Background:Adequate glucose control is an important, yet a challenging task, in the early postoperative care after liver transplantation (LTx). Potential of continuous glucose monitoring (CGM) in this context had not been fully explored because of concerns about sensors' precision in critical care. Objectives:We initiated a trial to assess feasibility, accuracy, and benefit of CGM used in addition to standard blood glucose (BG) management. Design:Prospective randomized trial. Methods:Patients undergoing LTx were included and randomized to wearing (1) unblinded ("active") CGM which could help guiding insulin therapy, (2) blinded CGM serving as controls. Dexcom G6 was applied immediately after surgery, arterial BG values measured with blood gas analyzer served as reference and for calibration. We evaluated mean absolute relative difference (MARD), Diabetes Technology Society (DTS) Error Grid zones, bias, 15/15 agreement rate, evolvement of accuracy over time, and possible interfering factors. Fisher test, Mann-Whitney test, DTS software, and linear mixed model were used for statistical analysis. Results:We included 155 LTx recipients, 13 were excluded (1 died during surgery, 12 experienced sensor failure-6 from each group), data from 142 patients (80 in active and 62 in blinded CGM group) were analyzed. Overall, MARD was 9.1% in active and 10.7% in the blinded group (p < 0.0001). DTS error grid in active group had shown 90% in zone A versus 85.3% in the blinded group. These results were consistent for reference glucose ranges 3.9-10 mmol/L and above 10 mmol/L, with less precision in the low ranges (these values were however rare). Sensor accuracy peaked on days 2-3 and deteriorated over time with significant worsening from day 7 on in both groups. Conclusion:Our study demonstrates feasibility and acceptable accuracy of CGM comparable to reports from the outpatient care. We believe this could be attributed to sensor calibration, reflected by more favorable outcomes in the active CGM group. In addition, we demonstrate decline in accuracy over time, suggesting their use in critical care could be limited to less days to secure sufficient reliability. Trial registration:This study is part of an ongoing prospective trial registered on ClinicalTrials.gov (NCT05585801) and was registered on October 12, 2022.

IntroductionChronic inflammation is increasingly recognized as a key contributor to the development and progression of heart failure (HF), with epicardial adipose tissue (EAT) emerging as an important local immunomodulatory organ. This study examined lymphocyte populations in EAT and subcutaneous adipose tissue (SAT) across different stages of HF and compared them with individuals without HF to clarify their potential role in HF progression.MethodsLymphocyte subsets in EAT, SAT, and peripheral blood were analyzed by flow cytometry in subjects with HF stage D, HF stage C, and subjects without HF. Circulating hormones and inflammatory proteins were quantified using ELISA and Luminex assays.ResultsSubjects with HF stage D exhibited a reduction in T helper (Th), cytotoxic T (Tc), natural killer T (NKT), and B cells in EAT compared with both HF stage C subjects and subjects without HF, alongside changes observed in the circulation. In contrast, HF stage C was characterized by a significantly increased presence of Th2 and Th17 lymphocytes in EAT, indicating active immune remodeling during intermediate stages of HF. This stage was also associated with elevated circulating levels of Intracellular Adhesion Molecule-1, suggesting enhanced lymphocyte trafficking into adipose tissue. Across all study groups, EAT consistently contained a higher proportion of pro-inflammatory lymphocytes compared with SAT.ConclusionTogether, these findings demonstrate that HF progression is accompanied by dynamic and stage-dependent changes in lymphocyte composition within adipose tissue, supporting the concept that a progressively pro-inflammatory EAT microenvironment may contribute to myocardial inflammation dysfunction-associated HF progression.

Introduction and Objective: Bariatric surgery is the most effective treatment for obesity, with novel endoscopic procedures also showing promising outcomes; however, direct randomized comparisons are limited. The SLAVIA randomized trial compares sleeve gastrectomy, endoscopic gastroplasty, and conservative therapy. This preliminary analysis reports outcomes in patients who have already finalized the 6-months trial period. Methods: Adults with BMI ≥35 kg/m² without contraindications were randomized 1:1:1 to laparoscopic sleeve gastrectomy (B), endoscopic gastroplasty (E; OverStitch or Endomina systems), or conservative weight-loss management (C). The primary endpoint was absolute weight change (kg) at 6 months. Secondary endpoints included change in total weight, BMI, percent body fat, and skeletal muscle mass measured by bioimpedance analysis. Results: Currently, follow-up was completed by 13 participants in C (age 44.8±7.2 years; body weight 126.2±22.3 kg; BMI 41.3±5.1 kg/m2), 7 in E (46.7±9.4 years; 126.6±24.1 kg; 42.5±5.6 kg/m2), and 9 in B (44.2±8.3 years; 124.5±23.1 kg; 41.6±5.1 kg/m2). Absolute weight change was −0.9±5.2 kg (C) vs −14.0±6.9 kg (E) vs −33.5±12.8 kg (B) (p<0.001 across groups). Percent weight change was 0.8±4.1% vs 11.1±5.4% vs 26.5±6.1% (p<0.001 across groups). BMI decreased after E (42.5±5.6 to 37.6±4.1 kg/m²; p=0.004) and B (41.6±5.1 to 30.3±3.5 kg/m²; p<0.001) as did body fat percentage (E: 46.0±8.9% to 43.4±7.9%; p=0.014 and B:44.6±9.1% to 32.6±11.0%; p<0.001) along with skeletal muscle mass (E: 38.7±11.0 to 35.8±10.5 kg; p=0.005 and B: 40.5±11.5 to 34.2±9.9 kg; p<0.001). No significant changes were observed in C. Conclusion: In this pilot SLAVIA cohort with class II or III obesity, both endoscopic gastroplasty and sleeve gastrectomy produced significant 6-month weight loss, with a more pronounced effect after surgery. Both procedures reduced fat mass, but were also associated with loss of skeletal muscle mass. Disclosure M. Haluzik: Advisory Panel; Current; Abbott Diabetes. Speaker's Bureau; Current; AbbVie Inc., Boehringer Ingelheim International GmbH, Berlin-Chemie AG, GlaxoSmithKline plc., Lilly. Advisory Panel; Current; Novo Nordisk. Speaker's Bureau; Current; Sanofi. Advisory Panel; Current; AstraZeneca. Research Support; Ended; Sanofi. L. Horvath: None. A. Nemcova: None. M. Mraz: None. P. Novodvorsky: None. J. Brezina: None. J. Kral: None. E. Machytka: None. J. Spicak: None. S. Frankova: None. E. Koblihova: None. J. Klouckova: None. I. Lankova: None. B. Akçora Veselá: None. I. Jakubikova: None. M. Kasalicky: None. T. Hucl: None. Funding Supported by MH CZ - DRO ("Institute for Clinical and Experimental Medicine – IKEM, IN 00023001")

BACKGROUND:This study aimed to explore the association of long-term left ventricular assist device (LVAD) support with changes in inflammation and cardiac remodelling in subjects with advanced heart failure (HF). METHODS:A single-centre prospective observational trial was conducted in 16 consecutive subjects with advanced HF who were indicated for implantation of HeartMate 3 LVAD. Blood samples were collected both during the procedure (V1) and 12 months postoperatively (V2) for comprehensive analysis. Additionally, in a subgroup of seven LVAD subjects listed for heart transplantation (HTx), a histological examination was performed on myocardial samples obtained during LVAD implantation and from the explanted heart following HTx. RESULTS:LVAD implantation was associated with reductions in brain natriuretic peptide (324.7±47.0 vs 124.6±50.3 pg/mL) and C reactive protein (15.2±3.8 vs 6.0±1.3 mg/L) levels. Decreased inflammation markers coincided with reduced levels of lymphocyte- and macrophage-derived cytokines and their stimulating factors. LVAD implantation was associated with modulation of circulating biomarkers related to negative cardiac remodelling processes, including reductions in fibrosis- and remodelling-associated mediators (Extracellular Matrix Metalloproteinase Inducer, fibroblast growth factor (FGF)-2, FGF-19, receptor for advanced glycation endproducts, suppression of tumourigenicity 2, interleukin 27) and angiogenesis-related factors (stromal cell-derived factor-1α, growth differentiation factor (GDF)-15, somatotropin, vascular endothelial growth factor, angiopoietin 1, hepatocyte growth factor). In parallel, markers of metabolism and systemic catabolic state were significantly modulated, with decreases in GDF-15, somatotropin, trefoil factor 3 and resistin and increases in leptin levels. Histological analysis of myocardial samples available from a subgroup of subjects showed reduced macrophage infiltration following LVAD implantation. CONCLUSIONS:Long-term LVAD support was associated with improved biochemical and haematological profiles and with coordinated changes in circulating markers of inflammation, metabolism and cardiac remodelling. These exploratory findings provide further insight into the biological changes associated with durable mechanical unloading in subjects with advanced HF.

Aims:Sodium-glucose cotransporter 2 inhibitors (SGLT2i) have demonstrated cardioprotective effects in heart failure (HF), yet the molecular mechanisms underlying these benefits remain incompletely understood. This study aimed to characterize cardioprotective effects of SGLT2i, changes of circulating growth and inflammatory factors, as well as adipose tissue gene expression, in subjects with advanced HF (stage D). Methods:27 subjects with HF undergoing cardiovascular surgery were included, comprising 17 subjects treated with SGLT2i and 10 untreated controls. Soluble factors were analysed using Luminex assay, and mRNA expression in subcutaneous (SAT) and epicardial adipose tissue (EAT) was assessed. Results:Subjects receiving SGLT2i exhibited a non-significant trend toward lower BNP concentrations (329.1 ± 78.7 vs. 514.2 ± 103.8 pmol/L, p = 0.079) and increased circulatory levels of anti-inflammatory IL-10 (7.2 ± 0.4 vs. 5.8 ± 0.7 pg/mL, p = 0.025) and cardioprotective TGF-α (3.5 ± 0.3 vs. 2.7 ± 0.4 pg/mL, p = 0.039). sVEGFR3 levels (82.3 ± 4.7 vs. 63.3 ± 3.9 pg/mL, p = 0.010) were higher in SGLT2i, suggesting altered lymphangiogenic signalling. Transcriptomic analysis showed lower expression of genes associated with inflammation (IL6, CCL2, CXCL2), cardiac hypertrophy (PKFP, NAMPT), fibrosis (TNC, TNFAIP3), and cellular senescence (ICAM1, CDKN1A), predominantly in SAT. Conclusions:SGLT2i therapy in advanced HF was associated with higher circulating IL-10, TGF-α and sVEGFR3 levels and with a more favourable adipose tissue gene expression profile characterized by lower expression of genes related to inflammation, fibrosis, and cellular senescence. These findings identify molecular pathways associated with SGLT2i therapy that warrant further mechanistic investigation.

Metabolic dysfunction, in particular obesity and type 2 diabetes mellitus, increases susceptibility to pulmonary fibrosis via chronic inflammation, oxidative stress, and the accumulation of senescence. Senescent cells promote secretion of pro-fibrotic mediators that impair lung structure and repair. Here, we investigated whether reducing senescent cell burden using the mitochondria-targeted senolytic agent MitoTam, or weight-loss-induced improvement after bariatric surgery, can attenuate metabolic-associated pulmonary injury. In mice with diet-induced obesity, MitoTam improved glucose homeostasis, reduced adiposity, and markedly decreased senescence markers in lungs. This was accompanied by reduced inflammatory and fibrotic gene expression, diminished myofibroblast accumulation, and alleviated lung hypoxia. MitoTam also lowered senescence and expression of key pro-fibrotic factors, including GDF15, FGF2, TGFβ, and endothelin-1 (EDN1) in subcutaneous adipose tissue, indicating both direct pulmonary and systemic endocrine effects. In patients with class III obesity, laparoscopic sleeve gastrectomy induced substantial body weight loss, improved metabolic parameters, and significantly reduced adipose tissue senescence and pro-fibrotic signaling, including EDN1 expression and its level in the circulation. These findings identify cellular senescence as a modifiable driver linking metabolic dysfunction to pulmonary fibrosis and highlight mitochondria-targeted senolysis with MitoTam as a promising therapeutic approach.

BACKGROUND:Early postoperative glycemic control after orthotopic liver transplantation (OLTx) is challenging because of surgical stress, corticosteroid and calcineurin-inhibitor immunosuppression, and parenteral nutrition. We evaluated whether adding real-time continuous glucose monitoring (rtCGM) to standard care increases time in the target glucose range. METHODS:In this single-center randomized controlled trial, OLTx recipients were randomized after surgery to open (Active) or blinded (Control) rtCGM (Dexcom G6); in the Active group, sensor data guided insulin titration. The primary endpoint was time in target range (TIR, 6.0-10.0 mmol/L), analyzed in a modified intention-to-treat population. Secondary endpoints included glycemic metrics, insulin requirements, and predefined clinical outcomes. RESULTS:We randomized 154 patients; 142 with available data were analyzed (82 Active, 60 Control). The Active group spent more time in target range (68.9% vs. 60.8%; median difference 7.2 percentage points [95% CI: 2.7-12.0]; P = 0.003), with less time in Level 1 hyperglycemia (P = 0.025) and fewer extended hyperglycemic episodes (incidence rate ratio 1.65 [1.03-2.65] for Control vs. Active; P = 0.039). TIR improved similarly in patients with and without pretransplant diabetes; the only significant treatment-by-diabetes interaction was a greater reduction in Level 2 hyperglycemia among patients with diabetes (P < 0.001). Hypoglycemia was minimal in both groups. Infectious complications were less frequent in the Active group (45.1% vs. 63.3%; P = 0.041). CONCLUSIONS:Adding rtCGM to standard postoperative care improved glycemic control after liver transplantation, with consistent benefit regardless of diabetes status and the greatest effect on Level 2 hyperglycemia in patients with diabetes. The lower infection rate is a hypothesis-generating finding warranting a dedicated trial.

AIMS:To evaluate the efficacy and safety of transitioning from multiple daily injections (MDIs) insulin regimen to once-daily, fixed-ratio combination of basal insulin analog glargine 100 U/mL and a glucagon-like peptide 1 receptor agonist lixisenatide (iGlarLixi) in people with type 2 diabetes (PwT2D). MATERIALS AND METHODS:Insulin therapy DE-intensificAtion with iglarLixi was a five-centre, open-label, parallel-group, active comparator, phase IV randomised controlled trial with a 24-week active treatment period. Eligible PwT2D (age 18-80 years, HbA1c ≤9% [75 mmol/mol], total daily dose of insulin ≤0.8 IU/kg, and fasting C-peptide above the lower limit of normal) were randomised in a 1:1 fashion to iGlarLixi initiation or continuation with MDI regimen. The primary endpoint was the mean change in HbA1c from baseline to 24 weeks after randomisation between the two treatment groups. RESULTS:Ninety individuals (n = 45 in both treatment groups), 71/91 (79.0%) male with mean (SD) age 66.2 (8.7) years, HbA1c 7.9 (1.0) % (62.8 [10.9] mmol/mol), diabetes duration 17.5 (8.7) years and body mass index (BMI) 33.6 (5.5) kg/m2 were analysed. The mean (95% confidence interval) difference in the change in HbA1c between the iGlarLixi and the MDI group was -0.12 (-0.48, 0.23)% (-1.39 [-5.21, 2.43] mmol/mol), indicating comparable glycaemic control in both treatment groups. Significant between-group differences in favour of iGlarLixi were observed in body weight: -4.19 (-5.95, -2.43) kg, BMI: -1.49 (-2.11, -0.86) kg/m2, total daily dose of insulin: -28.57 (-34.89, -22.24) IU, time spent in level 2 hyperglycaemia: -4.9 (-9.4, -0.34)%, and glycaemia risk index: -13.6 (-25.1, -2.1). CONCLUSIONS:Insulin therapy simplification from MDI regimen to once-daily iGlarLixi is an efficient and safe treatment option for PwT2D.

Introduction: The IDEAL RCT examined the efficacy and safety of MDI de-intensification into once-daily administered iGlarLixi in people with type 2 diabetes (PwT2D) and showed that it provides comparable glycemic control with the benefits of reduction of body weight, total daily insulin dose and number of insulin injections. Here we report CGM outcomes from the trial. Methods: IDEAL was a 5-centre, open-label, parallel-group, phase 4 RCT with a 24-week active treatment period. Participants were randomized in a 1:1 fashion into iGlarLixi or continuation with MDI and were applied professional CGM (Freestyle Libre Pro iQ) before the onset (BL) and for the last 2 weeks of the treatment period (W24). Participants in whom ≥ 72 hours of CGM data were available were included in the analysis. Results: Altogether 73/91 (80.2%) of IDEAL participants were analyzed. Median (IQR) %TIR increased in the iGlarLixi group (70 [57 - 88] at BL vs 80 [61 - 92] at W24, p = 0.039), but remained unchanged in the MDI group (78 [67 - 89] vs 82 [64 - 89], p = 0.728). In the iGlarLixi group reductions in %TAR (26 [11 - 44] vs 13 [6 - 35], p = 0.04), % of time in level 2 hyperglycemia (2 [1 - 9] vs 1 [0 - 4], p = 0.019), mean glucose (8.6 [7.4 - 10.1] vs 7.7 [6.9 - 9.2] mmol/L, p = 0.012) and glycemia risk index (GRI) (26 [10 - 46] vs 19 [8 - 35], p = 0.036) were detected. Median (IQR) %TBR (< 3.9 mmol/L) remained unchanged in iGlarLixi group (0 [0 - 1] vs 1 [0 - 2], p = 0.337) and MDI group (0.5 [0 - 2] vs 1 [0 - 3.75], p = 0.147). Statistically significant differences between the changes (BL - W24) in the following CGM metrics (iGlarLixi vs MDI) were observed: %CV (-0.8 [-3.4 - 0.75] vs 1.4 [-1.2 - 3.3], p = 0.016) and GRI (-3.2 [-22.4 - 2.4] vs 1.6 [-6.25 - 10.6], p = 0.045). Conclusion: Insulin therapy de-intensification from MDI into iGlarLixi in PwT2D showed an improvement in CGM outcomes vs baseline (TIR, TAR, level 2 hyperglycemia, mean glucose and GRI) and vs continuation with MDI (glycemic variability and GRI) without increase of time spent in hypoglycemia. Disclosure P. Novodvorsky: Speaker's Bureau; Sanofi, Boehringer-Ingelheim. Advisory Panel; Boehringer-Ingelheim. Speaker's Bureau; Novo Nordisk A/S. Research Support; Sanofi. Speaker's Bureau; Abbott, Medtronic, Berlin-Chemie AG, Viatris Inc., Novartis AG. L. Thieme: None. I. Lankova: None. A. Veselá: None. E. Zahumensky: None. T. Edelsberger: None. M. Löblová: None. F. Hrubý: None. M. Mraz: None. M. Haluzik: Advisory Panel; Sanofi, Novo Nordisk, Eli Lilly and Company, AstraZeneca, Bayer Inc., Johnson & Johnson Medical Devices Companies. Consultant; Merck & Co., Inc., Sanofi, Novo Nordisk, Eli Lilly and Company, AstraZeneca, Bayer Inc., Boehringer-Ingelheim, Johnson & Johnson Medical Devices Companies, Novatin. Research Support; Sanofi. Speaker's Bureau; Sanofi, Novo Nordisk. Funding Sanofi

Introduction and Objective: Glycemia management early after liver transplantation (LTx) is challenging due to patients' critical state and corticoid therapy. We evaluated the impact of actively used real-time continuous glucose monitoring (CGM) on glycemic control in LTx recipients at postoperative ICU in a prospective randomized trial (clinicaltrials.gov NCT05585801). Methods: LTx recipients were randomized to wearing an open-labelled or blinded CGM (Dexcom G6) added to standard care, placed in the infraclavicular region immediately after surgery. Data from the open-labelled CGM were used to adjust insulin therapy; blinded CGM data served as controls. Primary endpoint was > 7.5% difference in time in the target range 6-10 mmol/l. Results: We included 154 patients, 12 were excluded due to technical failures (6 from each arm), 142 patients were evaluated (active CGM n=82, control n=60), 28% with diabetes. All required vasopressors, mechanical ventilation and intravenous insulin therapy after transplantation. Patients with actively used CGM spent significantly more time in the target range compared to the control group (68.5% vs. 60.3%, p=0.003), meeting the primary endpoint, and significantly less time in level 1 hyperglycemia, see Table 1. Conclusion: Active use of CGM added to standard therapy significantly improved glycemic control in patients in critical state early after liver transplantation. B. Hagerf (Voglová): None. M. Protus: None. L. Nemetova: None. M. Mraz: None. P. Girman: Speaker's Bureau; Neovii. M. Haluzik: Research Support; Sanofi. Advisory Panel; Eli Lilly and Company. Speaker's Bureau; Novo Nordisk, Abbott. Advisory Panel; AstraZeneca. Speaker's Bureau; GlaxoSmithKline plc, Amgen Inc. Advisory Panel; Bausch Health. J. Franekova: None. A. Jabor: None. E. Kieslichova: None. CarDia (Programme EXCELES, Project No. LX22NPO5104); Funded by the European Union; Next Generation EUCooperatio Program, Charles University in Prague

Background Heart failure (HF) progression involves complex metabolic and multi-organ alterations, but the specific adaptations in adipose tissue are not fully understood. Aims We aimed to characterize the metabolic remodeling of epicardial (EAT) and subcutaneous (SAT) adipose tissues in HF with reduced ejection fraction (HFrEF), focusing on lipid metabolism, fatty acid oxidation, and ketogenesis. Methods Clinical and metabolomic profiling were performed on metabolically stable controls (n = 34), patients with mild HFrEF (n = 45), and severe HFrEF (n = 129). Metabolomics profiling identified over 800 metabolites in EAT and SAT. Clustering and pathway enrichment analyses defined depot-specific metabolic shifts across HF stages, while gene expression analyses provided mechanistic support. Results Advancing HF was associated with declining cardiac function, systemic congestion, and a metabolic shift toward catabolism. Metabolomics revealed depot-specific adaptations: SAT transitioned smoothly to enhanced lipolysis, whereas EAT demonstrated impaired triacylglycerol replenishment and disrupted final turn of β-oxidation spiral. Both depots increased reliance on acylcarnitine degradation and lipolysis; however, EAT was uniquely characterized by late-stage impairment in mitochondrial and peroxisomal fatty acid oxidation, leading to elevation of 3-hydroxybutyrate and hydroxybutyrylcarnitine tissue levels. Ex vivo analyses of EAT explants showed significantly increased fraction of L-3-hydroxybutyrate enantiomer, produced by EAT, compared to D-3-hydroxybutyrate enantiomer originating from the liver. Conclusions HF progression drives major, depot-specific metabolic remodeling in adipose tissue. In advanced HF, EAT shows impaired fatty acid oxidation and enhanced local production of L-3-hydroxybutyrate in the vicinity of myocardium, highlighting the close metabolic cooperation in nutrient supply between EAT and the heart muscle through the coronary circulation.

ABSTRACT Background Diabetes mellitus (DM) significantly impacts global health and economies. Despite various therapies, managing DM remains challenging. Bariatric surgery has shown efficacy in obese patients with type 2 diabetes mellitus (T2DM), but its utilization remains low. Innovative, less invasive endoscopic approaches such as duodenal mucosal resurfacing show potential in treating T2DM. This article presents the results of a First in Human (FIH) study using a duodenal submucosal laser ablation investigational device for T2DM treatment. Methods A prospective, single‐arm, open‐label study evaluated the safety and efficacy of the Digma System Endoscopic procedure for duodenal submucosal laser ablation in consecutive enrolled T2DM patients. Results The study was conducted from July 2017 to December 2020 and enrolled 31 patients for the Digma System Endoscopic procedure. The Dose Escalation Cohort (DEC) used sub‐therapeutic laser doses for training and safety. The Treatment Cohort (TC) of 25 patients received therapeutic doses, resulting in HbA1c reductions of −0.6% at 6 months ( p = 0.014) and −0.4% at 12 months ( p = 0.062). Fasting glucose dropped 17.3 mg/dL ( p = 0.173) at 6 months and 28 mg/dL ( p = 0.022) at 12 months. Post‐prandial glucose improvements were also observed. HOMA‐IR improved at 3 and 6 months. PAGI‐SYM and PAGI‐QOL showed stable to slightly improved GI symptoms and quality of life. Two severe adverse events were unrelated to the procedure. Conclusion The study demonstrates the safety, feasibility, and potential efficacy of the Digma System Endoscopic procedure. Evidence suggests improvements in HbA1c, fasting and post‐prandial glucose, and HOMA‐IR levels could be attributed to the Digma System Endoscopic procedure.

Objectives: Glycemia management in critical care is posing a challenge in frequent measuring and adequate insulin dose adjustment. In recent years continuous glucose measurement is gaining accuracy and reliability in outpatient and inpatient setting. The aim of this study was to assess the feasibility and accuracy of real-time continuous glucose monitoring in ICU patients after major abdominal surgery. Research design and methods: We included patients undergoing pancreatic surgery and solid organ transplantation (liver, pancreas, islets of Langerhans, kidney) requiring ICU stay after surgery. We used a Dexcom G6 sensor, placed in the infraclavicular region, for rtCGM. Arterial blood glucose measured by the amperometric principle (ABL 800, Radiometer, Copenhagen, Denmark) served as reference values and for calibration. Blood glucose was also routinely monitored by StatStrip bedside glucose meter. Sensor accuracy was assessed by mean absolute relative difference (MARD), bias, modified Bland-Altman plot and Surveillance Error Grid for paired samples of glucose values from CGM and ABL. Results: We analyzed data from 61 patients and obtained 1546 paired glucose values from CGM and ABL. Active sensor use was 95.1%. MARD was 9.4%, relative bias 1,4%, 92.8% values fell in zone A, 6.1% in zone B and 1.2% in zone C of Surveillance Error Grid. Median time in range was 78%, with minimum (<1%) time spent in hypoglycemia. StatStrip glucose meter MARD compared to ABL was 5.8%. Conclusions: Our study shows clinically applicable accuracy and reliability of Dexcom G6 CGM in postoperative ICU patients and a feasible alternative sensor placement site.