Coil embolization is widely used in the treatment of VAA because of its minimally invasive nature, short recovery time, and low rates of morbidity and mortality [15]. Most VAAs are asymptomatic [16], and 36.9% (38/103) of all VAA patients in this study had acute symptoms due to rupture and gastrointestinal bleeding. Symptomatic aneurysms can be an indication for intervention, although few studies have compared SVAA and ASVAA.
For VAAs that meet the indications, whether they are true aneurysms or pseudoaneurysms, intervention is recommended by guidelines as a matter of urgency due to their susceptibility to rupture. Mortality after VAA rupture is acknowledged to be high; the overall 30-day mortality rate in our study was approximately 3%. All deaths occurred in the A group; the mortality rate was significantly higher than the B group (P = 0.042); this result was similar to that published previously [6, 17]. The event-free survival rate was higher in the B group (84.1%) than in the A group (74.3%), although there was no significant difference between the two groups (P = 0.900). Importantly, the two patients who died in this study were also the patients who died in the A group; both had pseudoaneurysms, except that one was from the splenic artery and the other was from the hepatic artery. Considering the high mortality rate following the rupture of pseudoaneurysms, coil embolization is performed immediately after a confirmed diagnosis. In a previous study, Carr et al. demonstrated a 50% mortality rate (3/6) after the successful emergency embolization of pseudoaneurysms[18]; this is similar to the 40% mortality rate for pseudoaneurysms observed in the current study. Consequently, pseudoaneurysms still have a high mortality rate even when successfully treated with embolization. Based on our data, 60% (3/5) of patients with pseudoaneurysms require reintervention; this may be related to their specific and fragile structure.
Pseudoaneurysms are mainly caused by inflammation and trauma, with rupture of the intima and the resulting episcleral bulge, owing to the thinner abnormal vascular structures; the size of pseudoaneurysms is not related to the risk of rupture [19]. Smaller pseudoaneurysms tend to be detected only when they show dangerous symptoms such as bleeding, while larger pseudoaneurysms can be found incidentally on imaging. The incidence of pseudoaneurysm rupture can be as high as 80%, depending on the location, and the mortality rate can be as high as 100% if left untreated [20, 21]. In the last century, immediate open surgery was recommended for pseudoaneurysms due to war or traumatic causes that made them difficult to treat or impossible to heal. With the rapid development of endovascular techniques over the last two decades, and the fact that endovascular treatment has been proven to be safe and effective in most studies, endovascular treatment has become the first choice of more and more vascular surgeons for the treatment of pseudoaneurysms [22, 23]. Theoretically, the use of coils or hydrogels to occlude a pseudoaneurysm, followed by an endoluminal stent to maintain revascularization, is a safer and more reliable approach, and also frequently used in the treatment of intracranial aneurysms. One reason for this is that in some wider aneurysms of the neck, simple tamponade has the potential to allow the coil or tamponade to move into the vessel postoperatively, inadvertently increasing the risk of thrombosis or embolism. Direct embolization of vessels in focal sources such as the duodenal arteries appears to be a good approach, but some vessels are not suitable for such treatment, the anatomy of patients is diverse and complex, and many visceral arteries are too small or too tortuous to allow for successful stent placement, thus resulting in a limited selection of stent grafts.
Approximately 62% of aneurysms are reported to be caused by atherosclerosis [24]; lipoproteins are known to play an important role in atherosclerosis. The proportion of patients with dyslipidemia was higher in A group than in the B group (P = 0.010). Most studies have concluded that total cholesterol and low-density lipoprotein levels are positively associated with the risk of aneurysm. For example, Kubota et al. investigated 13,683 participants without a history of aneurysm surgery over a 2-year period; restricted cubic spline analysis demonstrated a positive dose-response relationship between plasma lipoprotein (a) with abdominal aortic aneurysm, with a steep increase in the risk of AAA above the 75th percentile [25]. In another study, Huang et al. concluded that high-density lipoprotein (HDL) was negatively associated with the risk of growth and rupture of intracranial aneurysms (P = 0.002)[26]. In contrast, however, other studies have shown that overly low triglyceride and low-density lipoprotein (LDL) levels significantly increase the risk of vascular rupture and bleeding. Rist et al. showed that LDL-C levels below 70 mg/dL and low triglyceride levels significantly increased the risk of hemorrhagic stroke; these authors suggested that low cholesterol leads to necrosis of the smooth muscle cells in the middle layer of the artery and that endothelial damage is more likely to lead to microaneurysms, which are often found in patients with cerebral hemorrhage [27]. We next plan to further specify the lipid data of VAA patients to analyze the effect of various lipoproteins on the prognosis of VAA.
In general, coil embolization therapy has a clear advantage for the parenchymal organs (e.g., splenic aneurysms, hepatic aneurysms), where open surgical treatment may sacrifice the spleen or part of the liver. Splenic infarction accounts for the majority of end organ ischemia and has the potential to occur when the embolization of more distal splenic artery lesions is performed. In a retrospective study of 253 visceral aneurysms, 20 SAA patients were treated with splenic artery embolization[6]. Two cases of splenic infarction and one case of pancreatic abscess were found in this group; all of these aneurysms occurrences were found in the splenic bed.
The mortality rate within 30 days after surgery in our study was approximately 3%, which is much lower than that in other studies [28, 29]. However, our study did not include all types of visceral aneurysms, such as mesenteric aneurysms, pancreaticoduodenal aneurysms, and gastroduodenal aneurysms. In addition, due to the low prevalence of VAA, the number of cases that could be included in this study was limited.