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. The aim of this systematic review and meta-analysis was to investigate short-, medium-and long-term outcomes, including morbidity, reintervention and mortality, associated with EVAR and open aneurysm repair. MethodsStandard reporting guidelines set by the Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) Group 7 were followed to identify RCTs and other high-level evidence reporting comparative outcomes of endovascular and open repair of AAA. Study titles and abstracts were searched using MEDLINE, Embase, and Health and Psychosocial Instruments databases, using Ovid Online (version: OvidSP_UI03.04.02.112) in July 2012, with the most recent search carried out on 31 December 2012, separately by two researchers. No language restrictions or filters used to restrict study designs were applied. Reference lists were searched for further studies to be included. Eligibility criteria and study selectionA comprehensive literature search was performed using the search terms 'endovascular AND open AND repair AND abdominal AND aortic AND aneurysm' AND 'randomised OR randomized' AND 'trial' NOT 'thoracic'. Two reviewers individually reviewed potential studies according to a set of eligibility criteria, with discussion of discrepancies. Inclusion criteria were that t...

Conclusions: Outcomes for repair of ruptured abdominal aortic aneurysms (rAAA) might be improved by wider use of local anesthesia for EVAR and by recognizing that a minimum blood pressure of 70 mmHg may be too low a threshold for permissive hypotension. Summary: Most data on outcomes of patients with rAAAs are singlecenter studies and as such may be too small to identify clinical factors that could improve overall patient outcomes. The IMPROVE study is a pragmatic multicenter randomized clinical trial in which eligible patients with a clinical diagnosis of rAAA were allocated to a strategy of endovascular repair of RAAAA (EVAR) or to open repair. IMPROVE showed no difference in 30-day mortality with a strategy incorporating EVAR for repair of a rAAAA compared to a strategy of open repair for ruptured abdominal aortic aneurysm (IMPROVE trial investigators, Brit Med J 2014;348:f7661). In this paper the IMPROVE investigators sought to analyze influences of time and manner of hospital presentation, fluid volume status, type of anesthesia, type of endovascular repair and time to aneurysm repair on 30-day mortality for rAAA. This was a prespecified plan of analyses to include only the patients who underwent aneurysm repair for a proven diagnosis of rAAA. Adjustments were made for potential confounding factors. In IMPROVE, 568 of 613 randomized patients had a symptomatic or rAAA and diagnostic accuracy was 91%. Patients randomized outside routine working hours had higher operative mortality (adjusted odds ratio, 1.47, 95% CI, 1.00-2.17). There was no difference in mortality rates between those patients admitted directly to a trial center versus those transferred to a trail center from a referring institution. Lowest systolic blood pressure was strongly and independently associated with 30-day mortality (51% among those with systolic blood pressures below 70 mmHg). In addition, patients who received EVAR under local anesthesia alone had reduced 30-day mortality compared to those who had EVAR under general anesthesia (adjusted odds ratio, 0.27; 95% CI, 0.10-0.70). In patients with confirmed rupture the time from randomization to the operating suite was not associated with 30-day mortality (P ¼ .415). Comment: The data indicate that blood pressure of 70 mmHg may be too low for optimal results in a patient with rAAA and permissive hypotensive levels should be above this. In addition, when EVAR is used to treat a rAAAA it may be best to do it, if possible, under local anesthesia. Finally, given the fact that results for repair of rAAA are no worse for a patient who is transferred than for those with a primary presentation to a specialist center, along with the fact that patients undergoing off-hours repair do more poorly suggests that a skilled multidisciplinary vascular team including specialists anesthesia services is likely to provide the best results for repair of a rAAA in any individual region. Outcomes for patients with rAAA therefore may be best served by a policy of regionalization of care for such patients to speci...

Conclusion:To potentially assess response to antiatherosclerotic therapy, measurement of total plaque volume is superior to both measurement of intima-media thickness (IMT) and total plaque area (TPA).Summary: Progression of IMT, TPA, and total plaque volume (TPV) have all been advocated as methods for risk prediction of cardiovascular events. In this study, the authors report a comparison of progression/ regression of carotid IMT, TPA, and TPV in patients attending vascular prevention clinics. The goal of the study was to determine which variable could be best used to assess response to antiatherosclerotic therapy. IMT, TPA, and TPV were measured at baseline in 349 patients attending vascular prevention clinics. To qualify for enrollment, a TPA of 40 to 600 mm 2 was required. Follow-up was for #5 years (median, 3.17 years). End points were vascular death, myocardial infarction, stroke, and transient ischemic attacks. Follow-up measurements at 1 year were available in 323 patients for IMT and TPA, and in 306 for TPV. Progression of TPV predicted stroke, death, or transient ischemic attack (TIA) (Kaplan-Meier log-rank P ¼ .001), stroke/death/myocardial infarction (MI) (P ¼ .008), and stroke/death/ TIA/MI (any cardiovascular event) (P ¼ .001). Progression of TPA weakly predicted stroke/death/TIA (P ¼ .097) but not stroke/death/MI (P ¼ .59) or any cardiovascular event (P ¼ .143). IMT also did not predict stroke/death/MI (P ¼ .13) or any cardiovascular event (P ¼ .455). With adjustment for coronary risk factors, TPV progression remained a significant predictor (P ¼ .001), but a change in TPA did not. Regression of IMT predicted events (P ¼ .004).Comment: The data suggest that TPV at the carotid bifurcation should be considered as the variable of choice to measure response to antiatherosclerotic therapy. Interestingly in this study, regression of IMT rather than progression predicted events. This may be consistent with the growing thought that IMT is more representative of hypertensive medial hypertrophy and is not truly representative of atherosclerosis (Finn AV et al, Arterioscler Thromb Vasc Biol 2010;30:177-81).

Background— Contemporary data from Western populations suggest steep declines in abdominal aortic aneurysm (AAA) mortality; however, international trends are unclear. This study aimed to investigate global AAA mortality trends and to analyze any association with common cardiovascular risk factors. Methods and Results— AAA mortality (1994–2010) using International Classification of Diseases codes were extracted from the World Health Organization mortality database and age standardized. The World Health Organization InfoBase and International Mortality and Smoking Statistics provided risk factor data. Nineteen World Health Organization member states were included (Europe, 14; Australasia, 2; North America, 2; Asia, 1). Regression analysis of temporal trends in cardiovascular risk factors (1946–2010) was done independently for correlations to AAA mortality trends. Global AAA mortality trends show substantial heterogeneity, with the United States and United Kingdom recording the greatest national decline, whereas internationally, male individuals and those <75 years of age demonstrated the greatest reductions. AAA mortality has increased in Hungary, Romania, Austria, and Denmark; therefore, the mortality decline is not universal. A positive linear relationship exists between global trends in systolic blood pressure ( P ≤0.03), cholesterol ( P ≤0.03), and smoking prevalence ( P ≤0.02) in males and females. Body mass index demonstrated a negative linear association with AAA mortality ( P ≤0.007), whereas fasting blood glucose showed no association. Conclusions— AAA mortality has not declined globally, and this study reveals that differences between nations can be explained by variations in traditional cardiovascular risk factors. Declines in smoking prevalence correlate most closely with declines in AAA mortality, and a novel obesity paradox has been identified that requires further investigation. Public health measures could therefore further reduce global AAA mortality, with greatest benefits in the younger age group.

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.