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Mortality remains high after emergency open surgery for a ruptured abdominal aortic aneurysm (RAAA). The aim of the present study was to assess, if intravenous (IV) Interferon (IFN) beta-1a improve survival after surgery by up-regulating Cluster of differentiation (CD73). This is a multi-center phase II double-blind, 2:1 randomized, parallel group comparison of the efficacy and safety of IV IFN beta-1a vs. placebo for the prevention of death after open surgery for an infra-renal RAAA. All study patients presented a confirmed infra-renal RAAA, survived the primary emergency surgery and were treated with IFN beta-1a (10 μg) or matching placebo for 6 days after surgery. Major exclusion criteria included fatal hemorrhagic shock, chronic renal replacement therapy, diagnosed liver cirrhosis, severe congestive heart failure, advanced malignant disease, primary attempt of endovascular aortic repair (EVAR), and per-operative suprarenal clamping over 30 min. Main outcome measure was all-cause mortality at day 30 (D30) from initial emergency aortic reconstruction. The study was pre-maturely stopped due to a reported drug-drug interaction and was left under-powered. Out of 40 randomized patients 38 were included in the outcome analyses (27 IFN beta-1a and 11 placebo). There was no statistically significant difference between treatment groups at baseline except more open-abdomen and intestinal ischemia was present in the IFN beta-1a arm. D30 all-cause mortality was 22.2% (6/27) in the IFN beta-1a arm and 18.2% (2/11) in the placebo arm (OR 1.30; 95% CI 0.21–8.19). The most common adverse event relating to the IFN beta-1a was pyrexia (20.7% in the IFN beta-1a arm vs. 9.1% in the placebo arm). Patients with high level of serum CD73 associated with survival (P = 0.001) whereas the use of glucocorticoids and the presence of IFN beta-1a neutralizing antibodies associated with a poor CD73 response and survival. The initial aim of the trial, if postoperative INF beta-1a treatment results on better RAAA survival, could not be demonstrated. Nonetheless the anticipated target mechanism up-regulation of CD73 was associated with 100% survival. According to present results the INF beta-1a induced up-regulation of serum CD73 was blocked with both use of glucocorticoids and serum IFN beta-1a neutralizing antibodies. The study was pre-maturely stopped due to interim analysis after a study concerning the use if IV IFN beta-1a in ARDS suggested that the concomitant use of glucocorticoids and IFN beta-1a block the CD73 induction. Trial registration: ClinicalTrials.gov NCT03119701. Registered 19/04/2017 (retrospectively registered).

Alajäseme arterite haigus on tänapäeval suureneva levimusega ning eelkõige aterosklerootilise etiopatogeneesiga haigus. Sümptomaatilistel juhtudel põhjustab haigus klaudikatsiooni- või rahuolekuvalusid, arteriaalseid haavandeid ja gangreeni. Samuti kaasneb haigusega suur haigestumus ja suremus teistesse südame-veresoonkonnahaigustesse (müokardiinfarkt, insult). Haiguse ennetuses ja ravis on olulisel kohal riskitegurite vähendamine, eluviisi muudatused ja medikamentoosne ravi, raskematel juhtudel ka endovaskulaarne ja/või kirurgiline ravi. Artikli eesmärk on anda ülevaade alajäseme arterite haigusega seotud mõistetest, haiguse epidemioloogiast ja riskiteguritest, kliinilisest pildist ning diagnostika ja ravi põhimõtetest., Eesti Arst, 2021: Jaanuar

Additional file 1: Table S1. Baseline values of acylcarnitines. Table S2. Non-substantial correlations between cardiac biomarkers (i.e. high sensitivity troponin T and NT-proBNP) and acylcarnitines.

Janno Jürgenson,1,2Martin Serg,3,4Priit Kampus,3,4Jaak Kals,4–6 Piibe Muda,7 Maksim Zagura,3,4Mehis Viru,1 Mihkel Zilmer,4,6Jaan Eha,3–4,7 Eve Unt2–3,8–91Institute of Sport Sciences and Physiotherapy, Medical Faculty, University of Tartu, Tartu, Estonia; 2Estonian Centre of Behavioural and Health Sciences, University of Tartu, Tartu, Estonia; 3Department of Cardiology, Institute of Clinical Medicine, Medical Faculty, University of Tartu, Tartu, Estonia; 4Endothelial Centre, University of Tartu, Tartu, Estonia; 5Department of Surgery, Institute of Clinical Medicine, Medical Faculty, University of Tartu, Tartu, Estonia; 6Department of Biochemistry, Institute of Biomedicine and Translational Medicine, Centre of Excellence for Genomics and Translational Medicine, Medical Faculty, University of Tartu, Tartu, Estonia; 7Heart Clinic, Tartu University Hospital, Tartu, Estonia; 8Department of Sports Medicine and Rehabilitation, Institute of Clinical Medicine, Medical Faculty, University of Tartu, Tartu, Estonia; 9Sports Medicine and Rehabilitation Clinic, Tartu University Hospital, Tartu, EstoniaAim: The purpose of this study was to evaluate the effect of a pre-seasonal 12-week supervised strength training program (SSTP) on arterial stiffness, brachial and central blood pressure, and systolic and diastolic function of the heart in elite powerlifting athletes.Methods: A descriptive study was performed in 19 elite male powerlifters, who exercised for 12 weeks, four days per week with an intensity of 60–90% assessed from 1 repetition maximum and 90–120 min per session. Carotid-femoral pulse wave velocity (cfPWV), augmentation index and central blood pressure were measured by applanation tonometry using the SphygmoCor device, and an echocardiographic examination was performed at baseline and after 12-week SSTP.Results: Subjects’ mean brachial and central systolic blood pressure decreased significantly after the training period (132.3±8.8 vs 124.3±8.7 mmHg, p=0.002 and 110.1±7.7 vs 104.5±8.7 mmHg, p=0.008, respectively). Strength training significantly improved systolic tricuspid annular velocity and mitral E/e’ ratio (p