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/Objectives: Inflammatory bowel disease (IBD) has widely been associated with various extraintestinal complications, including kidney disease. The literature suggests that IBD patients are at increased risk of developing chronic kidney disease (CKD). This study aims to assess the relationship between IBD and CKD, and to identify risk factors associated with CKD in patients with IBD. Methods: Data for hospitalized patients with IBD was obtained from The National Inpatient Sample (NIS) database from 2016 to 2020. Baseline risk factors were identified using ICD-10 codes. Patients were stratified into two groups: Crohn’s Disease (CD) and Ulcerative Colitis (UC). Primary outcomes were prevalence and risk factors of CKD. Secondary outcomes were mortality and length of hospital stay (LOS). Univariate and multivariate analyses were conducted using SPSS v. 30. Results: We identified 230,766 patients with IBD: 144,847 (63%) had CD and 85,919 (37%) had UC. After 1:1 matching, 148,498 patients were included: 74,249 with CD and 74,249 with UC. In this study group, the prevalence of CKD in patients with CD and patients with UC was the same (7.2%). CD patients with CKD had lower in-hospital mortality rates and lower in-hospital length of stay compared to UC patients with CKD. Conclusions: While the prevalence of CKD is similar amongst CD and UC patients, the risk factors and outcomes such as mortality and length of hospitalization differ significantly. This study emphasizes the need for tailored approaches and closer monitoring for the risk of developing CKD in IBD patients and especially patients with UC.
Mediastinal abscesses are life-threatening infections traditionally managed with surgical or percutaneous drainage. Endoscopic ultrasound (EUS)-guided drainage has emerged as a minimally invasive alternative for deep-seated collections, but experience with mediastinal abscesses remains limited. We present a case of successful EUS-guided transesophageal drainage of a posterior mediastinal abscess complicating vertebral osteomyelitis. A 50-year-old man with T3-T4 vertebral osteomyelitis and a posterior mediastinal abscess underwent EUS-guided drainage after percutaneous access was deemed unfeasible. A 19-gauge needle was used for aspiration, followed by guidewire placement and double-pigtail stent insertion. Technical success was achieved with placement of a 7-French × 4-cm double-pigtail stent. Blood and fluid cultures grew methicillin-sensitive Staphylococcus aureus . Complete radiographic resolution was confirmed at 3 days, the stent was removed, and an esophagram on the following day demonstrated no leak. The patient was discharged on a 6-week course of intravenous antibiotics with resolution of all clinical symptoms. EUS-guided drainage with short-interval double-pigtail stent placement is a safe and effective minimally invasive approach for posterior mediastinal abscesses when percutaneous access is not feasible.
The recent redefinition of steatotic liver diseases, introducing metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH), reflects a growing consensus among liver societies and marks a paradigm shift in disease classification. MASLD subsumes former categories of nonalcoholic fatty liver disease (NAFLD) and incorporates metabolic criteria alongside moderate alcohol intake, while MASH replaces nonalcoholic steatohepatitis (NASH), aligning terminology with disease mechanisms. This evolution clarifies the diagnostic criteria and minimizes stigma, facilitating more consistent epidemiological and clinical investigations. Recent advances in noninvasive diagnostics, including vibration-controlled transient elastography, magnetic resonance elastography, shear-wave elastography, and the Enhanced Liver Fibrosis test, have improved the identification and stratification of patients with advanced fibrosis. Current guidelines recommend targeted screening in populations at elevated metabolic risk, enabling earlier intervention and personalized management. Population studies indicate that MASLD affects over one-third of adults and is a major contributor to cardiovascular and metabolic morbidity. Therapeutic progress is highlighted by the approval of novel agents such as resmetirom and semaglutide for the treatment of MASH with fibrosis. Emerging dual and triple agonists, as well as sodium–glucose cotransporter inhibitors, offer additional promise, although further research is required to define their long-term efficacy and safety. As the disease prevalence escalates globally, the integration of multidisciplinary care, the ongoing refinement of diagnostic tools, and the expansion of therapeutic options will remain essential to optimizing outcomes for affected individuals.