Clinical features and management strategy of symptomatic spontaneous isolated celiac artery dissection

Abstract

Objectives

The aim of this study was to evaluate the clinical features and management strategy for patients with symptomatic spontaneous isolated celiac artery dissection (SICAD).

Methods

In this retrospective study, consecutive patients with symptomatic SICAD from two institutions were included. The demographics, clinical manifestations, comorbidities, imaging findings and treatment strategy selection were obtained from the medical records. The general epidemiological data, treatment regimens and clinical and follow-up outcomes were analysed.

Results

Patients were divided into the conservative treatment group (group A, n = 26) and endovascular treatment group (group B, n = 11). Of these 37 patients, extent of dissection in both groups included only celiac trunk (61.54%% vs. 18.18%, p = 0.03), common hepatic artery (CHA) and splenic artery (SA) (3.85%% vs. 54.55%, p = 0.001), CHA (7.69% vs. 18.18%, p = 0.57), SA (23.08% vs. 9.09, p = 0.65) and left gastric artery (LGA) (3.85% vs. 54.55%, p = 0.99). Of note, the extension of the lesion in group A was shorter than that in group B. In addition, there were significantly more type IIb in group A than in group B (42.31% vs. 9.09%, p = 0.06) and the mean length of dissection in group A was 42.3 ± 54.71 mm which was significantly shorter than that in the group B 58.45 ± 3.71 mm (p =0.04). During a median follow-up of 11.5 months, the 1, 3, 6 and 12 month follow-ups were completed in 100% (37/37), 100% (37/37), 94.59% (35/37) and 91.19% (34/37) of patients, respectively. The cumulative rate of persistent disease stability in patients with endovascular treatment group was higher than in that conservative treatment group at the 3, 6, 9 and 12 months (50% vs. 16.67%, p = 0.001; 80% vs. 37.5%, p =0.03; 100% vs. 62.5%, p = 0.012;100% vs. 91.67%, p = 0.02 respectively).

Conclusion

Most symptomatic SICAD have a tendency to persistent disease stability after conservative treatment. Risk factors for failed conservative treatment were length of dissection and branch involvement. Furthermore, endovascular treatment was associated with a high technical success and persistent disease stability rate, which might be reserved for patients with failed conservative treatment.

Keywords

Celiac artery dissection treatment

Introduction

Spontaneous isolated celiac artery dissection (SICAD), which is defined as a dissection in the celiac artery (CA) without the involvement of the aorta, is a rare disease but potentially catastrophic pathology.¹ The natural history of symptomatic SICAD is variable and unpredictable. Previous literature indicates that the incidence of SICAD was less than spontaneous isolated superior mesenteric artery dissection (SISMAD), and most were case reports or series.^2–5 The etiology remains largely unknown, several presumed risk factors include hypertension, smoking, atherosclerosis, vasculitis, dysplasia of myofibrillae fibers, arterial cystic degeneration, medial degeneration, pregnancy, connective tissue disease and autoimmune diseases.⁶

In clinical settings, SICAD is detected with contrast-enhanced computed tomography (CT) scans or angiography (CTA) when patients present with symptoms such as abdominal pain.⁷ However, there is no consensus on the treatment of this rare disease. Because it generally has a benign course, conservative management with or without antithrombotic agents (antiplatelet or anticoagulant) is recommend according to European Society for Vascular Surgery (ESVS) Guidelines, and yet in cases of emergent presentation, endovascular therapy is warranted.¹ In this study, we retrospectively analysed the clinical characteristics and outcomes of symptomatic SICAD based on our experience to propose an optimal therapeutic strategy of this condition.

Methods

Study design

The present retrospective study was approved by the institutional review board, and the requirement for written informed consent was waived. Between January 2012 to December 2019, consecutive patients with contrast-enhanced CT scans diagnosed symptomatic SICAD from two institutions were enrolled in the study. Two reviewers (DS and YJX) independently searched the EMRS (electronic medical record system) to identify patients with SICAD in two institutions, respectively. The demographics, initial symptoms, comorbidities, imaging characteristics and treatment strategy selection were obtained from the medical records. Treatment strategy (initial treatment choices, subsequent treatment and the use of antithrombotic agents that comprised antiplatelet or anticoagulant) and procedure related information and complications were recorded. The follow-up outcomes were recorded and analysed.

Image analysis

Two experienced radiologists and two vascular surgeons reviewed all CT examinations and reached consensus. The lesions were categorised based on the Yun classification as follows: type I, patent true and false lumen revealing entry and re-entry sites (entry and reentry tear visible, patent false lumen), type IIa (only entry tear visible, patent false lumen), type IIb (thrombosis of false lumen, patent true lumen) and type III (occlusion of true and false lumen).⁸ Imaging characteristics were analysed including ostial involvement (distance between the ostium of the CA and the origin of the dissection), dissection length, TLRD (true lumen residual diameter, true lumen size compared with the adjacent normal CA size),⁹ extent of dissection, signs in favour of the organ ischemia (defined as an organ with a complete or incomplete enhancement defect in the arterial and venous phases on initial contrast-enhanced CT scans but with enhancement improvement on follow-up CT scan)²,¹⁰ and dissecting aneurysm formation (at least 50% larger than the adjacent normal CA).¹¹

Definitions

Failure of conservative management was defined as the persistence or aggravation of symptoms and signs, increasing size of aneurysmal dilation, or appearance of peritonitis after conservative management. Persistent symptoms were defined as no change in or the aggravation of symptoms after a week of conservative treatment with antithrombotic agents.¹² Persistent disease stability was defined as the absence of symptoms or dissection positive remodelling after twice or more than twice thereafter. Positive remodelling was defined as complete remodelling and positive morphological changes.¹³ Technical success was defined as successful deployment of intervention content (stents, coils and thrombolytic catheters) to the target locations.¹⁴ Symptom duration was defined as the period from the onset of abdominal pain until disappeared. Procedure-related complications were classified as major and minor according to the guidelines of the Society of Interventional Radiology.¹⁵

Therapeutic schemes

Treatment decisions were based on the patient’s symptoms and imaging characteristics of the dissection. All patients initially underwent conservative treatment, which consisted of fasting, gastrointestinal decompression, analgesia, spasmolysis, parenteral nutrition and blood pressure control (systolic blood pressure and diastolic blood pressure should be 130–140 mmHg and 70–80 mmHg, respectively). Close surveillance range of seven days was used during the period of conservative treatment. After close surveillance, follow-up CTA was repeated to evaluate the morphological changes of the dissection, including dissection length, dissecting aneurysm formation, extent of dissection and true lumen stenosis. Conservative treatment was continued in patients with remission of symptoms and no deterioration of dissection morphology. However, conservative treatment failed were considered as candidates for endovascularly.

Endovascular intervention was performed through the right common femoral artery approach, and self-expandable stent Cordis SMART Control stent (Cordis Corporation, Warren, NJ, USA) or covered stents (Jostent, Abbott Vascular, Abbott Park, IL, USA (n = 2) were placed. In general, the stent diameter approximately 10% larger than that of normal CA routinely and was at least 5 mm longer than each at the distal and proximal margins. In addition, coiling (MicroVention, Aliso Viejo, CA, USA; Cook, Bloomington, IN, USA) was employed in patients with dissecting aneurysm and some with type IIa if the false lumen and/or entry tear were overwhelmingly large. Surgical treatment was to be used in patients with artery rupture or newly appearing peritonitis.

Anticoagulant regimen: during hospitalisation, low molecular weight heparin sodium (Sanofi, Paris, France) at a dose of 100 IU/kg, subcutaneous injection, every 12 h; after discharge, oral warfarin (Qilu Pharmaceutical, Shandong, China), INR (International Normalised Ratio) controlled at 2.0–3.0, for a time period of three months. Antiplatelet regimen: during hospitalisation, oral aspirin (Bayer Consumer Health, Germany) at a dosage of 100 mg/day after discharge, oral aspirin at a dosage of 100 mg/day, for a time period ≥ six months.

Follow-up

Patients were followed up for one, three and six months after discharge with CTA. If the symptom was stable or the lesion showed regression, then patients were scheduled for 12–24 months later. The criterion for termination of following up was persistent disease stability. Follow-up consisted of contrast-enhanced CT scanning and physical examination. More frequent evaluations were performed when needed. Those whose symptoms indicated worsening lesions underwent imaging evaluations immediately.

Statistical analyses

All statistical analyses were performed using SPSS 22.0 software (SPSS Inc., Chicago, IL, USA). Continuous variables are presented as the medians and ranges in the cases of nonparametric distributions, and comparisons were made using the Mann–Whitney test. Continuous variables are presented as the means and standard deviations in cases of parametric distributions, and comparisons were made using the independent t-test. Categorical variables were compared with the chi-square test or Fisher’s exact test, and they are reported as frequencies and percentages. The cumulative rate of persistent disease stability was calculated using a Kaplan–Meier curve generated with GraphPad Prism (7.0v; GraphPad Software Inc, La Jolla, CA, USA). A p value < 0.050 was considered to be statistically significant.

Results

Patients

Between January 2012 to December 2019, 37 consecutive patients with symptomatic SICAD from two institutions were enrolled in the study. Patients were divided into the conservative treatment group (group A, n = 26) and endovascular treatment group (group B, n = 11) (Figure 1). Of these 37 patients, the median age was 52.5 years old (ranging from 39 to 72) in group A and 47 years old (ranging from 36 to 63) in group B. Thirty-four (91.89%, 34/37) patients were men, and the misdiagnosis rate reached 13.51% in this study. Risk factor and comorbidities are associated with symptomatic SICAD include smoking history 13 (35.14%, 13/37), hypertension 17 (45.95%, 17/37), hyperlipidemia 4 (10.81%, 4/37) and food intake 4 (10.81%). There were no statistically significant differences between groups A and B. Furthermore, no patients were diagnosed as having connective tissue disease. Among the 37 patients, 32 (86.49%, 32/37) had abdominal pain as the initial symptom accompanied by nausea and vomiting 9 (23.32%) patients. Other symptoms included back pain 4 (10.81%, 4/37), chest pain 1 (2.7%, 1/37), abdominal distension 3 (8.11%, 3/37) and hematochezia 2 (5.41%, 2/37). Patient demographics, presentations, risk factors and comorbidities are summarised in Table 1.

Figure 1.

Study flowchart.

Table 1.

Baseline characteristics of patients admitted for symptomatic spontaneous isolated coeliac artery dissection.

Variable	Total (n = 37)	Group A (n = 26)	Group B (n = 11)	p value
Median age, years (min, max)	51 (36.72)	52.5 (39.72)	47 (36.63)	0.2
Male	34 (91.89%)	22 (84.62%)	11 (100%)	0.3
Misdiagnosis (yes)	5 (13.51%)	4 (15.38%)	1 (9.09%)	0.99
Symptoms
Abdominal pain	32 (86.49%)	22 (84.62%)	10 (90.9%)	0.99
Back pain	4 (10.81%)	4 (15.38%)	0	0.3
Chest pain	1 (2.7%)	0	1 (9.1%)	0.3
Abdominal distension	3 (8.11%)	3 (11.54%)	0	0.54
Hematochezia	2 (5.41%)	1 (3.85%)	1 (9.1%)	0.51
Nausea and Vomiting	9 (23.32%)	8 (30.77%)	1 (9.1%)	0.23
Risk factor and comorbidities
Smoking history	13 (35.14%)	9 (34.62%)	4 (36.36%)	0.92
Hypertension	17 (45.95%)	12 (46.15%)	5 (45.45%)	0.97
Hyperlipidaemia	4 (10.81%)	3 (11.54%)	1 (9.1%)	0.99
Food intake	4 (10.81%)	3 (11.54%)	1 (9.1%)	0.99

Note: Group A: conservative treatment group. Group B: endovascular treatment group. Misdiagnosis: the initial visit was misdiagnosed as another diseases.

With regard to confirmed gist, 16 (43.24%, 16/37) patients presented with intimal flap, 12 (32.43%, 12/37) patients presented with thrombosed false lumen, and 9 (24.32%, 9/37) patients presented with pseudoaneurysm. Extent of dissection in both groups included only celiac trunk (61.54%% vs. 18.18%, p = 0.03), common hepatic artery (CHA) and splenic artery (SA) (3.85%% vs. 54.55%, p = 0.001), CHA (7.69% vs. 18.18%, p = 0.57), SA (23.08% vs. 9.09, p = 0.65) and left gastric artery (LGA) (3.85% vs. 54.55%, p = 0.99). Of note, the extension of the lesion in group A was shorter than that in group B. Of these patients, 8 (21.62%, 8/37) had type I SICAD, 14 (37.84%, 14/37) had type IIa, 12 (32.43%, 12/37) had type IIb and 1 (2.7%, 1/37) patient had type III; however, there were significantly more type IIb in group A than in group B (42.31% vs. 9.09%, p = 0.06). Spleen infarction were seen in 18.92% (7/37), and aneurysm formation were seen in 5.41% (2/37). In addition, the mean length of dissection in group A was 42.3 ± 54.71 mm which was significantly shorter than that in the group B 58.45 ± 3.71 mm (p =0.04). The mean distance between the ostium of the CA and the origin of the dissection was 18.08 ± 1.44 mm, and the TLRD was 55.68 ± 7.23%. The clinical features and imaging findings of the patients are summarised in Table 2.

Table 2.

Imaging findings of symptomatic spontaneous isolated coeliac artery dissection patients.

Imaging finding	Total (n = 37)	Group A (n = 26)	Group B (n = 11)	p value
Confirmed gist
Intimal flap	16 (43.24%)	10 (38.46%)	6 (54.55%)	0.37
Thrombosed false lumen	12 (32.43%)	11 (42.31%)	1 (9.09%)	0.06
Pseudoaneurysm	9 (24.32%)	5 (19.23%)	4 (36.36%)	0.4
Ostial involvement (mm)	18.08 ± 1.44	17.65 ± 1.61	19.09 ± 3.11	0.65
Dissection length (mm)	47.14 ± 3.67	42.35 ± 4.71	58.45 ± 3.71	0.04
True lumen residual diameter (%)	55.68 ± 7.23	52.34 ± 6.79	58.12 ± 8.53	0.73
Extent of dissection
Only celiac trunk	18 (48.65%)	16 (61.54%)	2 (18.18%)	0.03
Extension to CHA and SA	7 (18.92%)	1 (3.85%)	6 (54.55%)	0.001
Extension to CHA	4 (10.81%)	2 (7.69%)	2 (18.18%)	0.57
Extension to SA	7 (18.92%)	6 (23.08%)	1 (9.09%)	0.65
Extension to LGA	1 (2.7%)	1 (3.85%)	0	0.99
Spleen infarction (yes)	7 (18.92%)	4 (15.38%)	3 (27.27%)	0.66
Morphological type
Type I	8 (21.62%)	6 (23.08%)	2 (18.18%)	0.74
Type IIa	14 (37.84%)	8 (30.77%)	6 (54.55%)	0.17
Type IIb	12 (32.43%)	11 (42.31%)	1 (9.09%)	0.06
Type III	1 (2.7%)	0	1 (9.09%)	0.3
Aneurysm formation	2 (5.41%)	1 (3.85%)	1 (9.09%)	0.51

Note: Group A: conservative treatment group. Group B: endovascular treatment group. Ostial involvement: the mean distance between the ostium of the coeliac artery and the origin of the dissection. Dissection length: the average length of the dissection. True lumen residual diameter (TLRD): true lumen size compared with the adjacent normal CA size. CHA: common hepatic artery; SA: splenic artery; LGA: left gastric artery.

Clinical outcomes

In the group A, conservative treatment was initially performed in 29 patients (Figure 2). However, three patients were switched to endovascular treatment because of persistent symptoms after primary conservatively during follow-up. In the group B, the overall technical success was 100%. Eleven (29.23%, 11/37) patients received endovascular treatment, which included 10 endovascular stentings (bare stent placement n = 8, Figure 3, cover stent placement n = 2) and one coiling placement. There was significant difference in the length of stay (11.38 ± 0.99 days vs. 15.36 ± 1.02; p = 0.02), symptom duration (6.38 ± 1.86 days vs. 9.53 ± 1.49; p = 0.03) between the two groups (Table 3). The bleeding complication rate was 18.18% (2/11) in group B experienced minor bleeding at the catheter insertion site, which was controlled in all of the cases by simple elevation of the limb and application of a compressive bandage and did not require further treatment.

Figure 2.

A 47-year-old man presented with acute epigastric pain that had lasted for approximately 3 h. Contrast-enhanced CT showed SICAD with intimal flap (a and b). Partial remodelling of the SICAD had occurred after 6 months (c and d). Complete remodelling of the SICAD was seen on contrast-enhanced CT 12 months later (e and f).

Figure 3.

A 42-year-old man presented with acute abdominal pain that had lasted for 6 h. Emergency contrast-enhanced CT revealed a dissection in the CA starting approximately 37 mm from its origin extending to the aortic orifice (a). After two months of conservative treatment, acute abdominal pain recurred. An 6 mm × 40 mm self-expanding bare stent was placed in the affected CA, which resulted in excellent distal blood flow (b–d). Follow-up contrast-enhanced CT showed that the stent placed had no stenosis or thrombosis, thrombus in the false lumen and blood flow in the distal end was unobstructed at six months postoperatively (e and f).

Table 3.

Treatment outcome of symptomatic spontaneous isolated coeliac artery dissection.

Treatment outcome	Total (n = 37)	Group A (n = 26)	Group B (n = 11)	p value
Length of stay (days)	12.57 ± 0.81	11.38 ± 0.99	15.36 ± 1.02	0.02
Symptom duration (days)	7.78 ± 1.58	6.38 ± 1.86	9.53 ± 1.49	0.03
Technical success	11 (29.73%)	0	11 (100%)
Complications	2 (5.41%)	0	2 (18.18%)	0.08

Note: Group A: conservative treatment group. Group B: endovascular treatment group.

Clinical follow-up

Clinical follow-up was scheduled on the first, third and sixth months after discharge and annually thereafter until persistent disease stability of the celiac artery had occurred. During a median follow-up of 11.5 months, the 1-, 3-, 6- and 12-month follow-ups were completed in 100% (37/37), 100% (37/37), 94.59% (35/37) and 91.19% (34/37) of patients, respectively. Three patients were lost to follow-up at the end of this study. During follow-up, no dissection related death, arterial rupture or evidence of distal organ ischemia was noted. A total of 10.81% (4/37) of patients experienced recurrent abdominal pain, in which three patients were relieved after conservative treatment, and one patient was transferred to endovascular treatment (Figure 4). The cumulative rate of persistent disease stability in patients with endovascular treatment group was higher than in that conservative treatment group at the 3, 6, 9 and 12 months (Figure 5; 50% vs. 16.67%, p = 0.001; 80% vs. 37.5%, p = 0.03; 100% vs. 62.5%, p = 0.012; 100% vs. 91.67%, p = 0.02 respectively).

Figure 4.

Example of failing conservative management of a symptomatic SICAD with development of celiac artery aneurysm. A 53-year-old man presented with acute abdominal pain that had lasted for 3 h. Contrast-enhanced CT scan showed a SICAD (typeIIa) (a). After conservative treatment for three months, contrast-enhanced CT scan showed false lumen diameter enlargement (b). Abdominal pain worsened after six months of conservative management (c), and angiography reveals celiac artery aneurysm with stenosis of the splenic arteries (d). Celiac artery angiogram after stent deployment and coil embolisation (e and f).

Figure 5.

Cumulative Kaplan–Meier estimate of patients with persistent disease stability of symptomatic SICAD treated conservative or endovascular treatment. The cumulative persistent disease stability was 16.67%, 37.5%, 62.5% and 91.67% at 3, 6 and 12 months after conservative treatment. The corresponding persistent disease stability in patients treated endovascular treatment was 50%, 80%, 100% and 100%.

Discussion

This study presented four findings regarding the clinical characteristics of symptomatic SICAD. First, due to the low incidence, initial visit physicians have insufficient knowledge of SICAD, especially in an emergency, which leads to being misdiagnosed easily. Second, most symptomatic SICAD has a tendency to persistent disease stability after conservative treatment. Third, dissection length and extension were two risk factors for failed conservative treatment. Finally, endovascular treatment was associated with a high technical success and persistent disease stability rate. This treatment strategy might be reserved for patients with failed conservative treatment.

SICAD was seen in middle aged male predominance with relevant risk factors, such as hypertension and smoking. Our series of patients had similar characteristics: the median age at diagnosis was 51 years old (ranging from 36–72), and male patients accounted for 91.89%. Although previous reports have demonstrated that hypertension and smoking were commonly observed in SICAD patients,⁵ the causal association is difficult to determine due to the low incidence. Unlike SISMAD, which occurs predominantly in Asia (China, Korea and Japan), SICAD appears to be few regional differences in the distribution of the reported cases.⁴ In the present study, four cases of SICAD occurred after a meal which was suggested that hemodynamic change might be a causative factor. The celiac artery originates from the aorta at a right angle as well as a rapid rise in arterial pressure, such as during or after a meal, weight lifting, could be a causative factor. Furthermore, several authors have indicated that celiac artery compression by the median arcuate ligament might be a predisposing factor for SICAD.¹⁶,¹⁷ However, because of the rarity of the disease, its exact aetiology remains unclear.

The most common chief complaint for patients with SICAD is abdominal pain, which is typically localised in the epigastrium. Severe abdominal pain may mislead initial visit physicians to think of traditional acute abdomen (such as gastroenteritis, cholecystitis, appendicitis and pancreatitis) that is one of the reasons for misdiagnosis. In the present study, the misdiagnosis rate was as high as 13.51% (5/37). The diagnosis of SICAD requires the collaborative efforts of a multidisciplinary team, particularly initial visit physicians, radiologists and vascular surgeons. The initial visit physicians should be aware of the clinical manifestation of SICAD and conduct targeted screening. Subsequently, radiologists must identify the morphological characteristics which guide treatment protocols to assist vascular surgeons in decision making. Vascular surgeons depend on radiologists to identify and characterise CA dissection and prioritise findings that guide the optimal treatment of patients. During this process, if any participator has insufficient knowledge of SICAD, there is a high risk of misdiagnosis. Clinicians should have a strong understanding of the relevant anatomy, as well as clinical presentations of SICAD will aid in making this rare diagnosis.¹⁸

Optimal treatment strategies for SICAD are still uncertain.¹ Various algorithms were proposed in previous literature reviews,¹⁹ but all these strategies were limited by small case numbers and retrospective study designs. The SICAD natural course is more indolent than that of aortic dissection. Given its self-limited, the majority of patients might be obtained persistent disease stability after conservative treatment, which had similar characteristics in our series of patients (70.27%, 26/37). Theoretically, SICAD rarely leads to severe ischemic complications in the distal organs because the organs supplying from the celiac artery are usually revascularised by sufficient collateral flow. However, in our study, 29.73% (11/37) underwent endovascular therapy, especially extension of the dissection into the CHA and SA (p = 0.001). Furthermore, it was found that dissection length was an independent risk factor for endovascular treatment (p = 0.04). An extended dissection length might be associated with more severe stenosis of the true lumen and subsequent intestinal ischaemia. Thus, patients with long dissection lengths should be treated more carefully.²⁰ Patient selection and timing of conservative or endovascular intervention is crucial in the management of SICAD. Previous studies reported that the conversion time from conservative to endovascular treatment varied from 3 days to 30 months.²¹According to the management strategy based on clinical stages previously reported by our team, the median time from conservative to endovascular treatment was 7.57 days.¹² However, our experience had some limitations; therefore, our results might be served only as a reference. Also, in the present study, endovascular treatment was associated with a high technical success and persistent disease stability rate. The cumulative rate of persistent disease stability in patients with endovascular treatment group was higher than in that conservative treatment group at the 3, 6, 9 and 12 months (Figure 5; 50% vs. 16.67%, p = 0.001; 80% vs. 37.5%, p = 0.03; 100% vs. 62.5%, p = 0.012; 100% vs. 91.67%, p = 0.02, respectively). This treatment strategy might be reserved for patients with failed conservative treatment.

Several limitations have to be noticed. First, the study is limited by its retrospective nature and its small sample size. Even so, prospective studies were impossible owing to the extremely low incidence of the disease. Second, the intensity of pain and the utility of blood examinations were not quantified for additional analysis. Additionally, morphological characteristics were determined by contrast-enhanced CT scan rather than by digital subtraction angiography. Third, we did not precisely evaluate the efficacy of surgical treatment for SICAD. Surgical treatment may be the optimal choice for peritonitis and ruptured dissecting aneurysm. However, in this study, no patients were diagnosed as having peritonitis and ruptured dissecting aneurysm. Finally, the clinical follow-up was arranged in the first and sixth months after discharge, and every year thereafter; therefore, the exact time of CA remodelling was unknown in this study.

Conclusion

Most symptomatic SICAD have a tendency to persistent disease stability after conservative treatment. Also, risk factors for failed conservative treatment were length of dissection and branch involvement. Furthermore, endovascular treatment was associated with a high technical success and persistent disease stability rate, which might be reserved for patients with failed conservative treatment.

Footnotes

Acknowledgements

The authors are grateful to all the participants for their involvement in the study. The authors would also like to thank the Union Hospital, Tongji Medical College, Huazhong University of Science and Technology for their collecting data. XG and WX contributed equally to this work.

Ethics approval

Ethics approval was provided by the Binzhou Medical University Hospital ethics committee.

Declaration of conflicting interests

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The author(s) received no financial support for the research, authorship, and/or publication of this article.

ORCID iD

Ying Jiang Xu

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