Background: Cardiac surgery often represents the only treatment option in patients with infective endocarditis (IE). However, IE surgery may lead to a sudden release of inflammatory mediators, which is associated with the severity of postoperative organ dysfunction. We investigated the impact of hemoadsorption during IE surgery on postoperative organ dysfunction. Methods: This multi-center, randomized, non-blinded, controlled trial assigned patients undergoing cardiac surgery for IE to hemoadsorption [integration of CytoSorb® to cardiopulmonary bypass (CPB)] or control. The Primary outcome (ΔSOFA) was defined as the difference between the mean total postoperative sequential organ failure assessment score (SOFA), calculated maximally to the 9th postoperative day, and the basal SOFA score. The analysis was by modified intention-to-treat. A predefined inter-group comparison was done using a linear mixed model for ΔSOFA including surgeon and baseline SOFA as fixed effect covariates and with the surgical center as random effect. The SOFA score assesses dysfunction in six organ systems, each scored from zero to four. Higher scores indicate worsening dysfunction. Secondary outcomes were 30-day mortality, durations of mechanical ventilation, vasopressor and renal replacement therapy. Cytokines were measured in the first 50 patients. Results: Between January 17, 2018 and January 31, 2020, A total of 288 patients were randomly assigned to hemoadsorption (n=142) or control (n=146). Four patients in the hemoadsorption and two in the control group were excluded as they did not undergo surgery. The primary outcome ΔSOFA did not differ between the hemoadsorption and the control group (1.79 ± 3.75 and 1.93 ± 3.53, respectively, 95% CI: −1.30 to 0.83, p=0.6766). Mortality at 30 days (21% hemoadsorption vs 22% control, p=0.782), the durations of mechanical ventilation, vasopressor and renal replacement therapy did not differ between groups. Levels of IL-1β and IL-18 at the end of CPB were significantly lower in the hemoadsorption than in the control group. Conclusions: This randomized trial failed to demonstrate a reduction in postoperative organ dysfunction through intraoperative hemoadsorption in patients undergoing cardiac surgery for IE. Although hemoadsorption reduced plasma cytokines at the end of CPB, there was no difference in any of the clinically relevant outcome points.

Background: Reduced exercise capacity in patients with heart failure (HF) could be partially explained by skeletal muscle dysfunction. We compared skeletal muscle function, structure, and metabolism among clinically stable outpatients with HF with preserved ejection fraction, HF with reduced ejection fraction, and healthy controls (HC). Furthermore, the molecular, metabolic, and clinical profile of patients with reduced muscle endurance was described. Methods: Fifty-five participants were recruited prospectively at the University Hospital Jena (17 HF with preserved ejection fraction, 18 HF with reduced ejection fraction, and 20 HC). All participants underwent echocardiography, cardiopulmonary exercise testing, 6-minute walking test, isokinetic muscle function, and skeletal muscle biopsies. Expression levels of fatty acid oxidation, glucose metabolism, atrophy genes, and proteins as well as inflammatory biomarkers were assessed. Mitochondria were evaluated using electron microscopy. Results: Patients with HF with preserved ejection fraction showed compared with HF with reduced ejection fraction and HC reduced muscle strength (eccentric extension: 13.3±5.0 versus 18.0±5.9 versus 17.9±5.1 Nm/kg, P =0.04), elevated levels of MSTN-2 (myostatin-2), FBXO-32 (F-box only protein 32 [Atrogin1]) gene and protein, and smaller mitochondrial size ( P <0.05). Mitochondrial function and fatty acid and glucose metabolism were impaired in HF-patients compared with HC ( P <0.05). In a multiple regression analysis, GDF-15 (growth and differentiation factor 15), CPT1B (carnitine palmitoyltransferase IB)-protein and oral anticoagulation were independent factors for predicting reduced muscle endurance after adjusting for age (log10 GDF-15 [pg/mL] [B, −54.3 (95% CI, −106 to −2.00), P =0.043], log10 CPT1B per fold increase [B, 49.3 (95% CI, 1.90–96.77), P =0.042]; oral anticoagulation present [B, 44.8 (95% CI, 27.90–61.78), P <0.001]). Conclusions: Patients with HF with preserved ejection fraction have worse muscle function and predominant muscle atrophy compared with those with HF with reduced ejection fraction and HC. Inflammatory biomarkers, fatty acid oxidation, and oral anticoagulation were independent factors for predicting reduced muscle endurance.

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The study demonstrates a time-dependent effect of RVP on microflow, leading to 50 and 25 % of baseline at 8 and 18 s of RVP, respectively. In a substantial proportion of patients, RVP is associated with microcirculatory arrest and a delayed recovery of microflow. Although the impact of these findings on outcome is yet unclear, TAVI operators should be aware of the potentially adverse effects of even short periods of RVP.

This study delivers cut-off values for VCA3D in patients with different types of MR. VCA3D is a robust parameter for quantification of MR, showing a good correlation with the reference method using 3D datasets of LV.