Short-Term Outcomes of Management of Endovascular Aneurysm Repair in Patients With Dilated Iliacs.

OBJECTIVES: This study aims to evaluate outcomes following endovascular aneurysm repair (EVAR) in patients with dilated but not aneurysmal common iliac arteries. METHODS: Data prospectively collected from 342 elective EVARs were analyzed retrospectively. Dilated common iliac anatomy was defined as 21 to 24 mm. Patients with iliac aneurysms or external iliac artery (EIA) extension were excluded. Patients were followed up using clinical review, plain radiographs, duplex imaging, and selective computed tomography scanning. RESULTS: Median age was 75 years with a mean follow-up of 3.6 years. In all, 33 patients had dilated common iliac arteries (DCIAs) and 309 had non-dilated common iliac arteries (NDCIA). There was no difference in aneurysm diameter or neck characteristics (length, diameter, angulation, thrombus, and flare) between the subgroups. There was no significant difference in technical success, 30-day mortality, late mortality, aneurysm-related mortality, 30-day reinterventions, stent graft migration, limb occlusion, sac expansion, graft rupture, type 1 endoleaks, type 3 endoleaks, and total reinterventions (all Ps > .05). There was a significant decrease in type II endoleaks in patients with DCIA compared to NDCIA (NDCIA 12.9% and DCIA 0.0%; P = .02). CONCLUSION: Patients presenting with abdominal aortic aneurysms with DCIA can be successfully treated with EVAR with no increase in complications without extension into the EIA.

Identification of microRNAs associated with abdominal aortic aneurysms and peripheral arterial disease.

BACKGROUND: MicroRNAs are crucial in the regulation of cardiovascular disease and represent potential therapeutic targets to decrease abdominal aortic aneurysm (AAA) expansion. The aim of this study was to identify circulating microRNAs associated with AAA. METHODS: Some 754 microRNAs in whole-blood samples from 15 men with an AAA and ten control subjects were quantified using quantitative reverse transcriptase-PCR. MicroRNAs demonstrating a significant association with AAA were validated in peripheral blood and plasma samples of men in the following groups (40 in each): healthy controls, controls with peripheral arterial disease (PAD), men with a small AAA (30-54 mm), those with a large AAA (over 54 mm), and those following AAA repair. MicroRNA expression was also assessed in aortic tissue. RESULTS: Twenty-nine differentially expressed microRNAs were identified in the discovery study. Validation study revealed that let-7e (fold change (FC) -1·80; P = 0·001), miR-15a (FC -2·24; P < 0·001) and miR-196b (FC -2·26; P < 0·001) were downregulated in peripheral blood from patients with an AAA, and miR-411 was upregulated (FC 5·90; P = 0·001). miR-196b was also downregulated in plasma from the same individuals (FC -3·75; P = 0·029). The same miRNAs were similarly expressed differentially in patients with PAD compared with healthy controls. Validated and predicted microRNA targets identified through miRWalk revealed that these miRNAs were all regulators of AAA-related genes (vascular cell adhesion molecule 1, intercellular cell adhesion molecule 1, DAB2 interacting protein, α1-antitrypsin, C-reactive protein, interleukin 6, osteoprotegerin, methylenetetrahydrofolate reductase, tumour necrosis factor α). CONCLUSION: In this study, circulating levels of let-7e, miR-15a, miR-196b and miR-411 were differentially expressed in men with an AAA compared with healthy controls, but also differentially expressed in men with PAD. Modulation of these miRNAs and their target genes may represent a new therapeutic pathway to affect the progression of AAA and atherosclerosis.

Meta-analysis and meta-regression analysis of biomarkers for abdominal aortic aneurysm.

BACKGROUND: Many studies have investigated the systemic and local expression of biomarkers in patients with abdominal aortic aneurysm (AAA). The natural history of AAA varies between patients, and predictors of the presence and diameter of AAA have not been determined consistently. The aim of this study was to perform a systematic review, meta-analysis and meta-regression of studies comparing biomarkers in patients with and without AAA, with the aim of summarizing the association of identified markers with both AAA presence and size. METHODS AND RESULTS: Literature review identified 106 studies suitable for inclusion. Meta-analysis demonstrated a significant difference between matrix metalloproteinase (MMP) 9, tissue inhibitor of matrix metalloproteinase 1, interleukin (IL) 6, C-reactive protein (CRP), α1-antitrypsin, triglycerides, lipoprotein(a), apolipoprotein A and high-density lipoprotein in patients with and without AAA. Although meta-analysis was not possible for MMP-2 in aortic tissue, tumour necrosis factor α, osteoprotegerin, osteopontin, interferon γ, intercellular cell adhesion molecule 1 and vascular cell adhesion molecule 1, systematic review suggested an increase in these biomarkers in patients with AAA. Meta-regression analysis identified a significant positive linear correlation between aortic diameter and CRP level. CONCLUSION: A wide variety of biomarkers are dysregulated in patients with AAA, but their clinical value is yet to be established. Future research should focus on the most relevant biomarkers of AAA, and how they could be used clinically.

Type II endoleak: conservative management is a safe strategy.

OBJECTIVE: Type II endoleak is the most common complication after endovascular abdominal aortic aneurysm repair (EVAR); however, its natural history is unclear. The aim of this study was to examine the incidence and outcomes of type II endoleak, at a single institution after EVAR. METHODS: A total of 904 consecutive patients who underwent EVAR between September 1995 and July 2013 at a single centre were entered onto a prospective database. All patients were followed up by duplex ultrasound (DUSS). Patients who developed type II endoleak were compared for preoperative demographics, mortality, and sac expansion. RESULTS: A total of 175(19%) patients developed type II endoleak over a median follow-up of 3.6 years (1.5-5.9 years); 54% of type II endoleaks spontaneously resolved within 6 months (0.25-1.2 years). No difference was found in preoperative demographics or choice of endograft between the two groups. Survival was significantly higher in the group with type II endoleak (94.1% vs. 85.6%; p = .01) and this effect was most pronounced in those with late type II endoleaks (97.7% vs. 85.6% p = .004). No difference was seen in aneurysm-related mortality or rate of type I endoleak between the two groups. Freedom from sac expansion (>5 mm from preoperative diameter) was significantly lower in the group of patients with type II endoleak (82.5% vs. 93.2%, p = .0001); however, at a threshold of >10 mm from preoperative diameter no difference was seen. CONCLUSIONS: Patients with isolated type II endoleak demonstrate equivalent aneurysm-related mortality and an improved survival.

National Vascular Registry Report on surgical outcomes and implications for vascular centres.

BACKGROUND: The National Vascular Registry Report on Surgical Outcomes (NVSRO) coincided with the update of the National Health Service Standard Contract for Specialized Vascular Services in Adults (NHSSCSVS). The latter promises patients minimum standards for vascular centres. The present study aimed to determine whether current data support the standards proposed in the NHSSCSVS. METHODS: Numbers of abdominal aortic aneurysm (AAA) repairs and carotid endarterectomies (CEAs) performed by hospital Trust and surgeon, and their outcomes were obtained from the NVRSO. These were assessed against NHSSCSVS recommendations that included: more than 60 AAA repairs per year per Trust, over 50 CEAs per year per Trust and at least six vascular surgeons per Trust. RESULTS: Based on NVRSO data, 107 hospital Trusts (92.2 per cent) would fail to meet the minimum standards required to achieve vascular centre status. Outcomes were poorer in these hospitals (overall mortality rate after AAA: 2.7 versus 1.3 per cent; P = 0.007). There were strong associations between number of AAA repairs or CEAs per Trust and better outcomes (AAA repair, P < 0.001; CEA, P = 0.004). These remained significant when analysed by individual surgeon (AAA repair, P < 0.001; CEA, P < 0.001). Trusts undertaking 60 or fewer elective AAA repairs per year had significantly higher elective AAA mortality rates (2.7 versus 1·7 per cent; P = 0.010). Trusts performing a minimum of 50 CEAs per year had significantly lower perioperative mortality/morbidity rates (1.9 versus 3.0 per cent; P = 0.032). Trusts with seven or more surgeons demonstrated lower AAA-related mortality rates (1.7 versus 2.7 per cent; P = 0.018). CONCLUSION: Data from the NVRSO suggest that the majority of hospital Trusts presently fail to meet the standards for vascular centre status. NVRSO data support a standard of more than 60 elective AAA repairs and 50 CEAs per Trust per year. A minimum of seven vascular surgeons per unit was associated with better outcomes. These data support the ongoing remodelling of vascular services in the UK.

A review of current reporting of abdominal aortic aneurysm mortality and prevalence in the literature.

BACKGROUND: It is common for authors to introduce a paper by demonstrating the importance of the clinical condition being addressed, usually by quoting data such as mortality and prevalence rates. Abdominal aortic aneurysm (AAA) epidemiology is changing, and therefore such figures for AAA are subject to error. The aim of this study was to analyse the accuracy of AAA prevalence and mortality citations in the contemporaneous literature. METHODS: Two separate literature searches were performed using PubMed to identify studies reporting either aneurysm prevalence or mortality. The first 40 articles or those published over the last 2 years were included in each search to provide a snapshot of current trends. For a prevalence citation to be appropriate, a paper had to cite an original article publishing its own prevalence of AAA or a national report. In addition, the cited prevalence should match that published within the referenced article. These reported statistics were compared with the most recent data on aneurysm-related mortality. RESULTS: The prevalence of AAA was reported to be as low as 1% and as high as 12.7% (mean 5.7%, median 5%). Only 47.5% of studies had referenced original articles, national reports or NICE, and only 32.4% of cited prevalences matched those from the referenced article. In total 5/40 studies were completely accurate. 80% of studies cited aneurysm mortality in the USA, with the majority stating 15,000 deaths per year (range 9,000 to 30,000). Current USA crude AAA mortality is 6,289 (2010). CONCLUSION: References for AAA mortality and prevalence reported in the current literature are often inaccurate. This study highlights the importance of accurately reporting mortality and prevalence data and using up-to-date citations.

Type II endoleak after endovascular aneurysm repair.

BACKGROUND: The aim was to assess the risk of rupture, and determine the benefits of intervention for the treatment of type II endoleak after endovascular abdominal aortic aneurysm repair (EVAR). METHODS: This systematic review was done according to PRISMA guidelines. Outcome data included incidence, spontaneous resolution, sac expansion, interventions, clinical success, and complications including conversion to open repair, and rupture. RESULTS: Thirty-two non-randomized retrospective studies were included, totalling 21 744 patients who underwent EVAR. There were 1515 type II endoleaks and 393 interventions. Type II endoleak was seen in 10·2 per cent of patients after EVAR; 35·4 per cent resolved spontaneously. Fourteen patients (0·9 per cent) with isolated type II endoleak had ruptured abdominal aortic aneurysm; six of these did not have known aneurysm sac expansion. Of 393 interventions for type II endoleak, 28·5 per cent were unsuccessful. Translumbar embolization had a higher clinical success rate than transarterial embolization (81 versus 62·5 per cent respectively; P = 0·024) and fewer recurrent endoleaks were reported (19 versus 35·8 per cent; P = 0·036). Transarterial embolization also had a higher rate of complications (9·2 per cent versus none; P = 0·043). CONCLUSION: Aortic aneurysm rupture after EVAR secondary to an isolated type II endoleak is rare (less than 1 per cent), but over a third occur in the absence of sac expansion. Translumbar embolization had a higher success rate with a lower risk of complications.

Systematic review and meta-analysis of the early and late outcomes of open and endovascular repair of abdominal aortic aneurysm.

BACKGROUND: Any possible long-term benefit from endovascular (EVAR) versus open surgical repair for abdominal aortic aneurysm (AAA) remains unproven. Long-term data from the Open Versus Endovascular Repair (OVER) trial add to the debate regarding long-term all-cause and aneurysm-related mortality. The aim of this study was to investigate 30-day and long-term mortality, reintervention, rupture and morbidity after EVAR and open repair for AAA in a systematic review. METHODS: Standard PRISMA guidelines were followed. Random-effects Mantel-Haenszel meta-analysis was performed to evaluate mortality and morbidity outcomes. RESULTS: The existing published randomized trials, together with information from Medicare and SwedVasc databases, were included in a meta-analysis. This included 25 078 patients undergoing EVAR and 27 142 undergoing open repair for AAA. Patients who had EVAR had a significantly lower 30-day or in-hospital mortality rate (1·3 per cent versus 4·7 per cent for open repair; odds ratio (OR) 0·36, 95 per cent confidence interval 0·21 to 0·61; P < 0·001). By 2-year follow-up there was no difference in all-cause mortality (14·3 versus 15·2 per cent; OR 0·87, 0·72 to 1·06; P = 0·17), which was maintained after at least 4 years of follow-up (34·7 versus 33·8 per cent; OR 1·11, 0·91 to 1·35; P = 0·30). There was no significant difference in aneurysm-related mortality by 2 years or longer follow-up. A significantly higher proportion of patients undergoing EVAR required reintervention (P = 0·003) and suffered aneurysm rupture (P < 0·001). CONCLUSION: There is no long-term survival benefit for patients who have EVAR compared with open repair for AAA. There are also significantly higher risks of reintervention and aneurysm rupture after EVAR.

International variations in AAA screening.

INTRODUCTION: Abdominal aortic aneurysm (AAA) screening programmes reduce AAA-related mortality and are cost-effective. This study aims to assess the state and variability of AAA screening programmes worldwide. METHODS: Data were obtained from an international expert group convened at the 34th Charing Cross Symposium as well as government websites and published reports on screening programmes. RESULTS: Six countries are in the process of implementing national AAA screening programmes, with Italy still performing screening trials. There is wide variability in inclusion criteria between countries with the majority screening only men in their 65th year, however 3 programmes include women, 2 programmes only include patients with high cardiovascular risk, and 2 trials are also screening for hypertension and lower limb atherosclerosis. Surveillance intervals vary between screening programmes, with the most common regimen being to vary the surveillance interval depending upon aneurysm size, however the optimum surveillance interval in terms of decreasing mortality and cost effectiveness remains uncertain. DISCUSSION: International dissemination of current AAA screening programme outcomes is required to inform developing programmes about optimum screening intervals, benefits of surveillance of the subaneurysmal aorta, and screening for other cardiovascular disease.

A multicentre observational study of the outcomes of screening detected sub-aneurysmal aortic dilatation.

OBJECTIVES: Currently most abdominal aortic aneurysm screening programmes discharge patients with aortic diameter of less than 30 mm. However, sub-aneurysmal aortic dilatation (25 mm-29 mm) does not represent a normal aortic diameter. This observational study aimed to determine the outcomes of patients with screening detected sub aneurysmal aortic dilatation. DESIGN AND METHODS: Individual patient data was obtained from 8 screening programmes that had performed long term follow up of patients with sub aneurysmal aortic dilatation. Outcome measures recorded were the progression to true aneurysmal dilatation (aortic diameter 30 mm or greater), progression to size threshold for surgical intervention (55 mm) and aneurysm rupture. RESULTS: Aortic measurements for 1696 men and women (median age 66 years at initial scan) with sub-aneurysmal aortae were obtained, median period of follow up was 4.0 years (range 0.1-19.0 years). Following Kaplan Meier and life table analysis 67.7% of patients with 5 complete years of surveillance reached an aortic diameter of 30 mm or greater however 0.9% had an aortic diameter of 54 mm. A total of 26.2% of patients with 10 complete years of follow up had an AAA of greater that 54 mm. CONCLUSION: Patients with sub-aneurysmal aortic dilatation are likely to progress and develop an AAA, although few will rupture or require surgical intervention.

Outcomes of endovascular aneurysm repair in patients with hostile neck anatomy.

OBJECTIVES: This study aims to evaluate outcomes following EVAR in patients with hostile neck anatomy (HNA). METHODS: Data prospectively collected from 552 elective EVARs were analysed retrospectively. Data regarding neck morphology was obtained from aneurysm stent plans produced prior to EVAR. HNA was defined as any of; neck diameter >28 mm, neck angulation >60°, neck length <15 mm, neck thrombus, or neck flare. RESULTS: 552 patients underwent EVAR. Mean age 73.9 years, mean follow-up 4.1 years. 199 patients had HNA, 353 had favourable neck anatomy (FNA). There was a significant increase in late type I endoleaks (FNA 4.5%, HNA 9.5%; P = 0.02) and total reinterventions (FNA 11.0%, HNA 22.8%; P < 0.01), and a significant decrease in late type II endoleaks in patients with HNA (FNA 16.7%, HNA 10.6%; P < 0.05). There was no significant difference in technical success (FNA 0.6%, HNA 2.0%; p = 0.12), 30-day re-intervention (FNA 2.8%, HNA 5.0%; P = 0.12), 30-day mortality (FNA 1.1%, HNA 0.5%; P = 0.45), 30-day type I endoleaks (FNA 0.8%, HNA 2.5%; P = 0.12), 5-year mortality (FNA 15.1%, HNA 14.6%; P = 0.86), aneurysm-related mortality (FNA 1.7% versus HNA 2.0%; P = 0.79), stent-graft migration (FNA 2.5%, HNA 3.0%; P = 0.75), sac expansion (FNA 13.0%, HNA 9.5%; P = 0.22), or graft rupture (FNA 1.1%, HNA 3.5%; P = 0.05). Binary logistic regression of individual features of HNA revealed secondary intervention (P = 0.009), technical failure (P = 0.02), and late type I endoleaks (P = 0.002), were significantly increased with increased neck diameter. CONCLUSIONS: HNA AAAs can be successfully treated with EVAR. However, surveillance is necessary to detect and treat late type I endoleaks in HNA patients.

Low density lipoprotein receptor related protein 1 and abdominal aortic aneurysms.

OBJECTIVES: A recent GWAS demonstrated an association between low density lipoprotein receptor related protein 1 (LRP1) and abdominal aortic aneurysm (AAA). This review aims to identify how LRP1 may be involved in the pathogenesis of abdominal aortic aneurysm. DESIGN AND MATERIALS: A systematic review of the English language literature was undertaken in order to determine whether LRP1 and associated pathways were plausible candidates for contributing to the development and/or progression of AAA. METHODS AND RESULTS: A comprehensive literature search of MEDLINE (since 1948), Embase (since 1980) and Health and Psychological Instruments (since 1985) was conducted in January 2012 identified 50 relevant articles. These studies demonstrate that LRP1 has a diverse range of biological functions and is a plausible candidate for playing a central role in aneurysmogenesis. Importantly, LRP1 downregulates MMP (matrix metalloproteinase) activity in vascular smooth muscle cells and regulates other key pathways involved in extracellular matrix remodelling and vascular smooth muscle migration and proliferation. Crucially animal studies have shown that LRP1 depletion leads to progressive destruction of the vascular architecture and aneurysm formation. CONCLUSIONS: Published evidence suggests that LRP1 may play a key role in the development of AAA.