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Objective:

The clinical efficacy of remote ischaemic preconditioning (RIPC) remains unclear. This pilot study, a substudy of a randomised controlled trial, tested whether repeated RIPC reduces arterial stiffness, end organ damage, and oxidative stress in patients with intermittent claudication (IC).

Methods:

In a single centre, randomised, sham controlled, double blind trial, 42 males with Fontaine stage IIa or IIb IC were allocated at a ratio of 1:1 to receive RIPC or sham using an automated device for 28 days in an outpatient setting (ClinicalTrials.gov ID NCT05084066). Secondary outcomes included changes in augmentation index (AIx), heart rate corrected AIx, carotid-femoral pulse wave velocity (cf-PWV), and biomarkers for cardiac (high sensitivity troponin T [hs-TnT], N-terminal pro B-type natriuretic peptide [NT-proBNP]), renal (creatinine, urea, cystatin C, b2 microglobulin, neutrophil gelatinase associated lipocalin, kidney injury molecule 1), and oxidative stress (high sensitivity C reactive protein, interleukin-6, interleukin-18, myeloperoxidase, adiponectin, oxidised low density lipoprotein).

Results:

Data from 41 patients (RIPC n = 23, sham n = 18) aged 64.9 +/- 7.4 years were analysed. The median change in cf-PWV was 0.2 m/s (interquartile range [IQR]-0.6, 0.6) in the RIPC group vs. 0.2 m/s (IQR-0.3, 0.8) in the sham group (p = .54). The median change in hs-TnT was 0 ng/L (IQR-1, 2) in the RIPC group vs. 1 ng/L (IQR-1, 2) in the sham group (p = .54). NT-proBNP showed a median change of-7 ng/L (IQR-32, 18) in the RIPC group vs. 6 ng/L (IQR-14, 35) in the sham group (p = .14). No statistically significant differences were observed between groups for arterial stiffness, oxidative stress, or renal biomarkers.

Conclusion:

Repeated RIPC did not significantly alter arterial stiffness, end organ damage, or oxidative stress biomarkers compared with sham treatment. It is possible that patients with IC already experience repeated RIPC from their ischaemic legs, thereby attenuating any additional effects from arm induced RIPC.

Importance Plasma levels of the gut microbiota-dependent metabolite trimethylamine N-oxide (TMAO) are associated with prevalent abdominal aortic aneurysms (AAA) in humans and fostering of AAA progression in animal models; therapeutic targeting of TMAO production blocks AAA progression and rupture in multiple mouse models. A blood biomarker that identifies individuals at risk for incident AAA development, accelerated AAA expansion, or recommendation for surgical AAA repair could be an asset for risk stratification. Objective To determine whether TMAO is associated with risk for AAA development, rapid AAA expansion, and risk for recommended surgical intervention. Design, Setting, and Participants This was a prospective cohort study using 2 independent clinical cohorts undergoing aorta imaging surveillance: a European cohort and a US cohort. Included in this study were patients undergoing serial imaging surveillance of the aorta and long-term outcome monitoring. Patients were recruited from single-center studies in Uppsala, Sweden, and Cleveland, Ohio. Study data were analyzed from October 2023 to May 2025. Exposures Plasma TMAO concentrations measured by stable isotope dilution liquid chromatography with tandem mass spectrometry. Main Outcomes and Measures The association of TMAO levels with AAA risk, fast-growing AAA (>= 4.0 mm per year), and recommended surgical intervention (>= 4.0 mm per year or >= 5.5 cm diameter). Results The European cohort included 237 individuals (median [IQR] age, 65 [65-73] years; 211 male [89.0%]), and the US cohort included 658 individuals (median [IQR] age, 63 [57-70] years; 523 male [79.5%]). In the European cohort, elevated circulating TMAO was significantly associated with AAA risk independent of traditional risk factors and kidney function. Moreover, elevated TMAO predicted both greater risk for fast-growing AAA (adjusted odds ratio [aOR], 2.75; 95% CI, 1.20-6.79) and recommended surgical intervention (aOR, 2.67; 95% CI, 1.24-6.09). Similar patterns were observed in the US cohort and the combined European and US cohort, with heightened circulating TMAO corresponding with significantly increased adjusted risk for fast-growing AAA (US cohort: aOR, 2.71; 95% CI, 1.53-4.80; combined cohort: aOR, 2.30; 95% CI, 1.47-3.62) and recommended surgical intervention (US cohort: aOR, 2.73; 95% CI, 1.56-4.80; combined cohort: aOR, 2.41; 95% CI, 1.55-3.74). Addition of TMAO to base models containing traditional cardiovascular risk factors resulted in significant improvement in both risk estimation for fast-growing AAA and predicting recommended surgical intervention. Conclusion and Relevance Results of this cohort study suggest that elevated circulating TMAO levels were associated with increased risk of AAA and identified patients at heightened risk for fast-growing AAA and recommended surgical intervention. TMAO may help identify individuals who may benefit from more frequent surveillance imaging and early surgical intervention to prevent aortic dissection or rupture.

BackgroundThe optimal strategy for initial treatment of acute occlusion of superior mesenteric artery (SMA) is debated. The aim of the study was to compare the effectiveness, timelines and outcomes of endovascular versus open surgical treatment in patients with acute SMA occlusion. This was a preplanned substudy of the prospective observational multicenter AMESI (Acute MESenteric Ischaemia) study.MethodsPatients with SMA occlusion were divided into surgical and endovascular treatment groups. The surgical group included patients initially subjected to open surgical treatment with surgical or hybrid revascularization or intestinal resection only. The endovascular group included patients initially revascularized endovascularly and was further divided according to treatment effectiveness. Patients were also categorized according to revascularization or no revascularization, and subanalysis performed for different revascularization methods. Baseline and outcome comparisons were made using Fisher and Mann-Whitney U tests. Risk-factors for in-hospital mortality were analysed using a logistic regression model.ResultsOf 158 patients 107 had surgical and 51 endovascular treatment. The surgical group had higher baseline illness severity scores, higher C-reactive protein and lactate values. The mortality in the endovascular effective, endovascular insufficient as monotherapy and surgical groups was 2.9%, 41.2% and 45.8%, respectively. In multivariable analysis surgery was not an independent risk factor for in-hospital mortality. The rate of arterial embolism was higher in the endovascular revascularization as monotherapy insufficient treatment group (10/17) compared to the endovascular revascularization as monotherapy effective (5/34) and surgical (27/107) groups. We could not identify useful best thresholds for discriminating between effective and insufficient endovascular treatment. Analysis comparing the effect of any revascularization versus no revascularization on in-hospital mortality did not show a clear benefit of revascularization and the method of revascularization did not independently influence mortality.ConclusionThe beneficial effect of endovascular compared to surgical treatment in unadjusted analyses is largely explained by selection of patients. None of the compared management approaches had an independent effect on mortality. The choice between endovascular and surgical treatment should not be based solely on the time elapsed from symptom onset but rather on the patient's general condition and possibly on the cause of SMA occlusion.

Objective: Manuscripts submitted to the European Journal of Vascular and Endovascular Surgery (EJVES) often contain shortcomings in baseline scientific principles and incorrectly applied methodology. Consequently, the editorial team is forced to offer post hoc repair in an attempt to support the authors to improve their manuscripts. This repair could theoretically have been prevented by providing more clear definitions and reporting standards to serve researchers when planning studies and eventually writing their manuscripts. Therefore, the general principles for EJVES publication standards are summarised here.

Methods: These publication standards did not follow a systematic approach but reflect the common opinion of the current Senior and Section Editors team. This team decided to only include recommendations regarding the most common pathologies in vascular surgery in this first edition of publication standards, namely carotid artery disease, abdominal aortic aneurysm (AAA), peripheral arterial occlusive disease (PAOD), and chronic venous disease. In future editions, the plan is to expand the areas of research.

Results: Presented are (1) a common set of minimum but required publication standards applicable to every interventions such as 30 day death and morbidity, and measures for completeness of data including outcome information, and (2) a common set of minimum publication standards for four vascular areas.

Conclusion: The editors of the EJVES propose universally accepted definitions and publication standards for carotid artery disease, AAA, PAOD, and chronic venous disease. This will enable the development of a convincing body of evidence to aid future clinical practice guidelines and drive clinical practice in the right direction. These first ever publication and reporting standards for EJVES aim to improve future research published in the journal.

Objective: The European Society for Vascular Surgery (ESVS) has developed clinical practice guidelines for the care of patients with diseases of the mesenteric and renal arteries and veins, in succession to the first 2017 guidelines, with the aim of assisting physicians and patients in selecting the best management strategy.

Methods: These guidelines are based on scientific evidence and expert opinion. By summarising and evaluating the best available evidence, recommendations for the diagnosis and treatment of patients have been formulated. The recommendations are graded according to the new ESVS clinical practice guidelines class of recommendation grading system, where the strength (class) of each recommendation is graded from Ito III, and the letter A to C marks the level of evidence.

Results: A total of 102 recommendations have been issued on the management of chronic arterial mesenteric ischaemia, median arcuate ligament syndrome, acute arterial mesenteric ischaemia, non-occlusive mesenteric ischaemia, venous mesenteric thrombosis and ischaemia, occlusive disease of the renal arteries and veins, visceral artery aneurysms, and spontaneous isolated dissection of the visceral arteries.

Conclusion: These 2025 ESVS clinical practice guidelines provide comprehensive and up to date advice to physicians and patients on the management of diseases of the mesenteric and renal arteries and veins. 

An association of coffee consumption with a risk of abdominal aortic aneurysm (AAA) is unknown. We hypothesized that coffee consumption influences aortic diameter and AAA risk, with smoking status as a modifier. The study included 42,723 Swedish men and 34,921 women (age 45-83 years) with infrarenal aortic diameter (IAD) measured in 8,109 men. Over 18.7 years, 1863 AAA cases (1585 non-ruptured, 278 ruptured) were identified. Among participants with coffee consumption ≤ 5 cups/day, current smokers versus never smokers had a 3-fold higher risk of non-ruptured and ruptured AAA (HR = 3.12, 95%CI = 2.62-3.71 and HR = 2.90, 95%CI = 1.95-4.31, respectively); the risk increased with coffee consumption > 5 cups/day and was a 4-fold higher (HR = 3.89, 95%CI = 3.12-4.85) for non-ruptured and a 4.6-fold higher (HR = 4.61, 95%CI = 2.72-7.86) for ruptured AAA (P-value- multiplicative-interaction = 0.009). 160 (2.0%) screened men had an IAD ≥ 30 mm. In men drinking daily ≤ 3 cups of coffee, current smokers versus never smokers had a 4-fold (OR = 4.09, 95%CI = 1.81-9.22) higher risk of IAD ≥ 30 mm; in men with higher coffee consumption (> 3 cups/day), the risk increased 6.6-fold (OR = 6.58, 95%CI = 2.98-14.6). In ex-smokers, the corresponding ORs were 1.67 (95%CI = 0.62-4.49) and 3.27 (95%CI = 1.27-8.40), respectively. In conclusion, high coffee consumption may increase risk of AAA and infrarenal aortic diameter in smokers.