Search Results (3,221)

Heart failure (HF) remains a global health challenge with high rates of hospitalization and mortality, particularly among the elderly. Many episodes of worsening HF occur before symptoms arise, underscoring the need for sensitive monitoring tools. Respiratory Stability Time (RST) is a novel index that quantifies the duration of stable respiration during sleep, reflecting pulmonary congestion and circulatory status. RST can be measured continuously and non-invasively using a contactless under-mattress sensor. Observational cohort studies show that low RST predicts poor prognosis, while its improvement parallels recovery from decompensation. Importantly, recent prospective multicenter observations involving 100 patients demonstrated that sustained RST decline often precedes HF readmission, probably enabling early intervention. A multicenter trial (ITMETHOD-HF III), involving 80 patients, is currently testing whether RST-guided therapy can reduce HF readmissions. RST might substantially enhance current HF management by enabling us to provide proactive therapeutic intervention, though further validation is warranted. Full article

Trail running involves constant changes in terrain and slope, complicating the accurate assessment of energy expenditure during performance. This study aimed to examine the relationship between running power output (RPO), oxygen consumption (VO₂), carbon dioxide production (VCO₂), and energy expenditure per minute (EE_min) across positive and negative slopes in trained trail runners under standardized laboratory conditions. Fifteen male trail runners performed five randomized 5 min treadmill runs at 70% of VO₂ maximal speed on −7%, −5%, 0%, +5%, and +7% slopes. VO₂, VCO₂, EE_min, respiratory exchange ratio (RQ), heart rate (HR), and RPO were recorded. Statistical analysis included Shapiro–Wilk tests for normality, repeated-measures ANOVA to compare variables across slopes, and Spearman or Pearson correlations between RPO and physiological variables. Moderate to strong positive correlations were found between RPO and VO₂ (Rho = 0.80–0.84, p < 0.001) and between RPO and EE_min (Rho= 0.74–0.87, p < 0.01) across all conditions. These findings suggest that RPO measured via a wearable device may reflect changes in energy expenditure and supports the integration of wearable power metrics into training and nutritional strategies for trail running. However, further studies in female athletes, outdoor settings, extreme slopes, and altitude conditions are needed to confirm the generalizability of these results. Full article

The peroxisome proliferator-activated receptor family of lipid-activated nuclear receptors (PPARs) plays a critical role in the regulation of cellular lipid metabolism. In cardiac muscle, PPARα is highly expressed and regulates genes involved in fatty acid oxidation, but its activity is downregulated in hypertrophic hearts; however, the consequences of chronic PPARα deficiency on the cardiac contractile apparatus remain unclear. This study aimed to investigate the PPARα role in hypertrophic phenotype and to evaluate the potential effects of the antioxidant Ebselen (Ebs) treatment on changes associated with PPARα depletion. We thus generated an in vitro model of cardiac hypertrophy by stable silencing of the PPARA gene in H9c2 rat cardiomyoblasts. We observed that PPARα silencing induces a hypertrophic phenotype, characterized by increased NPPB and decreased FBXO32 expression, mitochondrial dysregulation, impaired lipid metabolism, oxidative stress, and ferroptosis-related alterations. Epigenetically, H3K27ac levels increased while H3K27me3 decreased. Moreover, miR-34a, miR-132, and miR-331 were downregulated, implicating a miRNA-mediated mechanism in PPARα-linked cardiac hypertrophy. Treatment with Ebs, a redox-active compound with inhibitory effects on ferroptosis and epigenetics, reversed hypertrophic phenotype and restored miRNA levels. In conclusion, we found that PPARα depletion promotes oxidative stress and hypertrophic phenotype and that Ebs may act as a potential therapeutic agent. Full article

Virtual-reality exposure therapy (VRET) is an emerging treatment for psychiatric disorders that enables immersive and controlled exposure to anxiety-provoking stimuli. Recent developments integrate real-time physiological monitoring, including heart rate (HR), electrodermal activity (EDA), and electroencephalography (EEG), to dynamically tailor therapeutic interventions. This systematic review examines studies that combine VRET with physiological data to adapt virtual environments in real time. A comprehensive search of major databases identified fifteen studies meeting the inclusion criteria: all employed physiological monitoring and adaptive features, with ten using biofeedback to modulate exposure based on single or multimodal physiological measures. The remaining studies leveraged physiological signals to inform scenario selection or threat modulation using dynamic categorization algorithms and machine learning. Although findings currently show an overrepresentation of anxiety disorders, recent studies are increasingly involving more diverse clinical populations. Results suggest that adaptive VRET is technically feasible and offers promising personalization benefits; however, the limited number of studies, methodological variability, and small sample sizes constrain broader conclusions. Future research should prioritize rigorous experimental designs, standardized outcome measures, and greater diversity in clinical populations. Adaptive VRET represents a frontier in precision psychiatry, where real-time biosensing and immersive technologies converge to enhance individualized mental health care. Full article

Previous work has shown that mouse models fed a non-obesogenic high-fat diet have preserved cardiac function and no obesity-associated comorbidities such as diabetes. However, they do suffer increased cardiac vulnerability to ischemic reperfusion (I/R) injury, which has been attributed to changes in Ca²⁺ handling, oxidative stress, and mitochondrial transition pore activity. However, there have been no studies investigating the involvement of metabolites. Wild-type mice were fed either a control or a non-obesogenic high-fat diet for ~26 weeks. Key cardiac metabolites were extracted from freshly excised hearts and from hearts exposed to 30 min global ischemia followed by 45 min reperfusion. The extracted metabolites were measured using commercially available kits and HPLC. Hemodynamic cardiac function was monitored in Langendorff perfused hearts. Levels of energy-rich phosphates and related metabolites were similar for both hearts fed a control or a high-fat diet. However, the high-fat diet decreased cardiac glycogen and increased cardiac lactate, hypoxanthine, alanine, and taurine levels. Langendorff perfused hearts from the high-fat diet group suffered more ischemic stress during ischemia, as shown by the significantly shorter time needed for onset and for reaching maximal ischemic (rigor) contracture. Following I/R, there was a significant decrease in myocardial adenine nucleotides and a significant increase in the levels of alanine and purines for both groups. Most of the principal amino acids tended to fall during I/R. Hearts from mice fed a high-fat diet showed more changes during I/R in markers of energetics (phosphorylation potential and energy charge), metabolic stress (lactate), and osmotic stress (taurine). This study suggests that cardiac metabolic changes due to high-fat diet feeding, independent of obesity-related comorbidities, are responsible for the marked metabolic changes and the increased vulnerability to I/R. Full article

Galectin-3 (Gal-3), a multifunctional protein, plays a pivotal role in a wide range of physiological and pathological processes in the human body. Substantial evidence has linked its overexpression and secretion to the pathogenesis of various conditions, including diabetes mellitus, heart failure, fibrosis, atherosclerosis, and chronic kidney disease. Diabetes mellitus, a persistent metabolic disorder, exerts profound effects on both renal and cardiovascular systems. Contemporary research has investigated a range of various biomarkers aimed at predicting the early onset of renal and cardiac dysfunction in diabetic patients. An early decline in glomerular filtration rate (GFR) may occur even with normal urinary albumin excretion. Given that NT-proBNP concentrations are influenced by GFR, there is a critical need to identify biomarkers capable of detecting early cardio–renal injury in individuals with diabetes. Elevated Gal-3 levels in diabetic patients have been associated with an increased risk of all-cause mortality, cardiovascular disease, and progressive kidney failure and may serve as an indicator of subclinical cardiac and renal dysfunction. Incorporating Gal-3 assessment into clinical practice has the potential to improve diagnostic precision and support personalized management for cardiovascular, renal, and metabolic disorders. This review aims to elucidate the role of Gal-3 as a pivotal biomarker for diagnosis, prognosis, and therapeutic guidance in general in different types of diseases which involve cardio–renal complications. Full article

Background: Chronic heart failure (CHF) continues to present significant prognostic challenges despite advances in diagnosis and therapy. While the N-terminal prohormone of brain natriuretic peptide (NT-proBNP) is widely recognized as a key marker of cardiac stress, and serum albumin reflects systemic inflammation and nutritional status, their integration into a single parameter—the NT-proBNP-to-albumin ratio (NTAR)—may improve risk stratification. This study aimed to evaluate the NTAR as a novel biomarker for predicting in-hospital mortality in patients with CHF. Methods: We performed an exploratory, retrospective, observational, single-center study involving 542 patients (306 males) admitted for CHF between January 2022 and August 2024. NTAR was calculated as log₁₀(NT-proBNP/albumin). Statistical analyses included ROC curves, univariate and multivariable Cox regression, and Kaplan–Meier survival analysis. Sex-specific performance of NTAR was compared against NT-proBNP and serum albumin alone. Results: Females had significantly lower serum albumin levels than males, while NT-proBNP levels were similar across sexes. NTAR increased with NYHA functional class and was highest in patients with heart failure with reduced ejection fraction (HFrEF). NTAR showed very good discriminatory performance for predicting in-hospital mortality (AUC = 0.840, 95% CI: 0.794–0.879, p < 0.001), marginally but statistically outperforming NT-proBNP in the male subgroup. In univariate Cox regression analyses, higher serum albumin was significantly associated with reduced in-hospital mortality risk in males (HR = 0.352; 95% CI: 0.154–0.803; p = 0.010) and females (HR = 0.169; 95% CI: 0.072–0.399; p < 0.001). Elevated NT-proBNP levels were associated with increased mortality risk in males (HR = 8.627; 95% CI: 1.956–38.042; p < 0.001) and females (HR = 6.060; 95% CI: 1.498–24.521; p = 0.002) with similar findings in NTAR (HR_males = 10.318, 95% CI: 2.452–43.417, p < 0.001 and HR_females = 7.542, 95% CI: 1.874–30.358, p < 0.001). Multivariable analysis identified NTAR as the strongest independent predictor for in-hospital mortality among males. Conclusions: These findings suggest that NTAR effectively integrates cardiac and systemic dysfunction to improve mortality risk stratification in CHF, particularly in male patients. Its ease of calculation from routinely available biomarkers supports its clinical applicability. Full article

Background: Tacrolimus is a cornerstone of immunosuppressive therapy following heart transplantation. Despite routine therapeutic drug monitoring (TDM), substantial interindividual variability in tacrolimus pharmacokinetics presents a persistent challenge. Pharmacogenetic profiling—particularly of CYP3A5 and CYP3A4 polymorphisms—offers a promising approach to individualize tacrolimus dosing and improve clinical outcomes. Case Presentation: We describe a 54-year-old male heart transplant recipient with persistently subtherapeutic tacrolimus trough concentrations despite escalating standard doses. Tacrolimus dosing initially started at 3.5 mg twice daily, escalated to 7.0 mg twice daily, with final maintenance dosing at 6.5 mg twice daily. TDM values were persistently subtherapeutic at 3–5 ng/mL for over a month before achieving therapeutic targets >10 ng/mL. Pharmacogenetic testing revealed a CYP3A5 expresser genotype (*1/*3) and normal CYP3A4 activity (*1/*1), suggesting enhanced metabolic clearance. In accordance with CPIC guidelines, tacrolimus dosing was intensified and supported by co-administration of diltiazem (60 mg twice daily, later adjusted to 90 mg twice daily), a CYP3A4 inhibitor. Subsequent TDM confirmed achievement of therapeutic levels. At nine months post-transplant, the patient exhibited stable graft function and excellent clinical status. Discussion: This case underscores the value of genotype-informed tacrolimus dosing in clinical scenarios where standard TDM is insufficient. Pharmacogenetic variation—particularly involving CYP3A5 expression—has been consistently associated with altered tacrolimus exposure and dose requirements. The literature supports routine genotyping in solid organ transplant recipients, although implementation remains limited. Additional considerations include drug–drug interactions, notably with CYP3A-modulating agents such as diltiazem and antifungals, which may further influence tacrolimus pharmacokinetics. Current evidence suggests that the utility of CYP3A4 genotyping may be phase-dependent, being more impactful during early post-transplant periods. Conclusions: Incorporating pharmacogenetic data alongside TDM facilitates more precise and individualized tacrolimus therapy, optimizing immunosuppressive efficacy and minimizing risk. This case, supported by literature review, advocates for broader integration of genotype-guided strategies in transplant pharmacotherapy. Full article

Background: Ebstein’s anomaly (EA) is a rare congenital heart defect characterized by failure of tricuspid valve delamination during embryogenesis. Left ventricular (LV) hypertrabeculation results from incomplete myocardial compaction during fetal development. EA is associated with LV hypertrabeculation in 0.14% of cases, and EA is the most common congenital heart disease in LV hypertrabeculation (up to 29%), suggesting a shared embryogenetic pathway. Case Report: We describe a female patient prenatally diagnosed with EA and a large ventricular septal defect. Postnatal echocardiography confirmed EA with moderate regurgitation and revealed previously unnoticed left ventricular excessive trabeculations. Whole exome sequencing revealed a heterozygous never-described variant of unknown significance in the TNNC1 gene. Discussion: The genetic link between EA and LV hypertrabeculation remains unclear, though variants in sarcomeric or cytoskeletal genes like MYH7, TPM1, and NKX2.5—essential for cardiac development—have been implicated. A developmental hypothesis suggests that aberrant contraction during endocardial-to-mesenchymal and epicardial-to-mesenchymal transformation (5th–8th gestational weeks) may affect valve delamination and ventricular compaction via parallel signaling pathways. TNNC1 encodes troponin C1, a subunit of the troponin complex involved in muscle contraction. Its mutations are known to alter calcium sensitivity and impair cardiac contractility. Conclusions: EA and LV hypertrabeculation patients diagnosed in infancy have a greater risk of negative outcomes. Early, especially prenatal, diagnosis is crucial. Genetic analysis can provide fundamental insight into cardiac development. This new and rare variant of TNNC1 gene supports the hypothesis that early cardiomyocytes dysfunction disrupts both valve delamination and left ventricular compaction and that the two diseases share a common genetic pathway related to cardiomyocyte contraction. Full article

Background: Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by both motor and non-motor symptoms, including autonomic dysfunction. Structural alterations in the vagus nerve (VN) may contribute to PD pathophysiology, though existing data remain inconsistent. Objective: This study aimed to evaluate morphological changes in the VN using high-resolution ultrasound (USVN) and to investigate associations with autonomic symptoms, heart rate variability (HRV), and clinical characteristics in PD patients. Methods: A cross-sectional study was conducted involving 60 PD patients and 60 age- and sex-matched healthy controls. USVN was performed to assess VN cross-sectional area (CSA), echogenicity, and homogeneity bilaterally. Autonomic symptoms were measured using the Composite Autonomic Symptom Scale 31 (COMPASS-31). HRV parameters—SDNN, RMSSD, and pNN50—were obtained via 24 h Holter monitoring. Additional clinical data included Unified Parkinson’s Disease Rating Scale (UPDRS) scores, transcranial sonography findings, and third ventricle width. Results: PD patients showed significantly reduced VN CSA compared to controls (right: 1.90 ± 0.19 mm² vs. 2.07 ± 0.18 mm²; left: 1.74 ± 0.21 mm² vs. 1.87 ± 0.22 mm²; p < 0.001 and p < 0.02). Altered echogenicity and decreased homogeneity were also observed. Right VN CSA correlated with body weight, third ventricle size, and COMPASS-31 scores. Left VN CSA was associated with body size parameters and negatively correlated with RMSSD (p = 0.025, r = −0.21), indicating reduced vagal tone. Conclusions: USVN detects structural VN changes in PD, correlating with autonomic dysfunction. These findings support its potential as a non-invasive biomarker for early autonomic involvement in PD. Full article

Cirrhotic cardiomyopathy (CCM) is a cardiac dysfunction in patients with cirrhosis, occurring in the absence of structural heart disease. It increases perioperative risk, especially in liver transplantation, and may contribute to hepatorenal syndrome. Despite its clinical significance, CCM remains poorly understood and lacks effective treatments. This review aims to summarize recent findings on the pathogenesis of CCM and highlight potential therapeutic targets. A focused literature review was conducted using PubMed, Scopus, and Clarivate databases, selecting studies from the last five years. Included studies investigated molecular, cellular, and receptor-mediated mechanisms involved in CCM. Results: CCM results from neurohumoral, inflammatory, and electrophysiological disturbances. Key mechanisms involve dysfunction of β-adrenergic and muscarinic receptors, altered ion channels (potassium, L-type calcium), impaired sodium–calcium exchange, and suppression of the P2X7 receptor (P2X7R). Dysregulation of the CD73 (5’-nucleotidase, ecto-5’-nucleotidase)–A2 adenosine axis, along with effects from endocannabinoids, nitric oxide (NO) inhibition by tumor necrosis factor α (TNF-α) and interleukin-6 (IL-6), carbon monoxide (CO), and elevated galectin-3 (Gal-3), further contribute to myocardial dysfunction. Conclusions: CCM is a multifactorial condition linked to systemic and myocardial effects of cirrhosis. A deeper understanding of its mechanisms is essential for developing targeted therapies. Further research is needed to improve patient outcomes. Full article

Background/Objectives: The Internet of Things (IoT), integrated with application software, has increasingly been used to support health management through monitoring indicators like physical activity, sleep, and heart rate, in pregnant and postpartum women. However, limited evidence exists regarding its effectiveness in improving health outcomes for pregnant and postpartum women. The objective of this systematic review and meta-analysis was to evaluate and synthesize the role of IoT in enhancing the health outcomes of pregnant and postpartum women. Methods: A systematic search was conducted on 13 February 2023, across CENTRAL, CINAHL, ClinicalTrials.gov, Embase, MEDLINE, PsycINFO, PubMed, and WHO ICTRP to identify all randomized controlled trials. Studies were included if they involved pregnant or postpartum women in high-income countries and used sensor-based data collection via smartphones or wearable devices. Two reviewers independently selected the studies, extracted data, and assessed the risk of bias using the Cochrane Collaboration’s risk of bias assessment tool 2.0. We performed a pairwise meta-analysis using a random effects model. The findings were reported according to PRISMA guidelines. Results: Seven studies with 1638 pregnant and postpartum women were included in this review. Of the seven included studies, half targeted women with gestational diabetes and the other half targeted obese women. A meta-analysis revealed that IoT interventions may reduce gestational weight gain in women with obesity with a mean difference of −3.35 kg (95% confidence interval (CI): −5.23 to−1.46; I² = 36%; two studies; 242 women; moderate certainty of evidence). Conclusions: This review suggested that IoT interventions may limit gestational weight gain in pregnant women with obesity. Future studies should evaluate the long-term effects of IoT-based interventions on maternal and neonatal health outcomes. Full article

Cardiovascular diseases, which are among the most common diseases of the population and among the leading causes of death, are a constant topic of many research centers. A deeper understanding of their pathogenesis may contribute to the development of innovative diagnostic and therapeutic techniques. Recently, the role of myokines—a group of cytokines secreted mainly by muscle cells—has been increasingly emphasized in the development of these diseases. Both their excess and deficiency can cause undesirable effects that are involved in the pathomechanism of these diseases. In this review, we focus on the latest studies on the role of myonectin, irisin, musclin, follistatin-like1 (FSTL1), dermcidin, apelin, and myostatin in the pathogenesis of coronary artery disease, heart attack, heart failure, and hypertension. In particular, we look at myostatin and irisin in the context of the development of heart failure and decreased levels of apelin with higher cardiovascular risk in a group of patients with rheumatoid arthritis. Full article

Litopenaeus vannamei, commonly known as the Pacific white shrimp, is one of the most economically significant species in global aquaculture, valued for its rapid growth and adaptability. However, the mechanisms regulating its growth, especially under high-density farming and environmental stress, remain poorly understood. Previous study predicted that LvSlc12A2 was involved in growth regulation. To further reveal the function of this gene in the growth regulation of the whiteleg shrimp, in this study, we explore its function using RT-qPCR, RNA interference, overexpression, and tissue in situ hybridization. RT-qPCR results showed that LvSlc12A2 was highly expressed in gills (about 62%), followed by the hepatopancreas, with the lowest expression in muscle (0.08%, compared to the gills). Myostatin (LvMstn) was mainly expressed in the heart, and molt-inhibiting hormone (LvMIH) in the ventral nerve. In situ hybridization of gill tissues using the mRNA of the gene as a probe revealed strong LvSlc12A2 signals in the gill stratum and epithelial cells. Overexpression of LvSlc12A2, significantly decreased the osmotic gene aquaporin (LvAqp), while knockdown increased its expression. Additionally, levels of growth-related inhibitory genes LvMstn and LvMIH increased significantly after LvSlc12A2 overexpression and were downregulated after its knockdown, suggesting LvSlc12A2 negatively regulates growth, possibly in synergy with LvMstn and LvMIH. These findings indicate LvSlc12A2 influences growth both by negative regulation and by modulating osmotic balance in gill tissues. Full article

Obesity Hypoventilation Syndrome (OHS), also known as Pickwickian syndrome, is a complex disorder characterized by obesity (BMI > 30 kg/m²), daytime hypercapnia (PaCO₂ ≥ 45 mmHg), and sleep-disordered breathing, primarily affecting individuals with severe obesity. Its diagnosis requires the exclusion of other causes of alveolar hypoventilation and involves comprehensive assessments, including clinical history, physical examination, pulmonary function tests, arterial blood gases, and sleep studies. The pathophysiology of OHS involves mechanical constraints from excessive adipose tissue, diminished central respiratory drive often linked to leptin resistance, mitochondrial dysfunction, and oxidative stress, all contributing to impaired ventilation and systemic inflammation. The condition often coexists with obstructive sleep apnea (OSA), exacerbating nocturnal hypoxia and hypercapnia, which can lead to severe cardiopulmonary complications such as pulmonary hypertension and right-sided heart failure. Epidemiologically, the rising global prevalence of obesity correlates with an increased incidence of OHS, yet underdiagnosis remains a significant challenge, often resulting in critical presentations like acute hypercapnic respiratory failure. Management primarily centers on non-invasive ventilation modalities like CPAP and BiPAP, with an emphasis on individualized treatment plans, continuous monitoring, and addressing comorbidities such as hypertension and diabetes. Pharmacological interventions are still evolving, focusing on supportive care and metabolic regulation. Long-term adherence, psychological factors, and complications like ventilator failure or device intolerance highlight the need for ongoing multidisciplinary management. Overall, advancing our understanding of OHS’s multifactorial mechanisms and optimizing tailored therapeutic strategies are crucial for improving patient outcomes and reducing mortality associated with this increasingly prevalent syndrome. Full article