Heart failure (HF) continues to be a major global health burden, with persistent morbidity and mortality despite guideline-directed and device-based therapies. Evidence suggests the gut–heart axis is a critical and underrecognized contributor to HF progression. Alterations in cardiac output and systemic venous congestion in HF lead to intestinal hypoperfusion, mucosal edema, and loss of barrier integrity, increasing intestinal permeability, gut dysbiosis, and translocation of microbial products. This systemic translocation is associated with chronic low-grade inflammation that activates innate immune pathways that correlate with endothelial dysfunction, oxidative stress, fibroblast activation, and adverse cardiac remodeling. Gut-derived metabolites derived by microbial metabolism modulate cardiovascular health by altering the metabolic profiles. Dysbiosis results in loss of protective short-chain fatty acid (SCFA)-producing bacteria and enriches pro-inflammatory taxa such as trimethylamine N-oxide (TMAO)-producing bacteria. Elevated TMAO is associated with increased mortality and hospitalization in HF, whereas SCFAs enhance barrier integrity and immune tolerance. Secondary bile acids and uremic toxins such as indoxyl sulfate and p-cresyl sulfate further link dysbiosis to fibrosis and vascular stiffness. Circulating markers such as TMAO, lipopolysaccharide-binding protein (LBP), and soluble CD14 carry prognostic value beyond traditional cardiac biomarkers. This review highlights current experimental, translational, and clinical evidence describing gut dysbiosis and its molecular links to HF progression. Targeting the gut–heart axis represents a novel therapeutic approach in HF. Dietary modulation, probiotics/prebiotics, fecal microbiota transplantation, and inhibitors of microbial metabolic pathways show promise. Future research should emphasize microbiota-based interventions in HF management.

Background: Pressure-Adjusted Heart Rate (PAHR) is a novel hemodynamic index in cardiogenic shock (CS); however, its dynamic outcome remains underexplored. Methods: In this retrospective cohort study, which utilized the Medical Information Mart for Intensive Care IV (MIMIC-IV) database, PAHR was calculated using at least 12 time-matched values of mean arterial pressure (MAP), central venous pressure (CVP), and heart rate (HR) over the first 48 h. Patients receiving early mechanical circulatory support (MCS) were excluded. Multivariable regression assessed PAHR’s association with mortality, requirement of renal replacement therapy (RRT), and invasive mechanical ventilation. Effect estimates were reported per 10-unit increments of PAHR. Results: A total of 772 patients with CS were included. Mean PAHR was 15.9 ± 7.0. In our multivariable analysis, every 10-unit PAHR increase independently predicted in-hospital mortality (adjusted OR 1.97; 95% CI 1.45–2.68; p < 0.001). Using statistically comparable increments, PAHR showed strong association with in-hospital mortality (adjusted OR 1.97; 95% CI 1.45–2.68; p < 0.001) and ICU mortality (adjusted OR 1.85; 95% CI 1.35–2.54; p < 0.001). PAHR strongly predicted the use of RRT (aOR 2.69; p < 0.001) and invasive mechanical ventilation (aOR 2.11; p < 0.001). Among survivors, higher PAHR predicted prolonged ICU stay and vasopressor duration (p < 0.001). Conclusion: PAHR is a promising integrated marker of mortality and morbidity in patients with CS. It serves as a sustained predictor of outcomes, though external validation is required.

New-onset inflammatory bowel disease following Interleukin (IL)-17 inhibitor therapy is a rare iatrogenic complication occurring in 0.5%–1.5% of treated patients, reflecting IL-17's dual role as a systemic pro-inflammatory mediator and intestinal barrier protector. We report 2 cases: a 40-year-old woman who developed secukinumab-associated Crohn's disease and a 25-year-old woman who developed bimekizumab-associated ulcerative colitis, both without previous gastrointestinal history. IL-17 blockade disrupts intestinal homeostasis, triggering dysbiosis and paradoxical Th1/Th2-driven inflammation. Both patients achieved rapid remission following IL-17 inhibitor discontinuation and transition to IL-23 inhibitors. Clinicians should maintain heightened awareness of this complication.

Background: Inflammatory bowel disease (IBD) is a chronic inflammatory disorder that confers an increased risk of venous thromboembolism (VTE) and subsequent pulmonary embolism (PE). The risk stems from chronic systemic inflammation promoting endothelial dysfunction and hypercoagulability. Data on specific inpatient outcomes and procedural needs in patients with IBD with acute PE remains limited. This study explores these outcomes at a national level. Methods: We conducted a Nationwide Inpatient Sample (NIS) database analysis (2016–2020). Adult hospitalizations for acute PE were identified using ICD-10-CM codes and stratified based on IBD status. Multivariable regression analysis was performed to determine independent associations between IBD status and in-hospital mortality, length of stay (LOS), cardiac complications, and ICU-level interventions (intubation, central venous catheterization (CVC), arterial line placement, requirement of vasopressors), and blood transfusion. Results: Among 377,143 acute PE hospitalizations, 4123 (1.1%) had IBD. Patients with IBD were younger (58.72 vs. 62.78 years, p < 0.001) and had lower prevalence of diabetes mellitus, hypertension, end-stage renal disease (ESRD), dyslipidemia, overweight/obesity, coronary artery disease and smoking status (p < 0.05). Despite a favorable baseline profile, patients with IBD had a longer length of stay (LOS) (8.82 vs. 7.30 days, p < 0.001) but no significant association with in-hospital mortality (aOR = 0.93, p = 0.281). Multivariable analysis showed patients with IBD had higher odds of requiring CVC placement (OR = 1.42, p < 0.001), vasopressors (OR = 1.22, p = 0.05), and blood transfusions (OR = 1.78, p < 0.001). Conversely, they had lower odds of cardiac arrest (OR = 0.64, p < 0.001) and cor pulmonale (OR = 0.32, p = 0.012). Conclusions: patients with IBD with acute PE represent a complex population with high resource utilization. Future research is needed the development of IBD-specific PE risk stratification, targeted management, prophylactic and therapeutic anticoagulation guidelines.