Search

This study was an unplanned exploratory analysis of a subset of participants from the Telmisartan in the Management of Abdominal Aortic Aneurysm (TEDY) trial. It aimed to assess the efficacy of the angiotensin 1 receptor blocker telmisartan in reducing abdominal aortic aneurysm (AAA) peak wall stress (PWS) and peak wall rupture index (PWRI) among individuals with small AAAs.Participants with AAAs measuring 35 - 49 mm in maximum diameter were randomised to receive telmisartan 40 mg or identical placebo in the TEDY trial. Participants who had computed tomography angiography performed at entry and at least one other time point during the trial (12 or 24 months) were included in the current study. Orthogonal AAA diameter, PWS, and PWRI were measured using previously validated methods. The annual change in PWS and PWRI from baseline was compared between participants allocated telmisartan or placebo using linear mixed effects models. These models were either unadjusted or adjusted for risk factors that were different in the groups at entry (p.100) or systolic blood pressure (SBP) at one year.Of the 207 participants recruited to TEDY, 124 were eligible for inclusion in this study. This study included 65 and 59 participants from the telmisartan and placebo groups, respectively. The PWS and PWRI were not significantly different in the two groups at baseline. Participants allocated telmisartan had a slower annual increase in PWS (-4.19; 95% CI -8.24, -0.14 kPa/year; p = .043) and PWRI (-0.014; 95% CI -0.026, -0.001; p = .032) compared with those allocated placebo after adjusting for risk factors. After adjustment for SBP at one year, telmisartan did not significantly reduce annual increases in PWS or PWRI.The findings of this study suggest that telmisartan limits the rate of increase in PWS and PWRI of small AAAs by reducing blood pressure.

Background Depression is associated with an increased risk of cardiovascular events but its association with abdominal aortic aneurysm (AAA) progression is unknown. This study examined if a diagnosis of depression was association with more rapid AAA growth. Methods Patients with small AAA measuring between 30 and 50 mm were recruited from surveillance programs at 4 Australian centres. Maximum AAA diameter was measured by ultrasound imaging using a standardised and reproducible protocol to monitor AAA growth. Depression was defined from medical records of treatment for depression at recruitment. Linear mixed effects modelling was performed to examine the independent association of depression with AAA growth. A propensity matched sub-analysis was performed. Results A total of 574 participants were included of whom 73 (12.7%) were diagnosed with depression. Participants were followed with a median of 3 (Inter-quartile range (IQR): 2, 5) ultrasound scans for a median of 2.1 (IQR: 1.1, 3.5) years. The unadjusted model suggested that annual AAA growth was non-significantly reduced (mean difference: -0.3 mm/year; 95% confidence interval (CI): -0.7, 0.2; P = 0.26) in participants with a diagnosis of depression compared to other participants. After adjustment for covariates, depression was not significantly associated with AAA growth (mean difference: -0.3 mm/year; 95% CI: -0.8, 0.2; P = 0.27). Findings were similar in the propensity matched sub-analysis. Sensitivity analyses investigating the impact of initial AAA diameter and follow up on the association of depression with AAA growth found no interaction. Conclusions This study suggested that depression was not associated with faster AAA growth.

Iliac artery aneurysms (IAA) are associated frequently with abdominal aortic (AAA) and other degenerative large-vessel aneurysms. Concurrent fistulization of the aortoiliac tree into the gastrointestinal tract (GIT) and bladder is exceptionally rare. We herewith report a unique case of concurrent ilio-enteric and ilio-vesical fistula arising from a large aorto-iliac aneurysm.

Acquired arteriovenous fistulas involving the carotid artery are most frequently the result of trauma and iatrogenic causes such as central venous catheterisation. Occasionally, they may develop spontaneously due to erosion of an aneurysm into an adjacent vein. We report a rare case of an acquired carotid-jugular fistula secondary to a pseudoaneurysm that occurred four months following carotid endarterectomy

IntroductionGout is a systemic inflammatory disease which has been associated with an increased risk of cardiovascular events but its association with abdominal aortic aneurysm (AAA) progression is unknown. The aim of this study was to investigate the association of gout with growth of small AAA. MethodsPatients with initial AAA diameter measuring 30-54mm were recruited from surveillance programs at four Australian centres. Maximum AAA diameter was measured with a standardised and reproducible protocol to monitor AAA growth. Presence of gout was defined by clinical diagnosis by clinician or prescription of medications used to treat gout. Linear mixed effects modelling was performed to examine the independent association of gout with AAA growth. ResultsA total of 637 participants, including 66 (10.3%) diagnosed with gout, received a median of 4 (Inter-quartile range (IQR): 3, 6) scans over a median follow-up of 1.8 (IQR: 1.0, 3.0) years. In unadjusted analyses, participants with diagnosis of gout had a slower mean annual AAA growth of -0.3 mm/year (95% CI: -0.7, 0.2; p=0.25) than those without gout. After adjusting for potential confounders including initial AAA diameter, body mass index, prior stroke and anti-hypertensive medication prescription, gout was not significantly associated with AAA growth (-0.3 mm/year; 95% CI: -0.7, 0.2; p=0.24). Sensitivity analyses investigating the impact of initial AAA diameter on the association of gout with AAA growth found no interaction. ConclusionThis study suggests diagnosis of gout is not associated with growth of small AAA.

Objectives: Currently there is no drug therapy for abdominal aortic aneurysm (AAA) and most previous investigations have focused on imaging rather than clinical outcomes. The aim of this study was to assess whether AAA related clinical events were lower in patients prescribed metformin. Methods: This was a prospective cohort observational study performed in three cities in Australia, which was designed to study risk factors for clinical events not simply to focus on metformin. Patients with an asymptomatic unrepaired AAA of any diameter ≥30 mm were recruited from hospital outpatient clinics and surveillance programs run at four centres. The main outcome was the requirement for AAA repair or AAA related mortality (AAA events). The association between metformin prescription and AAA events was assessed using Kaplan-Meier analysis and Cox proportional hazard analysis. Results: Patients (1,080) with a mean (SD) initial AAA diameter of 46.1 (11.3) mm were followed for a mean (SD) of 2.5 (3.1) years until an AAA event (n ¼ 454), death (n ¼ 176), loss to follow up (n ¼ 128), or completion of current follow up (n ¼ 322). Patients with diabetes who were prescribed metformin (adjusted HR 0.63, 95% CI 0.44e0.93), but not patients with diabetes who were not prescribed metformin (adjusted HR 1.15, 95% CI 0.83e 1.59), had a lower incidence of AAA events compared with those without diabetes. Findings were similar in sensitivity analyses restricted to patients with an initial AAA diameter ≤ 50 mm and patients with a minimum follow up of six months before an AAA event. Conclusions: These findings suggest that clinically important AAA events may be reduced in patients with diabetes who are prescribed metformin, but not those with diabetes receiving other treatments. A randomised controlled trial is needed to definitively test whether metformin reduces AAA related clinical events in patients with small AAAs who do not have diabetes.

Background The aim of this study was to assess the relationship between serum lipoprotein (a) (Lp[a]) concentration and the requirement for peripheral artery disease ( PAD ) operations or incidence of major adverse cardiovascular events. Methods and Results A total of 1472 people with PAD presenting with intermittent claudication (n=355), abdominal aortic aneurysm (n=989) or critical limb ischemia (n=128) were prospectively recruited from 4 outpatient clinics in Australia. Lp(a) was measured in serum samples collected at recruitment using an immunoassay. Participants were followed for a median (interquartile range) of 2.4 (0.1–6.1) years to record requirement for any PAD operation, defined to include any open or endovascular PAD intervention (lower limb peripheral revascularization, abdominal aortic aneurysm repair, other aneurysm repair, or carotid artery revascularization). Myocardial infarctions, strokes, and deaths were also recorded. The association of Lp(a) with events was assessed using Cox proportional hazard analysis adjusting for traditional risk factors. Participants with Lp(a) ≥30 mg/dL had a greater requirement for any PAD operation (hazard ratio, 1.20, 95% CI , 1.02–1.41) and lower limb peripheral revascularization alone ( hazard ratio 1.33, 95% CI , 1.06–1.66) but no increased risk of major adverse cardiovascular events or all‐cause mortality. Lp(a) ≥50 mg/dL and a 40 mg/dL increase in Lp(a) were also associated with an increased risk of lower limb peripheral revascularization alone but not with other outcomes. Conclusions In participants with PAD referred for hospital management those with high Lp(a) had greater requirement for lower limb peripheral revascularization but Lp(a) was not consistently associated with other clinical events.

Background It has been suggested that diabetes medications, such as metformin, may have effects that inhibit abdominal aortic aneurysm (AAA) growth. The aim of this study was to examine the association of diabetes treatments with AAA growth in three patient cohorts. Methods AAA growth was studied using ultrasound surveillance in cohort 1, repeated CT in cohort 2 and more detailed repeat CT in cohort 3. Growth was estimated by the mean annual increase in maximum AAA diameter. Results A total of 1697 patients with an AAA were studied, of whom 118, 39 and 16 patients were prescribed metformin for the treatment of diabetes in cohorts 1, 2 and 3 respectively. Prescription of metformin was associated with a reduced likelihood of median or greater AAA growth in all three cohorts (cohort 1: adjusted odds ratio (OR) 0·59, 95 per cent c.i. 0·39 to 0·87, P = 0·008; cohort 2: adjusted OR 0·38, 0·18 to 0·80, P = 0·011; cohort 3: adjusted OR 0·13, 0·03 to 0·61, P = 0·010). No other diabetes treatment was significantly associated with AAA growth in any cohort. Conclusion These findings suggest a potential role for metformin in limiting AAA growth.

Background Hypertension is an important risk factor for cardiovascular events in patients with peripheral artery disease; however, optimal blood pressure targets for these patients are poorly defined. This study investigated the association between systolic blood pressure ( SBP ) and cardiovascular events in a prospectively recruited patient cohort with peripheral artery disease. Methods and Results A total of 2773 patients were included and were grouped according to SBP at recruitment (≤120 mm Hg, n=604; 121–140 mm Hg, n=1065; and >140 mm Hg, n=1104). Adjusted Cox proportional hazards analyses suggested that patients with SBP ≤120 mm Hg were at greater risk of having a major cardiovascular event (myocardial infarction, stroke, or cardiovascular death) than patients with SBP of 121–140 mm Hg (adjusted hazard ratio, 1.36; 95% CI, 1.08–1.72; P =0.009). Patients with SBP >140 mm Hg had an adjusted hazard ratio of 1.23 (95% CI, 1.00–1.51; P =0.051) of major cardiovascular events compared with patients with SBP of 121–140 mm Hg. These findings were similar in sensitivity analyses only including patients receiving antihypertensive medications or focused on patients with a minimum of 3 months of follow‐up. Conclusions This cohort study suggests that patients with peripheral artery disease and SBP ≤120 mm Hg are at increased risk of major cardiovascular events. The findings suggest caution in intensive SBP lowering in this patient group.

Background There is no drug therapy for abdominal aortic aneurysm ( AAA ). FAME‐2 (Fenofibrate in the Management of Abdominal Aortic Aneurysm 2) was a placebo‐controlled randomized trial designed to assess whether administration of 145 mg of fenofibrate/d for 24 weeks favorably modified circulating markers of AAA. Methods and Results Patients with AAA s measuring 35 to 49 mm and no contraindication were randomized to fenofibrate or identical placebo. The primary outcome measures were the differences in serum osteopontin and kallistatin concentrations between groups. Secondary analyses compared changes in the circulating concentration of AAA ‐associated proteins, and AAA growth, between groups using multivariable linear mixed‐effects modeling. A total of 140 patients were randomized to receive fenofibrate (n=70) or placebo (n=70). By the end of the study 3 (2.1%) patients were lost to follow‐up and 18 (12.9%) patients had ceased trial medication. A total of 85% of randomized patients took ≥80% of allocated tablets and were deemed to have complied with the medication regimen. Patients’ allocated fenofibrate had expected reductions in serum triglycerides and estimated glomerular filtration rate, and increases in serum homocysteine. No differences in serum osteopontin, kallistatin, or AAA growth were observed between groups. Conclusions Administering 145 mg/d of fenofibrate for 24 weeks did not significantly reduce serum concentrations of osteopontin and kallistatin concentrations, or rates of AAA growth in this trial. The findings do not support the likely benefit of fenofibrate as a treatment for patients with small AAA s. Clinical Trial Registration URL : www.anzctr.org.au . Unique identifier: ACTRN 12613001039774.

Background An abdominal aortic aneurysm (AAA) is a focal dilation of the abdominal aorta and is associated with a risk of fatal rupture. Experimental studies suggest that myo-inositol may exert beneficial effects on AAAs through favourable changes to biological pathways implicated in AAA pathology. The aim of the Inositol in the MAnaGemENt of abdominal aortic aneurysm (IMAGEN) trial is to assess if myo-inositol will reduce AAA growth. Methods/design IMAGEN is a multi-centre, prospective, parallel-group, randomised, double-blind, placebo-controlled trial. A total of 164 participants with an AAA measuring ≥ 30 mm will be randomised to either 2 g of myo-inositol or identical placebo twice daily for 12 months. The primary outcome measure will be AAA growth estimated by increase in total infrarenal aortic volume measured on computed tomographic scans. Secondary outcome measures will include AAA diameter assessed by computed tomography and ultrasound, AAA peak wall stress and peak wall rupture index, serum lipids, circulating AAA biomarkers, circulating RNAs and health-related quality of life. All analysis will be based on the intention-to-treat principle at the time of randomisation. All patients who meet the eligibility criteria, provide written informed consent and are enrolled in the study will be included in the primary analysis, regardless of adherence to dietary allocation. Discussion Currently, there is no known medical therapy to limit AAA progression. The IMAGEN trial will be the first randomised trial, to our knowledge, to assess the value of myo-inositol in limiting AAA growth. Trial registration Australian New Zealand Clinical Trials Registry, ACTRN12615001209583. Registered on 6 November 2015. Electronic supplementary material The online version of this article (doi:10.1186/s13063-017-2304-x) contains supplementary material, which is available to authorized users.

Australia is similar to other advanced Western countries in both prevalence of extracranial carotid artery atherosclerosis and the treatment options available. The historical model for the management of carotid artery disease has been a multi-disciplinary one, with a team comprised of stroke neurologist, interventional radiologist and vascular surgeon. In Australia, the vascular surgeon representing an independent subspecialty discipline evolved at an early stage in the global movement, and has therefore taken a leading role in the management of carotid disease. In this chapter we explore the local approach to carotid disease with a focus on revascularisation treatment comprising carotid artery endarterectomy and stenting.

Experimental studies suggest that angiotensin II plays a central role in the pathogenesis of abdominal aortic aneurysm. This trial aims to evaluate the efficacy of the angiotensin receptor blocker telmisartan in limiting the progression of abdominal aortic aneurysm.Telmisartan in the management of abdominal aortic aneurysm (TEDY) is a multicentre, parallel-design, randomised, double-blind, placebo-controlled trial with an intention-to-treat analysis. We aim to randomly assign 300 participants with small abdominal aortic aneurysm to either 40 mg of telmisartan or identical placebo and follow patients over 2 years. The primary endpoint will be abdominal aortic aneurysm growth as measured by 1) maximum infra-renal aortic volume on computed tomographic angiography, 2) maximum orthogonal diameter on computed tomographic angiography, and 3) maximum diameter on ultrasound. Secondary endpoints include change in resting brachial blood pressure, abdominal aortic aneurysm biomarker profile and health-related quality of life. TEDY is an international collaboration conducted from major vascular centres in Australia, the United States and the Netherlands.Currently, no medication has been convincingly demonstrated to limit abdominal aortic aneurysm progression. TEDY will examine the potential of a promising treatment strategy for patients with small abdominal aortic aneurysms.Australian and Leiden study centres: Australian New Zealand Clinical Trials Registry ACTRN12611000931976 , registered on 30 August 2011; Stanford study centre: clinicaltrials.gov NCT01683084 , registered on 5 September 2012.

The Australian and New Zealand Society for Vascular Surgery has incorporated a constitutional change to administer a self-funded compulsory vascular surgery audit since January 2010. This is a bi-national quality assurance activity that captures all procedures performed in both countries. Data is collected at two points in the clinical admission; at operation and at discharge and data entry is via the Internet. Security is stringent and confidentiality is guaranteed by Commonwealth privilege. Data privacy is maximized by encryption. The application is flexible and administered by a dedicated administrator with a help-desk facility. Reports are available to provide real-time feedback of user performance compared with the peer group data in key categories of arterial surgery. A structured hierarchy for data management has been established to assess four main categories of performance: mortality after aortic surgery, stroke and death after carotid surgery, patency and limb salvage after infrainguinal bypass and patency after arteriovenous access for haemodialysis. Data is analysed using risk-adjustment techniques and an algorithm for management of underperformance has been followed. Data validation has been performed. The outcomes in all categories have been of a high standard and correction of erroneous data in a single statistical outlier has negated underperformance. The audit has captured only 65% of the estimated procedures in Australia in the first year, but data quality is good. The feasibility of a complete compulsory bi-national audit has now been established and will be the benchmark for other craft groups in the current environment of accountability.

Objective The purpose of this study was to describe the development of the Australasian Vascular Audit that was created to unify audit activities under the umbrella of the Australian and New Zealand Society for Vascular Surgery as a Web-based application. Methods Constitutional change in late 2008 deemed participation in this audit compulsory for Society members. The Web-based application was developed and tested during 2009. Data for all open vascular surgery and for all endovascular procedures are collected at two points in the admission episode: at the time of operation and at discharge, and entered into the application. Data are analyzed to produce risk-adjusted outcomes. An algorithm has been developed to deal with outliers according to natural justice and to comply with the requirements of regulatory bodies. The Audit is protected by legislated privilege and is officially endorsed and indemnified by the Royal Australasian College of Surgeons. Confidentiality of surgeons and patients alike is ensured by a legally protected coding system and computer encryption system. Validation is by a verification process of 5% of members per year who are randomly selected. The application is completely funded by the Society. Results Data entry commenced on January 1, 2010. Over 40,000 vascular procedures were entered in the first year. The Audit application allows instantaneous on-line access to individual data and to deidentified group data and specific reports. It also allows real-time instantaneous production of log books for vascular trainees. The Audit has already gained recognition in the Australasian public arena during its first year of operation as an important benchmark of correct professional surgical behavior. Compliance has been extremely high in public hospitals but less so in private hospitals such that only 60% of members received a certificate of complete participation at the end of its first year of operation. Conclusion An Internet-based compulsory audit of complete surgical practice is possible to create and be maintained by a society of surgeons with a membership of just over 200. The 60% compliance rate for complete data entry has created an immediate constitutional challenge for the Society. Future challenges are to improve total participation to an acceptable level and to ensure accurate data entry via a robust validation system.

Background Experimental studies suggest that angiotensin II plays a central role in the pathogenesis of abdominal aortic aneurysm. This trial aims to evaluate the efficacy of the angiotensin receptor blocker telmisartan in limiting the progression of abdominal aortic aneurysm. Methods/Design Telmisartan in the management of abdominal aortic aneurysm (TEDY) is a multicentre, parallel-design, randomised, double-blind, placebo-controlled trial with an intention-to-treat analysis. We aim to randomly assign 300 participants with small abdominal aortic aneurysm to either 40 mg of telmisartan or identical placebo and follow patients over 2 years. The primary endpoint will be abdominal aortic aneurysm growth as measured by 1) maximum infra-renal aortic volume on computed tomographic angiography, 2) maximum orthogonal diameter on computed tomographic angiography, and 3) maximum diameter on ultrasound. Secondary endpoints include change in resting brachial blood pressure, abdominal aortic aneurysm biomarker profile and health-related quality of life. TEDY is an international collaboration conducted from major vascular centres in Australia, the United States and the Netherlands. Discussion Currently, no medication has been convincingly demonstrated to limit abdominal aortic aneurysm progression. TEDY will examine the potential of a promising treatment strategy for patients with small abdominal aortic aneurysms. Trial registration Australian and Leiden study centres: Australian New Zealand Clinical Trials RegistryACTRN12611000931976, registered on 30 August 2011; Stanford study centre: clinicaltrials.govNCT01683084, registered on 5 September 2012.

OBJECTIVE: To determine if overnight hospital stay after carotid endarterectomy (CEA) is feasible and safe in the Australian setting. DESIGN: Case series with follow-up of 4-11 months (mean, 7 months). PATIENTS AND SETTING: All patients undergoing primary CEA performed by a vascular surgeon (BMB) between 30 May and 11 November 1996. Surgery was performed in one of four hospitals (a district general public hospital with about 400 beds and three private hospitals) in the Gosford area of New South Wales. INTERVENTIONS: CEA using regional anaesthesia and sedation, after diagnosis by duplex ultrasound scan, avoiding cerebral angiography and intensive care; planned discharge after overnight hospital stay; review at one month and duplex ultrasound scan at four months. OUTCOME MEASURES: Length of hospital stay and complications. RESULTS: 65 patients were admitted for CEA during the study period and 59 were scheduled for overnight stay (one had "re-do" surgery, two remained longer for reasons unrelated to carotid artery disease, and three had been scheduled before the change to overnight stay). 54 (92%) were discharged on the first postoperative day, and only three required readmission within 30 days (for urinary retention, angina and reperfusion syndrome). There were no deaths, no myocardial infarctions and no recognised instances of cerebral ischaemia during follow-up. CONCLUSION: CEA can be performed safely without cerebral angiography or intensive care, with over 90% expectation of a single night's stay in hospital.

Background: Abdominal aortic aneurysms (AAAs) are a leading cause of mortality worldwide but have no recognised medical therapy. Pre-clinical studies indicate that osteopontin plays an important role in the pathogenesis of AAA via a number of mechanisms. This trial aims to assess the potential of fenofibrate to favourably alter biomarkers associated with AAA pathology. Methods: Fenofibrate in the management of AbdoMinal aortic anEurysm (FAME)-2 is a multi-centre, prospective, randomised, double-blind, placebo-controlled clinical trial to assess the effect of 24 weeks of oral therapy with 145 mg of fenofibrate on key pathological markers of AAA. A total of 140 participants with an AAA measuring between 35-49 mm will be randomly assigned to either 145 mg of fenofibrate once per day or identical placebo for a period of 24 weeks. Primary outcome measures will be serum concentrations of osteopontin and kallistatin. Secondary outcome measures will include serum levels of resistin, lipids, matrix metalloproteinases and pro-inflammatory cytokines, circulating concentrations of AAA biomarkers, and AAA diameter as assessed by ultrasound.Conclusions: This study represents the next step in the assessment of a potential novel medical therapy for AAA.

Purpose The purpose of this study was the report of the results of a consecutive series of carotid endarterectomy (CEA), performed by one surgeon and independently assessed by a neurologist, in which the achievability of selective early control of the distal internal carotid artery (ICA) was prospectively recorded. Methods All patients who underwent CEA by the surgical author between November 17, 1999, and November 15, 2001, were entered into a prospective study during which early selective exposure and clamping of the distal ICA were attempted (with initial avoidance of carotid bifurcation exposure and retraction), which allowed the remainder of the procedure (in patients without shunting) to be performed with ICA clamp protection and anticoagulation therapy. All the procedures were performed with local cervical block anesthesia, all the patients underwent a vein patch procedure, and, with one exception, cerebral angiography was not used. Major morbidity (stroke and myocardial infarction), mortality, and consecutiveness were independently verified by a neurologist. Results 148 consecutive CEAs were performed. In 142 cases (96%), the soft distal ICA could be initially isolated and controlled without dissection of the plaque-bearing bulb bifurcation area (group A), and in the remaining six cases, the carotid bifurcation had to be exposed and retracted to allow ICA clamping (group B). A shunt was needed in 15 cases (14 in group A, one in group B), which left 128 cases (86%) in which the procedure could be performed with the ICA clamped and the brain theoretically protected from particulate plaque embolism. There were no strokes or deaths, one patient had temporary vertebrobasilar ischemia, one patient had a myocardial infarct, one patient had a temporary accessory nerve palsy, one patient returned to the operating room for release of a cervical hematoma, and 94% spent one postoperative night in the hospital. Conclusion Early selective distal ICA control is highly achievable during CEA without apparently compromising clinical results. Its use is relevant when selective methods of shunting that do not need initial control of the common and external carotid arteries (eg, local cervical block anesthesia, electroencephalography/other monitoring) are used. Further evaluation with transcranial Doppler scan monitoring is suggested to substantiate the theoretic potential of this method in the reduction or elimination of particulate plaque embolism.

WHAT THIS PAPER ADDS This study examines the outcomes following off-licence use of rFVIIa to control critical bleeding in patients during abdominal aortic aneurysm (AAA) repair. Patients who stopped/attenuated bleeding after rFVIIa use had a lower mortality than those with continuous bleeding. However, predictive mortality models did not show improved survival after rFVIIa administration. Further studies are needed to more thoroughly explore the precise role of rFVIIa in these patients with high risk of mortality as clinicians are likely to continue using rFVIIa when conventional methods have failed and patient is at risk of exsanguination. Objective: To evaluate the outcomes following recombinant activated Factor VII (rFVIIa) use during abdominal aortic aneurysms (AAA) repair. Design: AAA patients were selected from the Australian and New Zealand Haemostasis Registry (ANZHR) who received off-licence rFVIIa to control critical bleeding. Methods: Patient characteristics and outcomes were compared between responders (bleeding stopped/ attenuated) and non-responders (bleeding continued) to rFVIIa, stratified by aneurysm status (ruptured (r-AAA) vs. non-ruptured (nr-AAA)). Patients were also scored using POSSUM (Physiological and Operative Severity Score for the enUmeration of Mortality and morbidity) and Hardman Index mortality predictive models. Results: In total, 77 AAA patients were included in the analysis. Approximately 73% (n ¼ 56) of them had ruptured aneurysms and about 50% (n ¼ 35/70 with known data) responded positively to rFVIIa. Eleven incidents of thromboembolic adverse events were reported in 9 patients (6 r-AAA and 3 nr-AAA). Responders in both ruptured and non-ruptured groups had significantly lower 28-day mortality than non-responders (r-AAA: 40% (10/25) vs. 92% (24/26); P < 0.001; nr-AAA: 30% (3/10) vs. 67% (6/9); P < 0.01). Mortality predictive models did not show any difference between overall observed and expected mortality in ANZHR patients. Conclusion: Patients who responded to rFVIIa had a lower mortality than those who did not respond to the treatment.