A Systematic Review of Open Versus Endovascular Repair of Inflammatory Abdominal Aortic Aneurysms

European Journal of Vascular and Endovascular Surgery(2009)

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Results The results were obtained from 35 studies comprising 999 patients and 21 studies with 121 patients who underwent OSR and EVAR, respectively. One-year CT follow-up was available for 124 and 52 patients from the two groups, respectively. Thirty-day mortality after OSR was 6% (95% confidence interval (CI); 6–13) and 2% (95% CI; 0–7) after EVAR ( p = 0.1). At 1 year, PAI regressed in 73% (95% CI; 64–80) in the OSR group compared to 65% (95% CI; 49–77) of the EVAR group ( p = 0.7). Conversely, inflammation progressed in 1% and 4%, respectively ( p = 0.1). Forty-five patients undergoing OSR and 29 EVAR were found to have preoperative hydronephrosis. This regressed postoperatively in 69% (95% CI; 53.3–81.8) and 38% (95% CI; 20.6–57.7), respectively ( p = 0.01). Hydronephrosis progressed in 9% of patients after OSR and in 21% after EVAR ( p = 0.1). New-onset hydronephrosis developed in 6% undergoing OSR compared to 2% with EVAR ( p = 0.2). One-year all-cause mortality after OSR was 14% (95% CI; 6–18) compared to 2% (95% CI; 0–13) after EVAR ( p = 0.02). Conclusion Either OSR or EVAR may be considered based on patient suitability. EVAR is associated with lower 1-year mortality compared to OSR. However, OSR may be preferred in those patients who have hydronephrosis and are deemed low risk. Keywords Inflammatory aneurysm Abdominal aortic aneurysm Surgery Endoluminal therapy EVAR Inflammatory abdominal aortic aneurysms (IAAAs), first described by Walker et al., in 1972, are characterised by marked thickening of the aortic wall and perianeurysmal fibrosis 1 and account for 3–10% of all abdominal aortic aneurysms (AAAs) with a male-to-female ratio ranging from 9:1 to 30:1. 2 IAAAs are associated with smoking, a positive family history and autoimmune diseases such as rheumatoid arthritis and systemic lupus erythematosus. 3,4 IAAAs are characterised by the presence of varying degrees of inflammatory infiltrates within the aneurysmal wall, the perivascular and the perineural tissues. 1,5,6 These infiltrates are predominantly constituted by plasma cells, lymphocytes and macrophages. Genetic and environmental aetiologies along with infections such as herpes simplex and cytomegalovirus have been proposed in their pathogenesis. 3 Patients usually present at a younger age compared to atherosclerotic aneurysms. 2 The classical triad of abdominal or back pain, weight loss and raised erythrocyte sedimentation rate in patients with AAA is highly suggestive. 2 Preoperative diagnosis can be established by ultrasound scan (US), computed tomography (CT) scan, intravenous urography (IVU) or gadolinium-enhanced magnetic resonance imaging. US and IVU have low sensitivities (13.5% and 25–30%, respectively) compared to CT, which has a sensitivity of up to 90% and is thus considered the gold standard. 7,8 Perianeurysmal adhesions invariably involve the duodenum, with additional involvement of the inferior vena cava 70%, left renal vein 50%, ureter 44% and sigmoid colon 20%. Up to 20% of patients with ureteral entrapment present with hydronephrosis. 2 Traditionally, IAAAs have been treated by conventional open surgical repair (OSR). 2,7 Due to the potential for iatrogenic injury in the presence of perianeurysmal adhesions, some authors recommend modified approaches such as avoidance of dissecting the duodenum and supracoeliac cross-clamping of the aorta. 9,10 Over the last 18 years, endovascular aneurysm repair (EVAR) has emerged as a treatment option and gained popularity due to favourable perioperative morbidity and mortality compared to OSR. 11,13 It is, however, unclear whether EVAR has similar benefit in patients with IAAA. Many individual series have reported a regression of periaortic inflammatory process with both OSR and EVAR. Hydronephrosis has also been noted to regress postoperatively with both approaches, though the extent is unknown. To date, there are no randomised controlled trials comparing OSR and EVAR for IAAA. This systematic study aims to evaluate current evidence for the outcomes of inflammatory aneurysms treated by OSR and EVAR. Further, the outcomes will be compared to determine whether either approach has any advantage over the other. Methods All publications in the English language related to IAAA, using MESH words: abdominal aortic aneurysm, inflammation, surgery and endoluminal repair were sought using OVID and MEDLINE. In order to maximise the search, inflammatory abdominal aortic aneurysm, EVAR and endoluminal therapy were used as keywords. ‘Related articles’ command was used to further broaden the search. References of relevant publications were used to obtain additional studies. Searches included studies from 1972 to date. The final search was conducted in May 2008. The flow chart for selection of studies is shown in Fig. 1 . Outcome measures - Thirty-day mortality: All studies presenting 30-day mortality were included for review. - Periaortic inflammation (PAI), hydronephrosis and 1-year mortality were recorded from studies with at least 1-year CT follow-up. Inclusion and exclusion criteria All studies presenting a minimum of 30-day follow-up data after elective OSR and EVAR were included. For late PAI and hydronephrosis, only studies presenting 1-year follow-up results with a CT scan were included. Individual patient data from the articles were reviewed and patients with less than 1-year follow-up were excluded. Studies presenting unclear follow-up data were also excluded. Results of ruptured IAAA, thoracic and complex thoraco-abdominal aneurysm morphologies were not considered. Studies with follow-up other than CT were excluded. Statistical analysis Three authors (SP, JG and DM) independently reviewed the abstracts of all relevant articles for inclusion. Any discrepancy was resolved by FSI and MGW. Data were collected (SP, JG) and analysed using STATSDIRECT statistical software (version 2.6.8, Cheshire, UK). Outcomes of OSR and EVAR were compared for statistical significance using Fisher's exact test; probability value less than 0.05 was considered significant. All results are reported as percentages and confidence intervals (CIs). As it was not intended to perform a meta-analysis, standard tests for heterogeneity and bias were not done. Results A total of 129 studies were identified of which 73 were excluded. Of the remaining 56, only one study 57 compared OSR with EVAR; thirty-five studies were related to OSR 1,4,5,7–10,14–41 and 21 to EVAR 11–13,42–58 ; 10 studies with OSR and 13 studies with EVAR presented follow-up data greater than 1-year duration. All the results are presented in Table 1 . Thirty-day mortality Thirty-five studies comprising 999 patients and 21 with 121 patients reported 30-day mortality after OSR and EVAR, respectively. Mortality rate was 6.2% (95% CI; 6–13) with OSR and 2.4% (95% CI; 0–7) with EVAR ( p = 0.1). Periaortic inflammation One-year follow-up on PAI was reported in 124 patients after OSR. Although 52 patients after EVAR with 1-year follow-up were available, details of PAI were only available in 48 patients. Only one study quantified the thickness of periaortic inflammatory tissue, 50 with the remainder only reporting whether the inflammatory status persisted, progressed or regressed. Therefore for this analysis, PAI was recorded as regressed, unchanged or progressed. PAI regressed in 73% (95% CI; 64–80) after OSR and 65% (95% CI; 49–77) after EVAR ( Tables 2 and 4 ) . Whilst PAI remained unchanged in 26% and 31% after OSR and EVAR, it progressed in 1% and 4%, respectively. None of the observed differences between groups were statistically significant. Hydronephrosis Seven studies after OSR 18,29,33,36,37,40,43 and 11 after EVAR 17,28,32,35,36,39,59 comprising 85 and 52 patients, respectively, reported the outcome of hydronephrosis. Of those, preoperative hydronephrosis was noted in 45 and 29 patients, respectively. None of the studies presented the grade of hydronephrosis. Hydronephrosis regressed in 69% (95% CI; 53.3–81.8) after OSR compared to 38% (95% CI; 20.6–57.7) after EVAR ( p = 0.01) ( Tables 3 and 5 ) . Ten patients in OSR group had concomitant ureterolysis, of whom improvement was noted in seven patients. Regression in hydronephrosis after OSR remained significantly higher compared to EVAR, on excluding those 10 patients ( p = 0.01). Hydronephrosis remained unchanged in 22% and 41%, respectively after OSR and EVAR ( p = 0.1). Progression was noted in 9% (95% CI; 2.4–21) and 21% (95% CI; 7.9–39.7), respectively ( p = 0.1). New-onset hydronephrosis was noted in 6% after OSR and 2% after EVAR ( p = 0.2). One-year mortality One-year mortality was reported in 23 studies. Whilst aneurysm-related mortality was 2% and 0%, respectively, with OSR and EVAR, all-cause mortality was 14% (95% CI; 6–18) and 2% (95% CI; 0–13), respectively after OSR and EVAR ( p = 0.01). Discussion This is the first comprehensive review comparing both 30-day and 1-year outcomes of IAAA after OSR and EVAR. These results demonstrate that both OSR and EVAR can be safely performed in IAAA. Safety of EVAR in IAAA has also been demonstrated in a recent meta-analysis, which showed similar results of 30-day mortality, PAI and hydronephrosis as above. 60 More than 1-year follow-up data were available in a minority of studies and therefore the status of PAI and hydronephrosis as well as mortality after this period remains unclear. The results of this review show that 30-day mortality of OSR and EVAR for IAAA were comparable to atherosclerotic aneurysm repair. This suggests that although the aetiology is unclear, perioperative mortality remains same, which may be attributed to the fact that most of these series were from high-volume centres. Although there was no significant difference for 30-day mortality between OSR and EVAR groups, this may be due to a type II error, as only 121 patients were in the EVAR group compared to 999 in OSR. It is likely that the benefit of EVAR over OSR for IAAA will be similar to that for non-inflammatory aneurysms. It is interesting to note that 1-year mortality favoured EVAR. The reasons for this are unclear since data provided regarding co-morbidities were insufficient to allow such a comparison between the two groups. PAI is considered to be responsible for abdominal or back pain and elevated ESR. Therefore, it is vital to determine the status of postoperative PAI. PAI is seen as a thickness from the tunica adventitia and is usually clearly seen on a CT scan. Although only 12% of OSR patients had CT follow-up, the available data showed that PAI regressed with both OSR and EVAR. However, contrary to the conventional belief that PAI completely regresses after OSR, this was noted in only 38%. This was akin to PAI regression noted following EVAR. Since there has been a suggestion that lipid deposition in the aortic media triggers the development of IAAA, 3,61 it may be hypothesised from these results that regression of the inflammatory process is dependent on aneurysm exclusion rather than the type of surgery. The degree of regression in PAI could not be quantified as only one study presented the baseline thickness of PAI. Whilst the studies have reported on postoperative periaortic thickening, none commented on patient symptomatology. A significant number of patients undergoing OSR had regression of their hydronephrosis compared to EVAR. This finding remained significant even when 10 patients who underwent ureterolysis in the OSR group were excluded. This finding questions the need for routine ureterolysis advocated by the Swedish registry. 25 Regression in hydronephrosis after EVAR as shown in some series could be a slow process. 11 Further, it is unclear whether EVAR alone has any beneficial effect on hydronephrosis, given the fact that in half of the number of patients, regression was noted only after initiating steroid therapy ( Table 6 ). Secondary intervention rate after EVAR was 22% and was due to the following reasons. One patient developed aorto-enteric fistula (2%) 8 months post-EVAR, which was treated successfully by performing an aorto-bi-femoral bypass after removing the infected stent graft. Four patients developed type III endoleak (8%) and three, type II endoleak (6%). Two patients had graft thrombosis (4%) and one patient developed stenosis of the graft (2%). These complication rates seem higher compared to the mid-term results of EVAR trial 1, 62 where type II endoleak in 3% and type III endoleak in 1% ( n = 505) was observed. Graft thrombosis and stenosis were noted in 2.5% and 0.2%, respectively. It is unclear whether increased incidence of complications in IAAA is secondary to the inflammatory nature of the aneurysm. A recent publication from EUROSTAR registry showed that IAAAs treated by EVAR have a higher incidence of stent stenosis compared to non-inflammatory aneurysms: 3.9% versus 0.3%, respectively. Progression of periaortic fibrosis may be a cause; however, such data were unavailable. Alternately, it may be a chance finding as the authors compared 52 inflammatory aneurysms with 3613 non-inflammatory aneurysms. 52 Traditionally, IAAAs have been treated by OSR as it was thought that inflammatory process would regress, and in presence of ureteral entrapment, concomitant ureterolysis could be performed. OSR for IAAA can pose a technical challenge depending on the degree of inflammation and the involvement of adjacent organs. EVAR has been increasingly employed in recent years due to low perioperative morbidity and mortality in non-inflammatory aneurysms. EVAR can also be of advantage in patients with hostile abdomen. This systematic study shows that OSR or EVAR can be performed; however, the results are limited by the non-availability of randomised controlled trials or case control studies comparing OSR with EVAR. Further, most of the studies were retrospective reviews. A number of case reports were included which may have led to selection bias. Furthermore, it should be noted that only 12% after OSR had CT follow-up, which may have underestimated the true regression or progression of PAI and hydronephrosis. Besides this, surgical technique and perioperative patient care have improved over decades and this may have confounded the results, especially of the OSR group. Conclusions Either OSR or EVAR may be considered based on patient suitability. EVAR is associated with lower 1-year mortality compared to OSR. However, OSR may be preferred in those patients who have hydronephrosis and are deemed low risk. Acknowledgements The authors would like to acknowledge the statistical input of Dr. Steve Roberts, Senior Lecturer in Medical Statistics, University of Manchester, in designing this study. Conflict of Interest None. Funding None. References 1 D.I. Walker K. Bloor G. Williams I. Gillie Inflammatory aneurysms of the abdominal aorta Br J Surg 59 1972 609 614 2 T.E. Rasmussen J.W. Hallett Jr. Inflammatory aortic aneurysms. A clinical review with new perspectives in pathogenesis Ann Surg 225 1997 155 164 3 T. Tang J.R. Boyle A.K. Dixon K. Varty Inflammatory abdominal aortic aneurysms Eur J Vasc Endovasc Surg 29 2005 353 362 4 E.S. Haug J.F. Skomsvoll G. Jacobsen T.B. Halvorsen O.D. Saether H.O. 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Inflammatory aneurysm,Abdominal aortic aneurysm,Surgery,Endoluminal therapy,EVAR
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