• Pericarditis may be adominant manifestation of severe acute respiratory syndrome coronavirus 2 infection. • Pericarditis should be considered in the patient with chest pain, a normal coronary angiogram, and ST elevation on electrocardiogram. • Basic clinical tools in the setting of the coronavirus disease 2019 epidemic should not be forgotten and may be of great help.

Autoimmune liver diseases involve a heterogeneous group of chronic inflammatory disorders, including autoimmune hepatitis, primary biliary cholangitis, and primary sclerosing cholangitis. Sometimes presented consistently as an overlapping syndrome, their pathogenesis is rather complex and has yet to be fully elucidated, despite extensive research efforts. This review article corroborates the molecular mechanisms of autoimmune liver diseases, as well as existing and potential therapeutic modalities.

Cirrhosis is no longer viewed solely as an isolated hepatic disorder but rather as a complex multisystemic disease that affects cardiovascular, renal, pulmonary, metabolic, and immune systems. One of its most clinically relevant but under-recognized consequences is cardiac dysfunction, manifesting as cirrhotic cardiomyopathy, portopulmonary hypertension, right ventricular (RV) failure, and impaired myocardial strain. Oxidative stress (OS) has recently emerged as a fundamental mechanistic link between hepatic fibrogenesis and myocardial remodeling, acting through mitochondrial injury, NADPH oxidase activation, nitric oxide dysregulation, iron-mediated ferroptosis, and inflammatory cytokines. These alterations lead to diastolic dysfunction, autonomic imbalance, myocardial fibrosis, electrophysiological abnormalities (including QTc prolongation), and impaired RV–pulmonary artery coupling. Redox biomarkers such as malondialdehyde (MDA), NOX2-derived peptides, GSH/GSSG ratio, sST2, NT-proBNP, and 8-isoprostanes hold promise in detecting early subclinical cardiac involvement in cirrhosis. Novel antioxidant therapies, including mitochondrial-targeted molecules, NOX inhibitors, and ferroptosis blockers, may improve myocardial remodeling and hemodynamic stability. This review explores the central role of redox imbalance in the cardiohepatic syndrome and its potential utility in diagnosis, monitoring, and therapy.

The heart and liver are closely interconnected through complex hemodynamic, neurohumoral, inflammatory, and metabolic mechanisms. Dysfunction of either organ may adversely affect the other, giving rise to a broad spectrum of cardiohepatic disorders with important diagnostic and prognostic implications. This narrative review is based on a literature search strategy of PubMed and the Web of Science Core Collection covering publications from January 2000 through June 2026, with a focus on hypoxic hepatitis, congestive hepatopathy, and cirrhotic cardiomyopathy. Cardiac diseases may induce liver injury through acute hypoperfusion or chronic venous congestion, resulting in distinct clinical entities characterized by different pathophysiological mechanisms, laboratory findings, imaging features, and therapeutic approaches. Conversely, advanced liver disease may be associated with impaired cardiovascular function, including cirrhotic cardiomyopathy, a condition that frequently remains clinically silent until physiological or therapeutic stress unmasks impaired cardiac reserve. Recent advances in multimodal imaging, including echocardiography with myocardial deformation analysis, abdominal ultrasonography with Doppler evaluation, elastography, computed tomography, and cardiac magnetic resonance, together with emerging biomarkers, have provided additional tools for the recognition and characterization of these disorders, although the clinical value of some newer techniques and biomarkers remains under investigation. Nevertheless, differentiating congestion-related liver injury from progressive fibrosis and identifying subclinical cardiac dysfunction remain important clinical challenges. A comprehensive understanding of the bidirectional interactions between the heart and liver is important for timely diagnosis, accurate risk stratification, and appropriate management. Future studies should focus on standardized diagnostic pathways, validation of novel imaging techniques and biomarkers, and multidisciplinary strategies that may improve outcomes in patients with complex cardiohepatic disease.

Background/Objectives: In heart failure with preserved ejection fraction (HFpEF), the gut–heart axis has emerged as a potential contributor to inflammation and cardiometabolic stress. We characterised gut microbiota composition, diversity, and predicted metabolic potential in HFpEF to assess their associations with disease status and clinical heterogeneity. Methods and Results: Faecal samples from 30 HFpEF patients and 28 healthy controls were profiled by means of bacterial ribosomal RNA gene sequencing. The groups were comparable in age (74 years in both groups) and sex (female: 60% vs. 60.7%). HFpEF patients exhibited lower community evenness (p = 0.04) and a trend toward lower diversity (p = 0.08), but no detectable shift in global community structure. The tested clinical and demographic variables explained only a modest proportion of the observed variation in community structure, with substantial residual variation across the beta-diversity analyses. No taxa were differentially abundant between groups at the predefined thresholds. Among clinical stratifications, New York Heart Association (NYHA) class showed the most consistent family-level associations, including stepwise depletion of Lachnospiraceae, Butyricicoccaceae, and Ruminococcaceae and enrichment of Akkermansiaceae; Enterobacteriaceae peaked in milder disease. These severity-associated taxonomic trajectories were accompanied by predicted functional shifts consistent with microbial adaptation to increasing metabolic constraints, including enrichment of stress-adaptation traits and, with increasing functional limitation, depletion of core metabolic and fermentative pathways and relative enrichment of oxidative stress-response pathways. Conclusions: HFpEF is associated with subtle gut microbiota alterations that appear to reflect severity- and context-dependent ecological reorganisation rather than uniform dysbiosis. These findings support severity-informed approaches targeting microbial metabolic function and ecological context rather than broad compositional changes.