In heart failure, impairment of cardiac muscle function leads to numerous neurohormonal and metabolic disorders, including an imbalance between anabolic and catabolic processes, in favour of the latter. These disorders cause loss of muscle mass with structural and functional changes within the skeletal muscles, known as skeletal myopathy. This phenomenon constitutes an important mechanism that participates in the pathogenesis of chronic heart failure. both its clinical symptoms and the progression of the disease. Attempts to reverse the above‐mentioned pathologic processes by exploiting the anabolic action of androgenic hormones could provide a potentially attractive treatment option. The current concepts of anabolic androgen deficiency and resultant skeletal myopathy in patients with heart failure are reviewed, and the potential role of anabolic‐androgenic hormones as an emerging therapeutic option for targeting heart failure is discussed.

(1) Background: Oxidative energy metabolism is presumed to rely on the optimal iron supply. Primary human cardiac myocytes (HCM) exposed to different iron availability conditions during mechanical stretch are anticipated to demonstrate expression changes of genes involved in aerobic and anaerobic metabolic pathways. (2) Methods: HCM were cultured for 48 h either in static conditions and upon mechanical stretch at the optimal versus reduced versus increased iron concentrations. We analyzed the expression of pyruvate kinase (PKM2), lactate dehydrogenase A (LDHA), and mitochondrial complexes I–V at the mRNA and protein levels. The concentration of l-lactate was assessed by means of lactate oxidase method-based kit. (3) Results: Reduced iron concentrations during mechanical work caused a decreased expression of complexes I–V (all p < 0.05). The expression of PKM2 and LDHA, as well as the medium concentration of l-lactate, was increased in these conditions (both p < 0.05). HCM exposed to the increased iron concentration during mechanical effort demonstrated a decreased expression of mitochondrial complexes (all p < 0.01); however, a decrement was smaller than in case of iron chelation (p < 0.05). The iron-enriched medium caused a decrease in expression of LDHA and did not influence the concentration of l-lactate. (4) Conclusions: During mechanical effort, the reduced iron availability enhances anaerobic glycolysis and extracellular lactate production, whilst decreasing mitochondrial aerobic pathway in HCM. Iron enrichment during mechanical effort may be protective in the context of intracellular protein machinery of non-oxidative metabolism with no effect on the extracellular lactate concentration.

Background: In total, 6.6% to 11% of patients with an initially implanted implantable cardioverter-defibrillator (ICD) will develop significant bradycardia and the need for pacing in subsequent years. As the leadless pacemaker (LP) and subcutaneous implantable cardioverter-defibrillator (S-ICD) population comorbidities are often similar, both groups would benefit from a hybrid solution. Unfortunately, currently, there is no commercially available and sufficiently validated interconnected set of S-ICD and LP. Methods: In this single-center, prospective observational study, 32 pacing-dependent patients after implantation of a Micra LP were screened for S-ICD on the left and right sides of the sternum using the EMBLEM Automated Screening Tool. At least one positive, both in the supine and standing positions, was considered a positive screening. The impact of various clinical variables and morphology of paced QRS on screening results was assessed. Moreover, the function of the tricuspid valve was evaluated before and after LP implantation to consider whether there is a relationship between paced QRS and worsening tricuspid regurgitation. Results: Patients with paced heart rhythm were divided into two groups based on screening results for S-ICD. The positive screening outcome was achieved in 10 patients (31.25%). No correlation between any clinical variable and screening results was found. However, right axis deviation [RAD] of paced QRS seems to be a strong predictor of positive S-ICD screening (RAD in 9/32 patients, sensitivity 90%, specificity 100%, PPV 100%, NPV 96% for passing screening), and negative polarity of paced QRS in inferior leads predicts negative screening results (positive polarity in II, III, and aVF in 12/32 patients, sensitivity 100%, specificity 90%, PPV 83%, NPV 100% for passing screening). Conclusions: Right axis deviation of the paced rhythm, positive QRS polarity of leads II, III, and aVF, and negative QRS polarity in leads I and aVL seem to predict a positive screening result for S-ICD. Such a position of LP does not seem to worsen tricuspid regurgitation.

Background. The complex clinical status of modern day patients hospitalized due to acute heart failure (AHF) results from their advanced age, comorbidities, frailty, heart failure symptoms (including massive swelling of the lower limb), and dramatic reduction of exercise tolerance. Hence, there is a need to implement physiotherapeutic procedures as early as possible, aiming to both accelerate the restoration of clinical stabilization and prevent post-hospital disability. Objectives. We investigated whether assisted lower limb exercises have an impact on perfusion and oxygenation in skeletal muscle and if they are feasible in patients with AHF. Materials and methods. We examined 34 men (age: 66 +/- 11 years; left ventricular ejection fraction (LVEF): 34 +/- 11%; clinical presentation: 31 wet-warm and 3 wet-cold). The intervention (carried out on the 2nd day of hospitalization) included: 1) a 3-minute rest period; 2) an exercise phase (45 repetitions of assisted flexion and extension of the lower limb; and 3) a 10-minute relaxation period. We analyzed blood pressure (BP), heart rate (HR), respiratory rate (RR), tissue oxygenation (reflected by oxygen saturation measured with a pulse oximeter), and changes in peripheral tissue perfusion (reflected by the tissue oxygenation index (TOI) measured with near-infrared spectroscopy (NIRS)). Results. The hemodynamic parameters (both Delta HR and Delta systolic BP) and oxygen saturation did not change (all p > 0.05), whereas the RR declined (p < 0.001). The exercises improved venous outflow (reflected by decreased oxygenated, deoxygenated and total hemoglobin, all p < 0.05) and increased peripheral tissue perfusion, as reflected by the TOI (p < 0.05). The patients reported relief and lack of dyspnea during and after the assisted exercises. Conclusions. The physiotherapeutic intervention improved both venous outflow and muscle oxygenation in men with AHF. The presented protocol was safe, feasible and well-tolerated, and resulted in relief for the patients. We believe that such procedures might be recommended for the initial period of rehabilitation in this challenging subgroup of patients.