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Heart failure is a multifaceted pathophysiologic syndrome, with prevalent dysfunction of other vital organs and systems. The role of the liver in this disease has been little investigated, although up to 80% of patients with heart failure present with some form of liver dysfunction. In addition to its multiple metabolic functions, the liver has a crucial role in the removal of circulating endotoxins and in regulating immune responses and iron homeostasis. Kupffer cells that constitute 80% to 90% of tissue macrophages in the human body play an important role in this regard. A disturbed microcirculation of the liver may decrease endotoxin clearance and increase the hepatic secretion of proinflammatory cytokines. Such an immune activation may in turn alter the expression of hepcidin in the liver, resulting in iron deficiency. The proinflammatory state also is associated with an augmented free radical formation. However, the antioxidant capacity of the liver seems to be inadequate because there is evidence for selenium deficiency in patients with heart failure. The aim of this article was to summarize the various aspects of liver dysfunction in heart failure and to highlight the role of liver-derived factors in the development of specific nutritional deficiencies. Nutritional strategies opposing these deficiencies might present promising additive treatments of heart failure.

Background Skeletal muscle wasting is an extremely common feature in patients with heart failure, affecting approximately 20% of ambulatory patients with even higher values during acute decompensation. Its occurrence is associated with reduced exercise capacity, muscle strength, and quality of life. We sought to investigate if the presence of muscle wasting carries prognostic information. Methods Two hundred sixty‐eight ambulatory patients with heart failure (age 67.1 ± 10.9 years, New York Heart Association class 2.3 ± 0.6, left ventricular ejection fraction 39 ± 13.3%, and 21% female) were prospectively enrolled as part of the Studies Investigating Co‐morbidities Aggravating Heart Failure. Muscle wasting as assessed using dual‐energy X‐ray absorptiometry was present in 47 patients (17.5%). Results During a mean follow‐up of 67.2 ± 28.02 months, 95 patients (35.4%) died from any cause. After adjusting for age, New York Heart Association class, left ventricular ejection fraction, creatinine, N‐terminal pro‐B‐type natriuretic peptide, and iron deficiency, muscle wasting remained an independent predictor of death (hazard ratio 1.80, 95% confidence interval 1.01–3.19, P = 0.04). This effect was more pronounced in patients with heart failure with reduced than in heart failure with preserved ejection fraction. Conclusions Muscle wasting is an independent predictor of death in ambulatory patients with heart failure. Clinical trials are needed to identify treatment approaches to this co‐morbidity.

The Otago program (OP) is evidence-based and focuses on fall prevention in older people. The feasibility and usability of a short-term digital program modeled after the principles of the OP in the setting of early geriatric rehabilitation (EGR) are unclear. This study investigated the feasibility and usability of an additional technology-based fall prevention program (FPP) in the setting of EGR. We performed a feasibility study in the setting of EGR. A sample of 30 patients (mobility at least by walker; mini-mental status test score >17) was recruited between March and June 2024 and compared with a retrospective cohort (n=30, former EGR patients). All patients in the intervention group (IG) received a supervised, OP-modified FPP thrice/week for 20 minutes using a technology-based platform called \"Pixformance.\" The device is a digital trainer and enables real-time corrections. The primary end point was the feasibility (given when 80% of the IG participated in 6 trainings within 2 weeks). Secondary outcomes were usability (patients' and facilitators' perspective; ≥75%), risk of falls (Berg Balance Scale), mobility (Timed Up and Go Test), functional independence (Functional Independence Measure), and activities of daily living (Barthel Index). Several further exploratory end points were analyzed including anxiety and depression (Four-Item Patient Health Questionnaire; PH-Q4). Data were accessed at entry to EGR and after 2 weeks prior to discharge. To analyze the pre-posttest results, the dependent Student t test and the Wilcoxon test were applied. A mixed ANOVA with repeated measurements was used for statistical analyses of time-, group-, and interaction-related changes. A cohort of 60 patients (mean 80.2, SD 6.1 y; 58% females, 35/60) was analyzed. The main indication for EGR was stroke (9/60, 15%). Patients were recruited into a prospective IG (n=30) and a retrospective control group (n=30). Of the 30 patients in the prospective IG, 11 patients (37%) completed 6 training sessions within 2 weeks. Reasons why participants did not complete 6 training sessions were diagnostic appointments (33%), pain/discomfort (33%), or fatigue (17%). EGR patients rated FPP usability at 84% and facilitators at 65% out of 100%. Pre-posttest analysis of the standard assessments showed a significant interaction in Berg Balance Scale (<.01). In both groups, a significant improvement over time was found in the Timed Up and Go Test (<.01), Barthel Index (<.01), and Functional Independence Measure (<.01). Likewise, in the IG, the PH-Q4 score (.02) improved. While the technology-based FPP in the EGR setting was generally well-accepted by patients, with high usability ratings, its feasibility was limited. Only 37% of participants completed the required additional training sessions. Further studies should test the technology-based FPP as an integrated part of the EGR complex therapy concept. Our findings suggest potential benefits of incorporating technology-based FPPs in EGR, but further refinement is needed to enhance participation and feasibility.

Maintaining cancer patients’ exercise capacity and therefore patients’ ability to live a self-determined life is of huge importance, but little is known about major determinants. We sought to identify determinants of exercise capacity in patients with a broad spectrum of cancer types, who were already receiving cancer treatment or about to commence such therapy. Exercise capacity was assessed in 253 consecutive patients mostly suffering from advanced cancer using the 6-min walk test (6-MWT). All patients underwent echocardiography, physical examination, resting electrocardiogram, hand grip strength (HGS) measurement, and laboratory assessments. Patients were divided into two groups according to the median distance in the 6-MWT (459 m). Patients with lower exercise capacity were older, had significantly lower HGS and haemoglobin and higher values of high sensitive (hs) Troponin T and NT-proBNP (all p  < 0.05). Whilst the co-morbidity burden was significantly higher in this group, no differences were detected for sex, body mass index, tumor type, or cachexia (all p  > 0.2). Using multivariable logistic regression, we found that the presence of anaemia (odds ratio (OR) 6.172, 95% confidence interval (CI) 1.401–27.201, p  = 0.016) as well as an increase in hs Troponin T (OR 3.077, 95% CI 1.202–5.301, p  = 0.019) remained independent predictors of impaired exercise capacity. Increasing HGS was associated with a reduced risk of a lower exercise capacity (OR 0.896, 95% CI 0.813–0.987, p  = 0.026). Screening patients for elevated hs troponin levels as well as reduced HGS may help to identify patients at risk of lower exercise capacity during cancer treatment.

Background Body weight loss is a frequent complication after stroke, and its adverse effect on clinical outcome has been shown in several clinical trials. The purpose of this prospective longitudinal single‐centre observational study was to investigate dynamical changes of body composition and body weight after ischemic stroke and an association with functional outcome. Methods Sixty‐seven consecutive patients (age 69 ± 11 years, body mass index 27.0 ± 4.1 kg/m2, 42% female patient, mean ± SD) with acute ischemic stroke with mild to moderate neurological deficit (National Institute of Health Stroke Scale median 4, ranged 0–12) were analysed in the acute phase (4 ± 2 days) and at 12 months (389 ± 26 days) follow‐up. Body composition was examined by dual energy X‐ray absorptiometry. Cachexia was defined according to the consensus definition by body weight loss ≥5% within 1 year and additional clinical signs. Lean tissue wasting was considered if a ratio of upper and lower limbs lean mass sum to squared height (kg/m2) was ≤5.45 kg/m2 for female patient and ≤7.25 kg/m2 for male patient. Results According to the body weight changes after 12 months, 42 (63%) patients had weight gain or stable weight, 11 (16%) patients had moderate weight loss, and 14 (21%) patients became cachectic. A relative decline of 19% of fat tissue and 6.5% of lean tissue was observed in cachectic patients, while no changes of lean tissue were observed in non‐cachectic patients after 12 months. The modified Rankin Scale was 48% higher (2.1 ± 1.6, P < 0.05), Barthel Index was 22% lower (71 ± 39, P < 0.01), and handgrip strength was 34% lower (21.9 ± 13.0, P < 0.05) in cachectic compared to non‐cachectic patients after 12 months. The low physical performance if defined by Barthel Index <60 points was linked to the lean tissue wasting (OR 44.8, P < 0.01), presence of cachexia (OR 20.8, P < 0.01), and low body mass index <25 kg/m2 (OR 11.5, P < 0.05). After adjustment for cofounders, lean tissue wasting remained independently associated with the low physical performance at 12 months follow‐up (OR 137.9, P < 0.05). Conclusions In this cohort study, every fifth patient with ischemic stroke fulfilled the criteria of cachexia within 12 months after index event. The incidence of cachexia was 21%. Cachectic patients showed the lowest functional and physical capacity.

Purpose Finerenone, a highly selective non‐steroidal mineralocorticoid receptor antagonist, was approved for the treatment of patients with chronic kidney disease (CKD) and type 2 diabetes mellitus (diabetic kidney disease, DKD). Finerenone reduced the composite endpoint of heart failure events and cardiovascular death in patients with heart failure with preserved or mildly reduced ejection fraction (HFpEF/HFmrEF). This study aimed to investigate the safety and cardiac effects of finerenone in patients with DKD with or without HFpEF/HFmrEF in a real‐world setting. Methods Patients with DKD were prospectively enrolled and were treated with finerenone according to best clinical practice. Clinical, laboratory and echocardiographic assessments were performed before, 4 weeks and 6 months after starting finerenone. Results Thirty‐one patients with DKD were included. At baseline, patients had a typical risk profile with arterial hypertension (90.3%) and hyperlipoproteinemia (87.1%). Most patients were treated with a sodium‐glucose cotransporter 2 (SGLT2) inhibitor (93.5%). Treatment with finerenone was safe and well tolerated: after 4 weeks, the glomerular filtration rate decreased slightly from 52 (43–78) mL/min/1.73 m2 to 48.0 (39.0–71.0) mL/min/1.73 m2 (P = 0.002 vs. baseline), but stabilized thereafter. Similarly, the median potassium value increased from 4.2 (3.8–4.5) mmol/L to 4.4 (4.2–4.8) mmol/L (P = 0.017) after 4 weeks, but remained stable thereafter [4.4 (4.1–4.6) mmol/L (P = 0.079)]. Only one patient (3.2%) had an unplanned hospitalization and concomitant hyperkalaemia up to 6.0 mmol/L. HFpEF/HFmrEF was frequently found in patients with DKD (71.0%), although most patients had a rather early stage with only mild symptoms and a median N‐terminal pro B‐type natriuretic peptide (NT‐proBNP) value of 150.8 (54.5–325.7) ng/L. During treatment with finerenone, NT‐proBNP and left ventricular mass index (LVMI) remained stable. In contrast, left atrial volume index (LAVI) decreased from baseline [31.2 (26.8–39.7) mL/m2] to 4 weeks follow‐up [29.7 (20.8–33.6) mL/m2, P = 0.027] and decreased further after 6 months [26.6 (20.8–34.9) mL/m2, P = 0.029]. In the subgroup of patients with HFpEF/HFmrEF, E/e′ decreased from 11.9 (8.7–14.5) at baseline to 9.9 (8.0–12.4) after 6 months (P = 0.043). Conclusions In a real‐world setting, treatment with finerenone is safe and well‐tolerated in patients with DKD and may improve functional and structural cardiac parameters. Further investigation is warranted.

Background C‐terminal Agrin Fragment (CAF) has been proposed as a novel biomarker for sarcopenia originating from the degeneration of the neuromuscular junctions. In patients with stroke muscle wasting is a common observation that predicts functional outcome. We aimed to evaluate agrin sub‐fragment CAF22 as a marker of decreased muscle mass and physical performance in the early phase after acute stroke. Methods Patients with acute ischaemic or haemorrhagic stroke (n = 123, mean age 70 ± 11 y, body mass index BMI 27.0 ± 4.9 kg/m2) admitted to inpatient rehabilitation were studied in comparison to 26 healthy controls of similar age and BMI. Functional assessments were performed at begin (23 ± 17 days post stroke) and at the end of the structured rehabilitation programme (49 ± 18 days post stroke) that included physical assessment, maximum hand grip strength, Rivermead motor assessment, and Barthel index. Body composition was assessed by bioelectrical impedance analysis (BIA). Serum levels of CAF22 were measured by ELISA. Results CAF22 levels were elevated in stroke patients at admission (134.3 ± 52.3 pM) and showed incomplete recovery until discharge (118.2 ± 42.7 pM) compared to healthy controls (95.7 ± 31.8 pM, p < 0.001). Simple regression analyses revealed an association between CAF22 levels and parameters of physical performance, hand grip strength, and phase angle, a BIA derived measure of the muscle cellular integrity. Improvement of the handgrip strength of the paretic arm during rehabilitation was independently related to the recovery of CAF22 serum levels only in those patients who showed increased lean mass during the rehabilitation. Conclusions CAF22 serum profiles showed a dynamic elevation and recovery in the subacute phase after acute stroke. Further studies are needed to explore the potential of CAF22 as a serum marker to monitor the muscle status in patients after stroke.

Aims Intravenous iron therapy (IVIT) is known to improve functional status in chronic heart failure (CHF) patients. The exact mechanism is not completely understood. We correlated magnetic resonance imaging (MRI) patterns of T2* iron signal in various organs to systemic iron and exercise capacity (EC) in CHF before and after IVIT. Methods and results We prospectively analysed 24 patients with systolic CHF for T2* MRI pattern of the left ventricle (LV), small and large intestines, spleen, liver, skeletal muscle, and brain for iron. In 12 patients with iron deficiency (ID), we restored iron deficit by IVIT using ferric carboxymaltose. The effects after 3 months were analysed by spiroergometry and MRI. Patients with vs. without ID showed lower blood ferritin, haemoglobin (76 ± 63 vs. 196 ± 82 μg/L and 12.3 ± 1.1 vs. 14.2 ± 1.1 g/dL, all P < 0.002), and in trend a lower transferrin saturation (TSAT) (19.1 [13.1; 28.2] vs. 25.1 [21.3; 29.1] %, P = 0.05). Spleen and liver iron was lower as expressed by higher T2* value (71.8 [66.4; 93.1] vs. 36.9 [32.9; 51.7] ms, P < 0.002 and 33.5 ± 5.9 vs. 28.8 ± 3.9 ms, and P < 0.03). There was a strong trend for a lower cardiac septal iron content in ID (40.6 [33.0; 57.3] vs. 33.7 [31.3; 40.2] ms, P = 0.07). After IVIT, ferritin, TSAT, and haemoglobin increased (54 [30; 104] vs. 235 [185; 339] μg/L, 19.1 [13.1; 28.2] vs. 25.0 [21.0; 33.7] %, 12.3 ± 1.1 vs. 13.3 ± 1.3 g/L, all P < 0.04). Peak VO2 improved (18.2 ± 4.2 vs. 20.9 ± 3.8 mL/min/kg−1, P = 0.05). Higher peak VO2 at anaerobic threshold was associated with higher blood ferritin, reflecting higher metabolic exercise capacity after therapy (r = 0.9, P = 0.0009). Increase in EC was associated with haemoglobin increase (r = 0.7, P = 0.034). LV iron increased by 25.4% (48.5 [36.2; 64.8] vs. 36.2 [32.9; 41.9] ms, P < 0.04). Spleen and liver iron increased by 46.4 and 18.2%, respectively (71.8 [66.4; 93.1] vs. 38.5 [22.4; 76.9] ms, P < 0.04 and 33.5 ± 5.9 vs. 27.4 ± 8.6 ms, P < 0.007). Iron in skeletal muscle, brain, intestine, and bone marrow remained unchanged (29.6 [28.6; 31.2] vs. 30.4 [29.7; 30.7] ms, P = 0.7, 81.0 ± 6.3 vs. 82.9 ± 9.9 ms, P = 0.6, 34.3 ± 21.4 vs. 25.3 ± 14.1 ms, P = 0.2, 9.4 [7.5; 21.8] vs. 10.3 [6.7; 15.7] ms, P = 0.5 and 9.8 ± 1.5 vs. 13.7 ± 8.9 ms, P = 0.1). Conclusions CHF patients with ID showed lower spleen, liver, and in trend lower cardiac septal iron. After IVIT, iron signal of the left ventricle as well as spleen and liver increased. Improvement in EC was associated with increase in haemoglobin after IVIT. In ID, liver, spleen, and brain but not heart iron were associated with markers of systemic ID.

Aims Increased sympathetic activation in patients with heart failure (HF) and sleep‐disordered breathing (SDB) provokes cardiac decompensation and protein degradation and could lead to muscle wasting and muscle weakness. The aim of this study was to investigate the differences in body composition, muscle function, and the susceptibility of preclinical congestion among patients with HF and SDB compared with those without SDB. Methods and results We studied 111 outpatients with stable HF who were enrolled into the Studies Investigating Co‐morbidities Aggravating Heart Failure. Echocardiography, short physical performance battery (SPPB), cardiopulmonary exercise testing, dual‐energy X‐ray absorptiometry, bioelectrical impedance analysis (BIA), tests of muscle strength, and polygraphy were performed. SDB was defined as apnoea/hypopnoea index (AHI) >5 per hour of sleep. Central sleep apnoea (CSA) and obstructive sleep apnoea (OSA) were defined as AHI >50% of central or obstructive origin, respectively. A total of 74 patients (66.7%) had any form of SDB [CSA (24 patients, 32.4%), OSA (47 patients, 63.5%)]. Patients with SDB showed increased muscle weakness (chair stand), reduced muscle strength, and lower values of SPPB score (P < 0.05). Patients with SDB did not show overt clinical signs of cardiac decompensation compared with those without SDB (P > 0.05) but had increased amounts of water (total body water, intracellular, and extracellular) measured using BIA (P < 0.05). Increased amounts of total body water were associated with the severity of SDB and inversely with muscle strength and exercise capacity measured by anaerobic threshold (P < 0.05). Altogether, 17 patients had muscle wasting. Of these, 11 (65%) patients had SDB (statistically not significant). Conclusions SDB is highly prevalent in patients with HF. Patients with SDB have lower muscle strength and tend to be more susceptible to preclinical congestion.