementation of this procedure is the presence of a normal aorta of sufficient length beneath the renal artery that can serve as a proximal anchorage zone for the stent to prevent ectopic stent grafts to the distal side and to prevent the occurrence of postoperative endoleaks. 7.2 Preoperative evaluation AAA EVAR has a low impact on the patient's systemic status and is only equivalent to moderate to low surgical trauma, with significantly lower perioperative mortality and complication rates than conventional open surgery. However, preoperative assessment of cardiac function is still required to understand whether the patient has a previous history of acute heart attack or heart failure. Other organ function should also be assessed, with particular attention to renal function, to prevent the development of postoperative contrast nephropathy. 7.3 Perioperative Outcomes Most of the data on comparing perioperative mortality between AAA open surgery and EVAR are non-randomized controlled studies, due to the fact that EVAR is chosen mostly for high-risk surgical patients. Nevertheless, the perioperative mortality rate after EVAR is less than 3%, which is lower than that of open surgery. In addition, EVAR has a lower rate of fatal perioperative complications compared to open surgery, patients recover quickly after surgery, and ICU treatment time and overall length of stay are greatly reduced [13-16]. 7.4 Long-term survival and postoperative complications The long-term survival of patients after AAA EVAR depends largely on preoperative high-risk factors, and comprehensive literature reports a significant difference in the 3-year survival rate after EVAR between high-risk and general patients, 68% and 83%, respectively [16].The main post-EVAR complications include endoleaks, stent graft ectasia, torsion, graft occlusion, and infection. It has been shown that the larger the preoperative AAA tumor diameter, the higher the incidence of postoperative endoleaks, stent ectasia, and other complications [17]. 7.5 Problems with EVAR With the continuous improvement of interventional devices and techniques, AAAEVAR has become increasingly mature, but there are still some problems with this procedure, which need to be further developed and improved. 7.5.1 Vascular anatomical limitations: Compared with traditional open surgery, EVAR requires higher vascular anatomical conditions. First, a normal aorta of at least 1.5 cm in length under the renal artery is required as the proximal anchorage area, i.e., the neck of the aneurysm must be at least 1.5 cm long; at the same time, the diameter of the neck is required to be less than or equal to 28 mm, while it must not be severely angulated. It is also required that the external iliac artery and the femoral artery have sufficient diameter to ensure the passage of the delivery vehicle carrying the stent graft. Because of the thin external iliac artery in women, the proportion of women who forgo endoluminal treatment due to poor delivery routes is substantially higher than that of men, with approximately 17% of women compared to 2.1% of men reported in the literature [18]. 7.5.2 Endoleaks: Endoleaks refer to persistent blood flow into the closed tumor cavity after AAAEVAR and can be classified into the following four types. type I endoleaks refer to blood flow into the tumor cavity due to failed closure of the proximal segment or distal anchorage area, which generally has high pressure in the tumor cavity and can easily lead to tumor rupture. Once detected, it needs to be corrected by adding extensions proximally or distally. Type II endoleaks refer to the return of blood into the tumor cavity through branch arteries (e.g., lumbar artery, inferior mesenteric artery, etc.) and occur in about 40% of cases. Most of them can close the lumen with prolonged thrombosis on their own, or selective branch artery embolization has been performed through catheterization. However, current evidence suggests that type II endoleaks do not increase the incidence of proximal or distal rupture of the tumor. type III endoleaks are leaks at the interface due to breakage or distortion of the stent vessel and require immediate interventional or surgical correction once they occur. type IV endoleaks are those in which blood enters the tumor lumen due to high permeability of the stent vessel and generally occur within 30 days of stent vessel placement. In addition, some patients with persistent luminal enlargement after AAAEVAR have not been found to have significant endotension by CT scan, which is referred to as endotension. In conclusion, it is due to the presence of inexact factors such as endotension that patients after AAAEVAR need to be followed up regularly. The follow-up interval is usually 3, 6, and 12 months after surgery, and annually thereafter. If the imaging data reveal progressive enlargement of the tumor, further investigations are needed to clarify the cause. 7.5.3 Stent graft occlusion: There is a high incidence of stent graft occlusion after early AAAEVAR. An important reason for occlusion is the twisting of the graft into an angle. It was later found that the use of a metal stent as an external support can reduce the twisting of the vascular graft, thus greatly reducing the incidence of graft thrombosis occlusion. 7.5.4 Aneurysmal neck dilatation: After AAAEVAR, the aorta in the proximal anchorage area will dilate further over time, which can lead to ectopic stent grafts distal to the stent. Currently, when EVAR is performed, the stent body diameter is generally selected to exceed the proximal aneurysm neck diameter by 10-20% to accommodate future aortic expansion, but even so, late ectopic stent grafts cannot be completely prevented.