Heart failure (HF) affects over 55 million individuals globally, with prevalence projected to exceed 11 million in the United States by 2050 and is increasingly recognized as a systemic disorder extending beyond hemodynamic dysfunction to encompass profound alterations in neural and gut physiology. Cognitive impairment affects nearly half of HF patients and represents a major determinant of morbidity, self-care capacity, and mortality. Recent advances suggest that the gut microbiome serves as a pivotal intermediary in the heart–brain crosstalk, influencing neurocognitive outcomes through inflammatory, metabolic, and neurohumoral pathways. Dysbiosis in HF disrupts intestinal barrier integrity, facilitating translocation of endotoxins and microbial metabolites such as trimethylamine-N-oxide (TMAO), short-chain fatty acids (SCFAs), and bile acids, which in turn modulate neuroinflammation, cerebral perfusion, and neuronal signaling. The gut–heart–brain axis provides an integrative framework linking HF and cognitive impairment pathophysiology through dysbiosis-driven systemic inflammation and metabolite dysregulation. Gut-derived biomarkers and microbiome-targeted interventions represent promising strategies for detection of early alterations and precision treatment, highlighting the urge for prospective, multi-omics studies to establish causality and therapeutic efficacy. This review synthesizes current evidence connecting gut microbiome dysbiosis and metabolite alterations to both HF and cognitive impairment pathophysiology and proposes translational strategies for integrating microbiome-targeted therapies in HF patients with cognitive dysfunction.

Background: Type II diabetes (T2DM) is one of the most prevalent metabolic disorders, and its multisystemic health consequences are widely known. Due to skeletal muscle's ability to sequester a vast amount of glucose, muscle function and exercise have become a subject of much research into strategies to prevent and treat T2DM. Myokines are bioactive molecules released by muscle during contraction and involved in several biological processes such as metabolism, inflammation and behaviour. Irisin, a recently discovered myokine, has been implicated in a vast array of physiological roles, including the ability to induce fat beiging. Since beige and brown fat both serve important roles in metabolic regulation, irisin's role in the context of T2DM is the subject of ongoing investigations.Methods: We systematically reviewed articles indexed in PubMed, Scopus and Web of Science that were published between 2011 and 2024 and compared circulating irisin levels in patients affected by T2DM and healthy subjects. As part of our systematic review of the literature, we performed meta‐analysis of the data across all included articles, as well as stratified by body mass index (BMI), country of origin and by average irisin concentration in the control group.Results: We discovered great variability across the included studies in the average irisin levels detected, which spanned four orders of magnitude, hence the attempt at reducing variability by stratifying based on average levels in the control group. While the statistical power of our meta‐analysis was decreased by the great variability in reported irisin concentrations, we nonetheless detected a consistent trend of decreased irisin concentration in T2DM patients compared with healthy controls, regardless of BMI, country of origin or average irisin concentration in the control group.Conclusions: With almost 60 articles included, ours is the first extensive systematic review and meta‐analysis of irisin in T2DM, yet a highly statistically significant association between circulating irisin levels and T2DM could not be established due to the great variability of the data across include articles. Nonetheless, we noticed a trend that is independent of BMI, suggesting a direct relationship between T2DM and irisin that is likely not secondary to diabetic sarcopenia. While our work encourages further research into irisin's potential role in T2DM pathogenesis, the reproducibility of irisin detection methods in biological samples should be determined and standardized protocols should be made available to the research and clinical communities.

Heart failure (HF) affects over 55 million individuals globally, with prevalence projected to exceed 11 million in the United States by 2050 and is increasingly recognized as a systemic disorder extending beyond hemodynamic dysfunction to encompass profound alterations in neural and gut physiology. Cognitive impairment affects nearly half of HF patients and represents a major determinant of morbidity, self-care capacity, and mortality. Recent advances suggest that the gut microbiome serves as a pivotal intermediary in the heart–brain crosstalk, influencing neurocognitive outcomes through inflammatory, metabolic, and neurohumoral pathways. Dysbiosis in HF disrupts intestinal barrier integrity, facilitating translocation of endotoxins and microbial metabolites such as trimethylamine-N-oxide (TMAO), short-chain fatty acids (SCFAs), and bile acids, which in turn modulate neuroinflammation, cerebral perfusion, and neuronal signaling. The gut-heart-brain axis provides an integrative framework linking HF and cognitive impairment pathophysiology through dysbiosis-driven systemic inflammation and metabolite dysregulation. Gut-derived biomarkers and microbiome-targeted interventions represent promising strategies for detection of early alterations and precision treatment, highlighting the urge for prospective, multi-omics studies to establish causality and therapeutic efficacy. This review synthesizes current evidence connecting gut microbiome dysbiosis and metabolite alterations to both HF and cognitive impairment pathophysiology and proposes translational strategies for integrating microbiome-targeted therapies in HF patients with cognitive dysfunction.

Background: The rapid expansion of telehealth has outpaced formal training in virtual interprofessional collaboration across health professions education. Although telehealth and interprofessional education (IPE) competency frameworks exist, limited evidence informs how longitudinal, virtual IPE curricula prepare learners for team-based telehealth practice. Objective: This study evaluated a longitudinal virtual interprofessional telehealth course to examine its impact on learners’ perceived telehealth competencies, understanding of interprofessional roles, and readiness for virtual team-based care. Methods: We conducted a mixed methods evaluation of a 4-week virtual IPE course involving graduate students from medicine, nursing, physical and occupational therapy, and social work. Learners participated in longitudinal standardized patient telehealth encounters, interprofessional debriefing sessions, and asynchronous learning activities. Quantitative outcomes were assessed using a validated postcourse survey. Qualitative data were obtained from open-ended survey responses and analyzed using thematic analysis. Results: Twenty-eight students completed the course and postcourse evaluation. Quantitative findings demonstrated high self-reported confidence in telehealth communication, ethical practice, interprofessional collaboration, and role clarity, with mean scores ranging from 4.4 (0.7) to 4.8 (0.6) on a 5-point Likert scale. Qualitative analysis identified three core themes: (1) development of interprofessional collaboration skills in virtual settings, (2) growth in telehealth-specific clinical and communication competencies, and (3) perceived value of longitudinal standardized patient encounters with iterative feedback. Conclusions: A longitudinal, standardized patient–based virtual IPE curriculum was associated with strong self-reported preparedness for interprofessional telehealth practice among health professions students. These findings support the use of structured, longitudinal virtual IPE models to address evolving educational needs in telehealth training.