Does a previous aortic endograft confer any protective effect during abdominal aortic aneurysm rupture? Systematic review and meta-analysis of comparative studies

Abstract

Objectives

Whether prior endovascular aneurysm repair confers a protective effect in patients with ruptured abdominal aortic aneurysm (rAAA) is not known. We aimed to systematically review and compare the outcomes of rAAA in patients with and without prior endovascular aneurysm repair.

Methods

We performed a systematic review that conformed to the Preferred Reporting Items for Systematic Reviews and Meta-analysis. We selected studies comparing the outcomes in patients with rAAA after prior endovascular aneurysm repair (group 1) and those with de novo rAAAs (group 2). We conducted a proportion meta-analysis of perioperative mortality and obtained summary estimates of odds ratios (ORs) and 95% confidence intervals (CIs) using random-effects models.

Results

We included four studies (retrospective observational studies) in quantitative synthesis reporting a total of 719 patients (group 1 (89) group 2 (630)). The perioperative mortality in groups 1 and 2 was 30.4% and 41%, respectively, and there was no statistical significant difference between the groups (OR 0.66, 95% CI 0.30–1.43, P = 0.29, I²=58%). However, patients presenting with rAAA following previous endovascular aneurysm repair were more hemodynamically stable (OR 0.33, 95% CI 0.12–0.90, P = 0.03, I²=74%). The choice between endovascular or open surgery treatment in group 1 did not affect the perioperative mortality (OR 1.12, 95% CI 0.41–3.04 P = 0.82, I²=0%). Endoleak types I and III were the main causes of rAAA in group 1.

Conclusions

Perioperative mortality was similar for rAAA either de novo or after prior endovascular aneurysm repair. However, ruptures in patients with prior endovascular aneurysm repair presented hemodynamically more stable.

Keywords

Endovascular aneurysm repair ruptured abdominal aortic aneurysm

Introduction

Endovascular aneurysm repair (EVAR) of abdominal aortic aneurysm (AAA) was first described almost three decades ago.¹ EVAR has evolved in the following years and became the most popular treatment modality for elective AAA treatment.² Despite the technological progress in EVAR devices and the improvement in procedural techniques, delayed aneurysm rupture has been reported by several studies.^3–6 Moreover, it may be associated with an inferior late survival benefit compared to open surgical treatment.⁷ The main causes of ruptured abdominal aortic aneurysm (rAAA) after EVAR include stent graft migration, endoleaks, endotension with sac enlargement or infection.^8,9 Mortality of patients with rAAAs varies by country but remains extremely high (>50%), despite the modern approaches in diagnosis and treatment of rAAAs.¹⁰

Taking into account the progressive increase in the number of patients treated with EVAR and the longer follow-up currently available, a potential effect of a previous endograft implantation on the outcomes of AAA rupture becomes relevant and important.² In other words, the speculation that previous EVAR may have a protective role at the time of rupture is intriguing. Nevertheless, a hypothesis that the presence of an endograft inside the ruptured aorta may limit the blood loss and subsequently decrease the disastrous effects of rapid extravasation needs scientific documentation and stronger evidence.

We aim to perform a systematic review and meta-analysis of available literature in order to investigate the outcomes of AAA rupture in patients with prior EVAR (group 1) compared to those with de novo (group 2) ruptures.

Methods

Design

The objectives and methodology of our review were prespecified in a protocol, which we registered with the registration number CRD42019130832 at the International Prospective Register of Systematic Reviews in Health and Social Care (PROSPERO).We conducted and reported our review in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines.¹¹

Criteria for considering studies

Types of studies

We considered any type of studies comparing outcomes of patients treated for rAAA with and without prior EVAR.

Types of participants

Eligible participants were male or female patients of any age presented with rAAA either with prior EVAR or with de novo ruptures. They underwent treatment for rAAA with open repair or endovascular procedures. We excluded patients treated for symptomatic non-ruptured AAA.

Types of prognostic factor

The main prognostic factor of interest was antecedent EVAR, which could have been performed with any commercially available bifurcated or aorto-uni-iliac device, under different types of anaesthesia (local, regional or general) using a percutaneous access or surgical exposure of the femoral arteries.

Types of outcome measures

The primary outcome in this study was perioperative (in-hospital or within 30 days of treatment) mortality.

The secondary objectives were perioperative morbidity, hemodynamic instability following rAAA and the association between postoperative mortality and treatment modality for rAAA in these groups. Perioperative morbidity refers to the total number of perioperative complications reported by each study, while hemodynamic instability was considered taken into account the definitions each study used.

Search methods for identification of studies

The literature search strategy was developed by two authors independently to interrogate the National Library of Medicine’s database (MEDLINE), ExcerptaMedica Database (EMBASE) and the Cochrane Register of Studies (CRS) (CENTRAL). The search string that was applied was “((Rupture) AND (abdominal aortic aneurysm)) AND ((Secondary rupture) OR (Previous EVAR) OR (Late rupture) OR (Prior EVAR)) AND ((Primary) OR (de Novo))”. A second level search consisting of interrogation of bibliographic lists of selected articles was performed to identify additional material. No language constraints were applied. The literature search was last run in February 2019.

Study selection and data management

Two authors conducted the prespecified literature searches and evaluated the eligibility of studies for inclusion independently (NG, NK). When disagreement arose, a third author acted as an arbitrator (CI). One author extracted data from selected studies (NK). The collected data were then crosschecked by a second author (NG). Retrieved data were entered into a spread sheet. Only published data were considered. We extracted the following information:

Study-related data: year and journal of publication, single- or multi-centre study, prospective or retrospective study design, time period over which patients underwent the index procedure, inclusion and exclusion criteria for patient enrolment, total number of patients in the study, number of patients in the study groups.

Data related to risk of bias assessment (see “Assessment of risk of bias” section).

Clinical characteristics of the study populations: gender; age; smoking history; co-morbidities including diabetes mellitus, coronary artery disease, hypertension, chronic obstructive pulmonary disease and chronic kidney disease; haemodynamic status at presentation.

Data related to the EVAR procedure in antecedent EVAR group and treatment (open or endovascular) after rupture in both groups: type of aortic endovascular device, bifurcated or aorto-uni-iliac endovascular device, tube or bifurcated graft for open aneurysm repair, supra- or infra-renal aortic clamping.

Outcome data, as outlined in the “Criteria for considering studies” section.

Assessment of risk of bias

The validity and bias in selected studies were evaluated using the Quality in Prognosis Studies (QUIPS) tool.¹² The tool consists of six domains that can inform judgments of risk of bias in prognostic research: study participation, study attrition, prognostic factor measurement, outcome measurement, study confounding and statistical analysis and reporting. Each domain consists of items for which the adequacy of reporting can be judged as yes, no or unsure. The potential risk of bias in each of the six domains is rated as high, moderate or low considering all relevant issues. The risk of bias assessment was performed by two review authors independently and discrepancies were resolved with discussion.

Data synthesis

Measures of treatment effect

We calculated pooled estimates of dichotomous outcomes data using the odds ratio (OR) and associated 95% confidence interval (CI).

Assessment of heterogeneity

In-between study, heterogeneity was examined with the Cochrane’s Q (χ²) test. We quantified inconsistency by calculating I² and interpreted it using the following guide: 0% to 40% might not be important; 30% to 60% may represent moderate heterogeneity; 50% to 90% may represent substantial heterogeneity and 75% to 100% may represent considerable heterogeneity.

Assessment of reporting bias

For each study, we plotted the effect (or proportion) by the inverse of its standard error (SE). We assessed publication bias by both visually evaluating the symmetry of the funnel plot and mathematically using the Egger’s regression intercept for the outcomes reported in >10 studies.

Missing data

We made no attempt to contact authors of included studies to inquire about missing or incomplete data.

Statistical models

In view of the anticipated variability in applied treatments and patient characteristics and the methodological diversity among the selected studies, we calculated the summary estimates using the random-effects models of DerSimonian and Laird.¹³

Moreover 2 × 2 contingency tables were constructed in order to investigate whether treatment modality during rAAA repair was related to the type of rupture (post-EVAR vs. de novo), and the significance of these relations was evaluated with the chi-square test.

Sensitivity and subgroup analysis

We sequentially excluded studies of low methodological quality in three or more domains of the QUIPS tool and performed a pooled sensitivity analysis in order to assess whether the included studies, deemed to be biased, impacted the final analysis. We also conducted a subgroup analysis of patients that underwent open surgical repair and those that underwent endovascular treatment because of rAAA in the antecedent EVAR group.

Statistical software

For data synthesis, we used the Review Manager (RevMan) computer program (Version 5.3, Copenhagen: The Nordic Cochrane Centre, The Cochrane Collaboration, 2014).

Results

Results of the literature search

Search of the literature applying the defined strategy retrieved 270 reports. After reviewing titles, abstracts and full-text versions of these articles, five studies fulfilled the inclusion criteria and were included in qualitative synthesis.^14–18 Two studies originated from the same institution, and the data from the older study were included in the more recent report which was finally included in the quantitative synthesis which involved four studies. The literature flow chart is presented in Figure 1.

Study characteristics

All selected articles employed retrospective studies which were published between 2009 and 2017, enrolling a total of 719 patients presenting with rAAA (Table 1). Demographics of patients are summarized in Table 2. Among them, 89 patients had undergone EVAR before AAA rupture (group 1) and 630 presented with de novo rAAA (group 2). Various devices were used in patients in group 1 such as Graft attachment device (White/Yu) (n = 6), Stentor/Vanguard (Mintec Marseille, Boston) (n = 14), AneuRx (Medtronic) (n = 20), Talent (Medtronic) (n = 13), Endologix (Endologix, Inc.) (n = 3), Ancure (Guidant) (n = 9), Zenith (Cook) (n = 14), Powelink (Endologix, Inc.) (n = 4), Endurant (Medtronic) (n = 3) and Excluder (W.L.) (n = 3). In all rAAAs following EVAR, an endoleak or stent-graft migration was found. Among patients in group 1, all but one presented endoleak at the time of rupture, such as type Ia (n = 38), Ib (n = 18), II (n = 5), III (n = 18), IV (n = 1), V (n = 3) and there were seven cases of stent-graft migration. Endoleak types I and III were the main cause of rAAA in patients with previous EVAR (Table 3). Time from index operation to rupture ranged from 42 months to 4.9 years among patients with previous EVAR. About one-third of patients had been lost to follow-up before the secondary rupture. This information is reported in Table 4.

Table 1.

Characteristics of the included studies.

Study	Journal	Published year	Study period	Design	Outcome	Patients
Study	Journal	Published year	Study period	Design	Outcome	De novo	Post-EVAR
Coppi et al.¹⁵	J Vasc Surg	2009	1999–2007	Retrospective	30-Day	155	14
Cho et al.¹⁶	J Vasc Surg	2010	2001–2008	Retrospective	30-Day OR in-hospital	233	18
Catanescu et al.¹⁷	Ann Vasc Surg	2017	2001–2015	Retrospective	30-Day	104	17
Rajendran and May¹⁸	J Vasc Surg	2017	1992–2014	Retrospective	30-Day	138	40
Total						630	89

EVAR: endovascular aneurysm repair.

Table 2.

Demographics and comorbidities of patients reported in the primary studies.

	Coppi et al.¹⁵			Cho et al.¹⁶			Catanescu et al.¹⁷			Rajendran and May¹⁸
	Post-EVAR (n = 14)	De novo (n = 155)	P	Post-EVAR (n = 18)	De novo (n = 232)	P	Post-EVAR (n = 17)	De Novo (n = 104)	P	Post-EVAR (n = 40)	De novo (n = 138)	P
Age	83	79	0.154	78	75	0.17	75	72	0.25	76	73	NS
Smoking	14%	35%	0.146	11%	34%	0.06	12%	13%	0.868	NR	NR	–
HP	71%	61%	0.571	78%	79%	0.99	88%	78%	0.663	65%	53%	NS
HL	0%	29%	0.022	NR	NR	–	29%	45%	0.349	NR	NR	–
CAD	50%	46%	0.763	72%	55%	0.22	76%	49%	0.278	48%	46%	NS
Diabetes	0%	9%	0.609	22%	15%	0.50	6%	16%	0.512	15%	9%	NS
Renal disease	0%	12%	0.372	22%	15%	0.49	12%	9%	0.737	20%	9%	NS

Note: P-values indicate no significant differences between the groups.

NR: not reported; HP: hypertension; HL: hyperlipidemia; CAD: coronary artery disease; NS: non-significant; EVAR: endovascular aneurysm repair.

Table 3.

Endoleaks detected at the last follow-up and at the time of rupture.

Study	No. of pts in group 1	Endoleak at last follow-up	Endoleak at the time of rupture
Study	No. of pts in group 1	Endoleak at last follow-up	Ιa	Ib	II	III	IV	V	Migration
Coppi et al.¹⁵	14	7	5	2		7
Cho et al.¹⁶	18	13	9	6	2	3		1	2
Catanescu et al.¹⁷	17	NR	9	4	3	1
Rajendran and May¹⁸	40	13	15	7		7	1	3	5
Total	89	33	38	18	5	18	1	3	7

Table 4.

Summary of the time from initial procedure to rupture, rate of secondary interventions and rate of patients that did not attend follow-up.

Study	Time from index procedure to rupture	Rate of secondary interventions	Lost follow-up
Coppi et al.¹⁵	50 months	6/14	5/14
Cho et al.¹⁶	4.0 years	4/18	3/18
Catanescu et al.¹⁷	42 months	3/17	5/17
Rajendran and May¹⁸	2.4 and 4.9 years^a	NR	13/40

^aDuring the first and the second period of the study.

Methodological quality assessment

The summary and results of methodological quality assessment of the four included studies are displayed in Figure 2(a) and (b). Overall, the methodological quality of included studies was reasonably good. However, there was moderate to high risk of bias for the domain of study participation regarding the inclusion and exclusion criteria of studies and the adequate number of patients in group 1. Justification for methodological quality assessment is provided in online Appendix 1.

Effects of interventions

Forest plots of primary and secondary outcomes are presented in Figure 3.

Perioperative mortality

The perioperative mortality for group 1 was 30.4% and for group 2 was 41%. However, there was no statistically significant difference in perioperative mortality between these groups (OR 0.66, 95% CI 0.30–1.43, P = 0.18, I²=58%).

Hemodynamic instability

At presentation, hemodynamic instability was found in 34.8% of patients in group 1 and in 59.7% of patients in group 2. Three out of four studies defined hemodynamic instability as systolic blood pressure <80 mmHg and one study as systolic blood pressure <100 mm Hg. EVAR was associated with reduced hemodynamic instability in patients with rAAAs compared to de novo ruptures (OR 0.33, 95% CI 0.12–0.90, P = 0.03, I²=74%).

Periprocedural complications

Total periprocedural systematic complications were reported in two out of four studies, and no significant differences were found between groups (OR 1.72, 95% CI 0.82–3.63, P = 0.15, I²=0%).^15,16 Complications mainly regarded renal failure, stroke, myocardial infarction, abdominal compartment syndrome and intestinal ischemia. One study reported information on complications, but a total number of perioperative morbidity was not provided, while another study did not report such information. These studies were excluded from this comparison.^17,18

Subgroup analysis

Following rupture, 48 patients in group 1 underwent surgical treatment and 41 patients underwent endovascular treatment. The choice between endovascular or open surgery did not affect the perioperative mortality (OR 1.12, 95% CI 0.41–3.04, P = 0.82, I²=0%) in patients with previous EVAR.

Sensitivity analysis

After excluding the study from Catanescu et al. which presented low methodological quality in three different domains, no significant effect was obtained in the outcome estimate of perioperative mortality (OR 0.54, 95% CI 0.22–1.34, P = 0.18, I² = 60%). The difference in hemodynamic instability lost statistical significance during sensitivity analysis (OR 0.36, 95% CI 0.10–1.32, P = 0.12, I² = 82%).

Type of rupture vs. type of treatment

Comparisons of frequency of open repair and EVAR in groups of de novo vs. post-EVAR ruptures indicated that endovascular repair was significantly more common among patients presenting secondary ruptures vs. those with primary ruptures. Interaction was significant in three out of four studies (in the study of Catanescu et al., statistical significance was marginally lost), which was also the case when the numbers for all four studies were summarized (P-value >0.001) (online Appendix 2).

Discussion

The main finding of the present report is the fact that previous EVAR does not confer any protective effect at the time of AAA rupture. Periprocedural mortality seems to be as high as during de novo rupture. Taking into account the progressively higher proportion of patients treated by endovascular means as well as the longer follow-up currently available, this finding may be of clinical relevance.² Indeed, late complications and late rupture risk are the Achilles’ heel of EVAR. According to randomized and observational data, late rupture is significantly higher among patients undergoing endovascular vs. open AAA repair.^7,19 Specifically, the long-term follow-up of the EVAR-1 randomized trial suggested a secondary rupture rate of 7% during 15 years after the index procedure.⁷ Analysis of data derived from large administrative databases indicated a rupture rate of 1.8% during four years of follow-up. In the light of the present findings, these data highlight the significance of strict surveillance protocols after EVAR in order to detect complications and take appropriate actions early.¹⁹

Among the patients included in the current review, a significant minority of those with rAAA post-EVAR were lost to follow-up. Nevertheless, most patients had regular follow-up. It is not clear from the data reported in the primary studies if this involved ultrasound or CT imaging. Notably, only half of the patients presented an endoleak at the time of the last follow-up, while all patients presented some kind of endoleak or endotension at the time of rupture. The vast majority of them were type I or III, suggesting that early detection and treatment of these endoleaks may prevent a late rupture. Since CTA has been shown to be a more accurate method to detect and identify the type of endoleak, a strategy of follow-up with ultrasound alone should be critically viewed, while a low threshold for additional CT imaging in the presence of US findings or lack of necessary expertise may better serve patients’ interest.^20,21 The included studies mention some diagnostic inaccuracies with ultrasound imaging, which resulted in missing important findings, which could be related to the subsequent AAA ruptures.¹⁷

Surprisingly, a previous meta-analysis suggested that patients compliant with EVAR surveillance programmes may have an increased re-intervention rate and do not appear to have better survival rates than non-compliant patients. A possible explanation given by the authors is that patients who were asymptomatic and potentially healthier were less likely to attend surveillance, which may result in the trend of better survival rates in non-compliant patients and more complications in the compliant group.²²

An interesting finding of the current report is the fact that patients in the post-EVAR group presented hemodynamically more stable at the time of rupture compared to those with primary rAAAs. This observation may not be surprising taking into account that the pressurization of the aneurysmal sac is significantly reduced after the implantation of an endograft compared to the native aneurysmal aorta, even in the presence of an endoleak. Specifically, Dias et al., with the use of direct intra-aneurysm sac pressure with tip sensors, have indicated a mean 26%–63% reduction of sac pressurization after EVAR even in the presence of endoleaks.²³ Therefore, extravasation may occur at a slower pace due to the lower intra-sac pressure in the post-EVAR group. Since hemodynamic instability has been directly related to worse outcomes after rAAA, this should normally lead to improved outcomes among patients previously having been treated with EVAR.²⁴ Nevertheless, this is not the case according to our results, indicating similar perioperative mortality in both groups. This could be related to technical challenges encountered during repair of a rAAA that has been previously undergone EVAR. Supra-renal clamping and endograft explantation are only few of the possible intra-operative challenges that the surgeon has to deal with. Remarkably, a mortality rate as high as 10% has been reported for late conversion even in the elective setting, while the need for supra-renal clamping has been identified as a significant predictor of operative mortality after open conversion.^25,26

Another finding that worth’s mentioning is the fact that repair with endovascular techniques is significantly more common among patients in the post-EVAR ruptured group. In other words, rAAAs in the presence of a previous endograft are usually repaired by endovascular interventions and not open surgery. Taking into account the anticipated complexity of open surgical correction, this could lead to improved results, but again this is not confirmed by the present analysis.²⁷ Specifically, when we examined the effect of the treatment modality on the outcomes in the group of secondary ruptures, no significant effect was observed. This could be explained by the fact that rupture confers a significant systematic insult, resulting in a high mortality irrespective of treatment modality. Another possible explanation is the low number of patients included in this specific outcome.

The findings of the present report should be viewed in the light of its limitations. Firstly, the limited comparative data that we could retrieve from the literature may narrow the applicability of our conclusions. Secondly, the observational design of all included studies makes them prone to selection bias. Last but not least, missing data about causes of rupture and their relation to the outcome may have hidden essential information. For example, it would be critical to examine if the outcomes of rupture are the same in case of a type I or type II endoleak, but such analysis could not been performed based on available data.

Future studies should explicitly examine the relation between specific causes of rupture after previous rAAA (i.e. type of endoleak, migration, sac enlargement) and outcome. The effect of treatment modality during the management of rAAA after previous EVAR has not been adequately examined and should also be evaluated in future studies to guide treatment of these patients.

Conclusion

Data regarding a possible effect of previous EVAR during AAA rupture are limited. Available evidence suggests that secondary ruptures confer a similar risk of mortality compared with de novo, primary AAA ruptures. The fact that patients with ruptured AAAs after a previous EVAR present hemodynamically more stable may be counterbalanced by an increased surgical complexity which results in similar perioperative outcomes. The need for adherence in follow-up protocols and early intervention to correct complications may reduce late ruptures after EVAR.

Supplemental Material

VAS896464 Supplemental Material1 - Supplemental material for Does a previous aortic endograft confer any protective effect during abdominal aortic aneurysm rupture? Systematic review and meta-analysis of comparative studies

Supplemental material, VAS896464 Supplemental Material1 for Does a previous aortic endograft confer any protective effect during abdominal aortic aneurysm rupture? Systematic review and meta-analysis of comparative studies by Nikolaos Galanakis, Nikolaos Kontopodis, Emmanouil Tavlas, Dimitrios Tsetis and Christos V Ioannou in Vascular

Supplemental Material

VAS896464 Supplemental Material2 - Supplemental material for Does a previous aortic endograft confer any protective effect during abdominal aortic aneurysm rupture? Systematic review and meta-analysis of comparative studies

Supplemental material, VAS896464 Supplemental Material2 for Does a previous aortic endograft confer any protective effect during abdominal aortic aneurysm rupture? Systematic review and meta-analysis of comparative studies by Nikolaos Galanakis, Nikolaos Kontopodis, Emmanouil Tavlas, Dimitrios Tsetis and Christos V Ioannou in Vascular

Footnotes

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 iDs

Nikolaos Galanakis

Nikolaos Kontopodis

Christos V Ioannou

Supplemental material

Supplemental material for this article is available online.

References

Parodi

Palmaz

Barone

HD.

Transfemoral intraluminal graft implantation for abdominal aortic aneurysms. Ann Vasc Surg 1991; 5: 491–499.

Sachs

Schermerhorn

Pomposelli

, et al. Resident and fellow experiences after the introduction of endovascular aneurysm repair for abdominal aortic aneurysm. J Vasc Surg 2011; 54: 881–888.

Bernhard

Mitchell

Matsumura

, et al. Ruptured abdominal aortic aneurysm after endovascular repair. J Vasc Surg 2002; 35: 1155–1162.

Fransen

Vallabhaneni

Sr van Marrewijk

, et al. Rupture of infra-renal aortic aneurysm after endovascular repair: a series from EUROSTAR registry. Eur J Vasc Endovasc Surg 2003; 26: 487–493.

Szmidt

Galazka

Rowinski

, et al. Late aneurysm rupture after endovascular abdominal aneurysm repair. Interact Cardiovasc Thorac Surg 2007; 6: 490–494.

Schlosser

Gusberg

Dardik

, et al. Aneurysm rupture after EVAR: can the ultimate failure be predicted? Eur J Vasc Endovasc Surg 2009; 37: 15–22.

Patel

Powell

Sweeting

, et al. The UK EndoVascular Aneurysm Repair (EVAR) randomised controlled trials: long-term follow-up and cost-effectiveness analysis. Health Technol Assess 2018; 22: 1–132.

Harris

Vallabhaneni

Desgranges

, et al. Incidence and risk factors of late rupture, conversion, and death after endovascular repair of infrarenal aortic aneurysms: the EUROSTAR experience. European Collaborators on Stent/graft techniques for aortic aneurysm repair. J Vasc Surg 2000; 32: 739–749.

Hinnen

Koning

van Bockel

, et al. Aneurysm sac pressure after EVAR: the role of endoleak. Eur J Vasc Endovasc Surg 2007; 34: 432–441.

10.

Karthikesalingam

Holt

Vidal-Diez

, et al. Mortality from ruptured abdominal aortic aneurysms: clinical lessons from a comparison of outcomes in England and the USA. Lancet 2014; 383: 963–969.

11.

Liberati

Altman

Tetzlaff

, et al. The PRISMA statement for reporting systematic reviews and meta-analyses of studies that evaluate healthcare interventions: explanation and elaboration. BMJ 2009; 339: b2700.

12.

Hayden

van der Windt

Cartwright

, et al. Assessing bias in studies of prognostic factors. Ann Intern Med 2013; 158: 280–286.

13.

DerSimonian

Laird

Meta-analysis in clinical trials. Control Clin Trials 1986; 7: 177–188.

14.

May

White

Stephen

, et al. Rupture of abdominal aortic aneurysm: concurrent comparison of outcome of those occurring after endovascular repair versus those occurring without previous treatment in an 11-year single-center experience. J Vasc Surg 2004; 40: 860–866.

15.

Coppi

Gennai

Saitta

, et al. Treatment of ruptured abdominal aortic aneurysm after endovascular abdominal aortic repair: a comparison with patients without prior treatment. J Vasc Surg 2009; 49: 582–588.

16.

Cho

Park

Kim

, et al. Prior endovascular abdominal aortic aneurysm repair provides no survival benefits when the aneurysm ruptures. J Vasc Surg 2010; 52: 1127–1134.

17.

Catanescu

Long

Bove

, et al. Rupture of abdominal aortic aneurysm in patients with and without antecedent endovascular repair. Ann Vasc Surg 2017; 39: 99–104.

18.

Rajendran

May

Late rupture of abdominal aortic aneurysm after endovascular repair. J Vasc Surg 2017; 65: 52–57.

19.

Schermerhorn

O'Malley

Jhaveri

, et al. Endovascular vs. open repair of abdominal aortic aneurysms in the Medicare population. N Engl J Med 2008; 358: 464–474.

20.

Abraha

Luchetta

De Florio

, et al. Ultrasonography for endoleak detection after endoluminal abdominal aortic aneurysm repair. Cochrane Database Syst Rev 2017; 6: CD010296.

21.

Kapetanios

Kontopodis

Mavridis

, et al. Meta-analysis of the accuracy of contrast-enhanced ultrasound for the detection of endoleak after endovascular aneurysm repair. J Vasc Surg 2019; 69: 280–294.

22.

Grima

Boufi

Law

, et al. Editor's choice – the implications of non-compliance to endovascular aneurysm repair surveillance: a systematic review and meta-analysis. Eur J Vasc Endovasc Surg 2018; 55: 492–502.

23.

Dias

Ivancev

Kölbel

, et al. Intra-aneurysm sac pressure in patients with unchanged AAA diameter after EVAR. Eur J Vasc Endovasc Surg 2010; 39: 35–41.

24.

Luebke

Brunkwall

Risk-adjusted meta-analysis of 30-day mortality of endovascular versus open repair for ruptured abdominal aortic aneurysms. Ann Vasc Surg 2015; 29: 845–863.

25.

Moulakakis

Dalainas

Mylonas

, et al. Conversion to open repair after endografting for abdominal aortic aneurysm: a review of causes, incidence, results, and surgical techniques of reconstruction. J Endovasc Ther 2010; 17: 694–702.

26.

Gambardella

Antoniou

Gaudino

, et al. State of the art and meta-analysis of secondary open aortic procedure after abdominal endovascular aortic repair. J Vasc Surg 2019; 70: 1341–1350.

27.

Kontopodis

Tavlas

Georgakarakos

, et al. Has anatomic complexity of abdominal aortic aneurysms undergoing open surgical repair changed after the introduction of endovascular treatment? Systematic review and meta-analysis of comparative studies. Ann Vasc Surg 2018; 52: 292–301.

Supplementary Material

Please find the following supplemental material available below.

For Open Access articles published under a Creative Commons License, all supplemental material carries the same license as the article it is associated with.

For non-Open Access articles published, all supplemental material carries a non-exclusive license, and permission requests for re-use of supplemental material or any part of supplemental material shall be sent directly to the copyright owner as specified in the copyright notice associated with the article.

0.00 MB

0.14 MB

0.28 MB