第一部分 腹主动脉瘤的解剖形态与破裂的相关性分析

目的

本研究旨在评估腹主动脉及髂动脉的解剖形态与腹主动脉瘤（abdominal aortic aneurysm，AAA）破裂风险之间的关联，为未来的预测模型寻找风险因素。

方法

本研究对46对性别、年龄和最大动脉瘤直径1:1 匹配的破裂腹主动脉瘤（ruptured abdominal aortic aneurysm, rAAA）患者和稳定腹主动脉瘤（stable abdominal aortic aneurysm, sAAA）患者进行了回顾性分析。并根据AAA最大直径分为小腹主动脉瘤组（≤ 55mm）与大腹主动脉瘤组（>55mm）进行分层分析。使用卡方检验、配对t检验和Wilcoxon符号秩检验比较相应变量。进行Logistic回归来评估可能与 AAA 破裂相关的变量。使用受试者工作特征曲线分析和曲线下面积（area under the curve, AUC）来评估回归模型。

结果

与sAAA组相比，rAAA 组的近端瘤颈较短（中位数（四分位距）：24.0 (9.4-34.2) mm vs. 33.3 (20.0-52.8) mm，p = 0.004），动脉瘤扭曲度较高（中位数 (四分位距)：1.35 (1.23 -1.49) vs. 1.29 (1.23-1.39)，p = 0.036)，双侧髂总动脉的最小血流腔面积较小（右侧：中位数 (四分位距)：86.7 (69.9-126.4) mm² vs. 118.9 ( 86.3- 164.1)mm², p = 0.001) (左侧：中位数(四分位距): 92.2 (67.3-125.1) mm² vs. 110.7 (80.12-161.1) mm², p = 0.010)。多元回归分析表明，髂总动脉的最小血流腔面积（比值比 [odds ratio, OR] = 0.996，95%置信区间 [confidence interval, CI] 0.991–0.999，p = 0.037）、瘤颈长度（OR = 0.969，95% CI 0.941–0.993，p = 0.017）以及动脉瘤扭曲度（OR = 1.031，95% CI 1.003–1.063，p = 0.038）与动脉瘤破裂之间存在显著相关性。该回归模型的AUC为0.762（95% CI 0.664–0.860，p < 0.001）。亚组分析表明，rAAA和sAAA的解剖形态在大腹主动脉瘤（n=82）中的差异与未分层前一致，在小腹主动脉瘤（n=10）中无明显差异。

结论

本研究表明，较短的动脉瘤颈、较小的流出道参数和较高的扭曲度与腹主动脉瘤破裂风险增加有关。综合纳入瘤颈长度、动脉瘤扭曲度与流出道参数的回归模型可有效判别腹主动脉瘤的破裂风险本研究强调了利用流出道参数作为风险评估的新颖和附加工具的潜力。为进一步加强该领域的研究提供了令人信服的理由。

第二部分 腹主动脉瘤的瘤囊变化与腔内修复术预后的关系分析

目的

本研究的主要目的是描述腹主动脉瘤（abdominal aortic aneurysm, AAA）患者在接受腹主动脉腔内治疗术（endovascular abdonimal aortic repair, EVAR）后的瘤囊变化情况，包括早期与长期影像学随访结果以及动态变化，并分析瘤囊行为与腔内修复术预后的关系。

方法

回顾且连续性纳入了自2010年1月至2020年12月在我院确诊为AAA并接受EVAR的患者。基线瘤囊直径的测量基于术后1月的主动脉计算机断层扫描血管成像（computed tomography angiography, CTA）。收集并测量了有至少术后1年主动脉随访CTA的AAA瘤囊直径、瘤颈直径、双侧髂总动脉直径以及有无内漏等数据。将术后瘤囊直径减小或增加超过5mm定义为瘤囊收缩或瘤囊扩张。主要结局指标为全因死亡（包括AAA相关死亡、非AAA相关死亡和死因不详）。次要结局指标为复合主动脉事件（再干预、AAA破裂、髂支闭塞、支架感染、支架移位、迟发I型或III型内漏、迟发或持续性II型内漏）。使用相应的统计方法描述EVAR术后瘤囊行为变化，并按照术前AAA直径大小进行亚组分析。

结果

最终纳入术后CTA随访时间 ≥ 1年的患者共297例。在外院复查主动脉CTA的外地患者由于影像资料获取困难未被纳入本研究。男性患者所占比例为88.2%，平均年龄为66.4 ± 7.6岁，多数患者有既往吸烟史(66.7%)、合并高血压(70.4%)以及高脂血症(65.7%)。末次随访时，40.7%（121/297）的患者出现瘤囊收缩，中位随访时间 40（IQR, 22-54）月，平均术前AAA最大直径为50.7mm，在瘤囊收缩患者中出现内漏的比例为13.2% (16/121)，瘤囊收缩的五年累积发生率为53.9%（95%CI，45.5%-61%）；13.5 % (40/297)的患者出现瘤囊扩张，中位随访时间47（IQR, 36-58）月，平均术前AAA最大直径为57.9mm（显著大于瘤囊收缩患者的AAA直径，p = 0.023），80% (32/40)的瘤囊扩张的患者在随访过程中有内漏（显著高于瘤囊收缩患者的内漏比例，p < 0.001)。瘤囊扩张的五年累积发生率为28.7%（95%CI，19%-37.3%）。在初始瘤囊收缩后发生瘤囊扩张的患者共2例，另外有3例初始瘤囊收缩后瘤囊收缩幅度减少的患者。

根据EVAR术后1年瘤囊行为将患者分为两组：瘤囊收缩组（n= 70）和无瘤囊收缩组（n = 135，包括1例瘤囊扩张），中位随访时间分别为50 (IQR, 36, 70) 月和52 (IQR, 35, 71) 月，两组患者在全因死亡方面无显著统计学差异 (7.1% vs 10.4%, p = 0.450)，无瘤囊收缩组的动脉瘤相关死亡率显著高于瘤囊收缩组 (35.7% vs 0%, p = 0.050) 。瘤囊收缩组和无瘤囊收缩组的术后5年累积生存率分别为94.8% (95%CI, 87.9% - 100%) 和 88.8% (95%CI, 81.5% - 96.7%)。无瘤囊收缩组的复合主动脉事件发生率显著高于瘤囊收缩组(20% vs 10%, p = 0.028)。瘤囊收缩组的迟发或持续性II型内漏的比例显著低于无瘤囊收缩组 (10.4% vs 2.9%，p = 0.037)。瘤囊收缩组和无瘤囊收缩组的术后5年免于复合主动脉事件的累积概率分别为92.3% (95%CI， 86.1% - 99.1%) 和78.5% (95%CI, 70.5% - 87.3%)。

以AAA直径为分组标准，将患者分为三组：≤ 50mm (n = 113)，50-60mm (n = 107)，>60mm(n = 77)。直径大于60mm组的瘤囊收缩比例显著小于50-60mm组和≤ 50mm组(31.2% vs 48.6% vs 38.9%, p = 0.055),  I型内漏或III型内漏比例显著高于另外两组(16.9% vs 6.5% vs 2.7%, p < 0.001)，动脉瘤相关再干预比例显著高于另外两组(11.7% vs 1.9% vs 0.9%, p < 0.001)。三组患者在瘤囊扩张、II型内漏、全因死亡、动脉瘤破裂、支架感染、支架移位、髂支闭塞等晚期事件的发生率方面无明显差异。

结论

本研究调查了国内单中心EVAR术后AAA瘤囊回缩与瘤囊扩张的长期随访结果，为EVAR术后个性化随访方案的制定提供了数据依据。鉴于瘤囊收缩患者更低的复合主动脉事件发生率，可以考虑延长随访间期；另外由于瘤囊收缩患者的远期再扩张可能，因此长期随访必不可少。直径超过60mm的AAA患者，术后I型或III型内漏及动脉瘤相关再干预风险较高，应考虑规律严密随访。

第三部分 影响腹主动脉腔内修复术后髂支闭塞的手术与解剖因素分析

目的

调查腹主动脉腔内修复术（endovascular abdominal aortic repair, EVAR）后髂支闭塞（endograft limb occlusion, ELO）的发生率，分析解剖形态因素以及对吻球囊技术对ELO的影响。

方法

本研究回顾并连续性纳入了2010年1月至2020年12月在阜外医院接受EVAR治疗的腹主动脉瘤患者。根据EVAR术中的球囊策略，将患者分为三组：对吻球囊组、单个球囊组和不采用球囊组，以ELO为结局进行生存分析；采用巢式病例对照研究分析潜在的解剖形态及手术相关危险因素，包括踝肱指数（ankle brachial index, ABI）、瘤颈角度、腹主动脉分叉直径、髂动脉锚定区直径、髂外动脉直径、髂动脉扭曲度、髂支锚定于髂外动脉等因素。闭塞患者的所有随访影像均由资深外科医师检查，记录潜在的机械性原因，包括支架移植物受压、扭折（kinking）或无。 通过Kaplan-Meier生存分析法评估组间差异。条件Logistics回归被用于检验与结局相关的潜在变量。

结果

832名接受标准分叉型EVAR治疗的腹主动脉瘤和/或髂动脉瘤的患者被纳入研究，按照术中球囊策略分组：对吻球囊组 (n = 451)、单球囊组 (n = 253) 或不采用球囊组 (n = 128)。术后平均随访时间35月，共32名 (3.8%) 患者出现 ELO，其中12名 (2.7%) 发生在对吻球囊组，11名 (4.3%) 在单球囊组，9 名 (7%) 在不采用球囊组（总体log-rank检验，p = 0.026）。在ELO患者中，不采用球囊组(6[67%])比对吻球囊组 (1[8%], p < 0.05) 更有可能出现支架移植物受压。巢式病例对照的结果表明，ELO组闭塞髂支的术前ABI显著低于对照组相应髂支术前ABI (0.97 ± 0.19 vs 1.08 ± 0.09, p = 0.018)；ELO组的对吻球囊应用比例明显低于对照组 (37.5% vs 65.6%)，无球囊应用的比例明显高于对照组 (28.1% vs 9.4%，p = 0.052)；ELO组的AAA最大直径明显小于对照组(50 ± 12 mm vs 57 ± 15 mm, p = 0.064) , 瘤颈角度α角明显大于对照组 (25 ± 20 度 vs 14 ± 8 度，p = 0.065)。两组患者在髂支锚定于EIA的比例、瘤颈直径和长度、瘤颈β角、腹主动脉分叉处直径、髂动脉锚定区直径、髂外动脉直径以及髂动脉扭曲度等解剖形态特征方面无显著统计学差异。多因素回归分析结果显示ABI < 0.9与ELO风险增高相关(OR, 13.99, 95%CI, 1.33-147.2, p = 0.028), 对吻球囊技术的应用与ELO风险减低相关(OR, 0.24, 95%CI, 0.03-0.87, p = 0.021)。

结论

EVAR术前踝肱指数和术中对吻球囊技术的应用与ELO的发生显著相关。术前ABI < 0.9是ELO发生的独立危险因素，对这部分患者应考虑更加严密的随访，及时调整药物与手术治疗方案。EVAR 术中应用对吻球囊技术的患者 ELO 的发生率明显低于未进行球囊扩张的患者。对吻球囊技术作为EVAR的辅助策略是 ELO 发生的独立保护因素，可作为有效手段预防术后闭塞事件的发生。

Part One: Correlation analysis between anatomical morphology and rupture of abdominal aortic aneurysm

Objective

This study aimed  to compare outflow parameters between ruptured and stable AAAs and to assess their association with the risk of AAA rupture.

Methods

We retrospectively analyzed 46 patients with ruptured AAAs and 46 patients with stable AAAs using a 1:1 match for sex, age, and maximum aneurysm diameter. The chi-square test, paired t-test, and Wilcoxon signed-rank test were used to compare variables. According to the maximum diameter of AAA, the patients were divided into small abdominal aortic aneurysm group (≤55mm) and large abdominal aortic aneurysm group (>55mm) for stratified analysis. Logistic regression was performed to evaluate variables potentially associated with AAA rupture. Receiver operating characteristic curve analysis and the area under the curve (AUC) were used to assess the regression models.

Results

Ruptured AAAs had a shorter proximal aortic neck (median (interquartile range, IQR): 24.0 (9.4-34.2) mm vs. 33.3 (20.0-52.8) mm, p = 0.004), higher tortuosity (median(IQR): 1.35 (1.23-1.49) vs. 1.29 (1.23-1.39), p = 0.036), and smaller minimum luminal area of the right common iliac artery (CIA) (median (IQR): 86.7 (69.9-126.4) mm2 vs. 118.9 ( 86.3-164.1)mm2, p = 0.001) and left CIA (median(IQR): 92.2 (67.3,125.1) mm2 vs. 110.7 (80.12, 161.1) mm2, p = 0.010) than stable AAA did. Multiple regression analysis demonstrated significant associations of the minimum luminal area of the bilateral CIAs (odds ratio [OR] = 0.996, 95% confidence interval [CI] 0.991–0.999, p = 0.037), neck length (OR = 0.969, 95% CI 0.941–0.993, p = 0.017), and aneurysm tortuosity (OR = 1.031, 95% CI 1.003–1.063, p = 0.038) with ruptured AAAs. The AUC of this regression model was 0.762 (95% CI 0.664–0.860, p < 0.001). Subgroup analysis showed that the anatomical differences between rAAA and sAAA in large AAAs (n=82) were consistent with those before stratification, but there was no significant difference in small AAAs (n=10).

Conclusions

This study demonstrates that shorter aneurysm neck, smaller outflow parameters, and higher tortuosity are associated with an increased risk of abdominal aortic aneurysm rupture. A regression model that comprehensively incorporates aneurysm neck length, aneurysm tortuosity, and outflow parameters can effectively identify the rupture risk of abdominal aortic aneurysms. This study highlights the potential of utilizing outflow parameters as a novel and additional tool for risk assessment. Compelling reasons are provided for further strengthening research in this area.

Part Two: Analysis of the relationship between aneurysm sac changes and prognosis of endovascular repair of abdominal aortic aneurysm

Objective

The main purpose of this study was to describe the changes in the aneurysm sac in patients with abdominal aortic aneurysm (AAA) after endovascular abdominal aortic repair(EVAR), including early and long-term imaging follow-up results and dynamic changes, and analyzes the relationship between aneurysm sac behavior and the prognosis of EVAR.

Methods

Patients diagnosed with AAA and undergoing EVAR in our hospital from January 2010 to December 2020 were retrospectively and consecutively included. Baseline sac diameter measurements were based on computed tomography angiography (CTA) of the aorta 1 month postoperatively. Data such as sac diameter, neck diameter, bilateral common iliac artery diameter, and endoleaks were collected and measured for patients with follow-up CTA for at least 1 year after surgery. The postoperative reduction or increase of the sac diameter by more than 5 mm was defined as sac shrinkage or expansion. The primary outcome was all-cause death (including AAA-related death, non-AAA-related death, and unknown cause of death). The secondary outcome was a composite aortic event (reintervention, AAA rupture, endograft limb occlusion, stent infection, stent migration, late-onset type I or III endoleak, late-onset or persistent type II endoleak). Corresponding statistical methods were used to describe the changes in sac behavior after EVAR, and subgroup analysis was performed according to the preoperative AAA diameter.

Results

A total of 297 patients with postoperative CTA follow-up time ≥ 1 year were finally included. Non-local patients who underwent aortic CTA review in other hospitals were not included in this study due to difficulties in obtaining imaging data. The proportion of male patients was 88.2%, and the average age was 66.4 ± 7.6 years old. Most patients had a history of smoking (66.7%), hypertension (70.4%), and hyperlipidemia (65.7%). At the last follow-up, 40.7% (121/297) of the patients had sac shrinkage, the median follow-up time was 40 (IQR, 22-54) months, the average preoperative maximum diameter was 50.7 mm, the proportion of endoleak was 13.2%, and the five-year cumulative incidence of sac shrinkage was 53.9% (95%CI, 45.5%-61%); 13.5% (40/297) of patients had sac expansion, the median follow-up time was 47 (IQR, 36-58) months, the average preoperative maximum AAA diameter was 57.9mm (significantly larger than the AAA diameter in patients with sac contraction, p = 0.023), the proportion of endoleak was 80% (significantly higher than the proportion of endoleaks in patients with sac shrinkage, p < 0.001). The five-year cumulative incidence of sac expansion was 28.7% (95% CI, 19%-37.3%). There were 2 patients with sac expansion after initial sac shrinkage, and another 3 patients with reduced sac contraction after initial sac shrinkage.

The patients were divided into two groups according to the sac behavior 1 year after EVAR: sac shrinkage group (n = 70) and no sac shrinkage group (n = 135, including 1 case of sac expansion). The median follow-up time was respectively 50 (IQR, 36, 70) months and 52 (IQR, 35, 71) months, there was no significant statistical difference in all-cause death between the two groups (7.1% vs 10.4%, p = 0.450). The aneurysm-related mortality rate in the aneurysm sac shrinkage group was significantly higher (35.7% vs 0%, p = 0.050). The 5-year cumulative survival rates for the sac shrinkage group and no sac shrinkage group were 94.8% (95%CI, 87.9% - 100%) and 88.8% (95%CI, 81.5% - 96.7%) respectively. The incidence of composite aortic events in the group without aneurysm sac shrinkage was significantly higher than that in the group with aneurysm sac shrinkage(20% vs 10%, p = 0.028). The proportion of late-onset or persistent type II endoleaks in the sac shrinkage group was significantly lower than that in the no sac shrinkage group (10.4% vs 2.9%, p = 0.037). The 5-year cumulative probabilities of freedom from composite aortic events in the aneurysm sac shrinkage group and the no sac shrinkage group were 92.3% (95%CI, 86.1% - 99.1%) and 78.5% (95%CI, 70.5% - 87.3%) respectively.

Using AAA diameter as the grouping standard, patients were divided into three groups: ≤ 50mm (n = 113), 50-60mm (n = 107), and >60mm (n = 77). The sac shrinkage ratio in the diameter >60mm group was significantly smaller than that in the 50-60mm group and ≤ 50mm group (31.2% vs 48.6% vs 38.9%, p = 0.055), and the proportion of type I endoleak or type III endoleak was significantly higher than that of the other two groups (16.9% vs 6.5% vs 2.7%, p < 0.001), and the proportion of aneurysm-related reintervention was significantly higher than the other two groups (11.7% vs 1.9% vs 0.9%, p < 0.001). There was no significant difference in the incidence of late events such as sac expansion, type II endoleak, all-cause death, aneurysm rupture, stent infection, stent migration, and engraft occlusion among the three groups of patients.

Conclusion

This study investigated the long-term follow-up results of AAA sac shrinkage and sac expansion after EVAR in a single center in China, and provided data basis for the development of a personalized follow-up plan after EVAR. In view of the lower incidence of composite aortic events in patients with sac shrinkage, extending the follow-up interval can be considered; in addition, because of the possibility of long-term re-expansion in patients with sac shrinkage, long-term follow-up is essential. Patients with AAA whose diameter exceeds 60 mm have a higher risk of type I or type III endoleak and aneurysm-related re-intervention after surgery, and regular and close follow-up should be considered.

Part Three: Analysis of surgical and anatomical factors predisposing endograft limb occlusion after endovascular abdominal aortic repair

Objective

To investigate the incidence of endograft limb occlusion (ELO) after endovascular aneurysm repair (EVAR) and analyze the impact of anatomical morphological factors and kissing balloon technology on ELO.

Methods

All consecutive patients who underwent EVAR from January 2010 to December 2020 at Fuwai Hospital were reviewed in this study. Patients were divided into three groups according to the balloon strategy used during EVAR: kissing balloon, single balloon, and no balloon, survival analysis was conducted with ELO as the outcome; A nested case-control(NCC) study was used to analyze potential anatomical morphology and surgery-related risk factors, including ankle brachial index (ABI), aneurysm neck angulation(α and β angle), abdominal aortic bifurcation diameter, iliac artery landing zone diameter, external iliac artery(EIA) diameter, tortuosity of the iliac artery, and stent extension to the EIA. All follow-up images of occluded patients were checked by senior surgeons, and the potential mechanical cause was noted as limb graft compression, kinking, or none. Kaplan-Meier survival estimates with the log-rank test were calculated to analyze the difference between groups. Conditional logistic regression was used to examine potential variables associated with outcome.

Results

832 patients who underwent bifurcated EVAR for AAA and/or iliac aneurysms with kissing balloon (n = 451), single balloon (n = 253), or none balloon angioplasty (n = 128) were included. During the mean follow-up of 35 months, a total of 32 (3.8%) patients presented with ELO, 12 (2.7%) treated with kissing balloon, 11 (4.3%) with a single balloon, and 9 (7%) without balloon angioplasty (overall log-rank test, p = .026). ELO patients of the none balloon angioplasty group were more likely to have compression (6[67%]) than the kissing balloon group (1[8%], p < 0.05 ).

The results of NCC cohort showed that the preoperative ABI of the occluded limb in the ELO group was significantly lower than that of the corresponding limb in the control group (0.97 ± 0.19 vs 1.08 ± 0.09, p = 0.018); The proportion of the kissing balloon application in the ELO group was significantly lower than that of the control group (37.5% vs 65.6%), and the proportion of non-balloon application was significantly higher than that of the control group (28.1% vs 9.4%, p = 0.052); the maximum diameter of AAA in the ELO group was significantly smaller than that of the control group (50 ± 12 mm vs 57 ± 15 mm, p = 0.064), and the α angle was significantly greater than that of the control group (25 ± 20 degrees vs 14 ± 8 degrees, p = 0.065). There is no obvious difference in morphological characteristics including the proportion of stent extension to EIA, aneurysm neck diameter and length, β angle, abdominal aortic bifurcation diameter, iliac artery landing zone diameter, EIA diameter, and iliac artery tortuosity. Multivariate regression analysis results showed that ABI < 0.9 was associated with an increased risk of ELO (OR, 13.99, 95%CI, 1.33-147.2, p = 0.028), and the application of kissing balloon technology was associated with a reduced risk of ELO (OR, 0.24, 95 %CI, 0.03-0.87, p = 0.021).

Conclusion

Preoperative ABI and intraoperative application of kissing balloon technique were significantly associated with the occurrence of ELO. Preoperative ABI < 0.9 is an independent risk factor for the occurrence of ELO. Closer follow-up should be considered for these patients, and drug and surgical treatment plans should be adjusted in a timely manner. The incidence of ELO in patients using the kissing balloon technique during EVAR was significantly lower than that in patients without balloon dilatation. Kissing balloon technology as an auxiliary strategy for EVAR is an independent protective factor for the occurrence of ELO and can be used as an effective means to prevent the occurrence of postoperative occlusive events.