Heart failure with preserved ejection fraction is increasingly recognized as a systemic disorder driven by inflammation, congestion, and metabolic dysbiosis along a hepato-pancreato-cardiac axis.
Abstract It has become increasingly recognized that heart failure with a preserved ejection fraction (HFpEF) results from an inflammatory process, congestion, and metabolic dysbiosis rather than an intrinsic structural heart abnormality. Recent studies have highlighted the close link between the heart, the liver, and the pancreas, which are organically connected via the same inflammatory processes and pathways. Liver congestion and fibrosis are responsible for the inflammatory process and the lack of metabolic adaptation, whereas pancreatic ischemia and insufficiency of the exocrine glands aggravate malnutrition and cachexia, worsening the heart condition. Acute pancreatitis may cause heart failure and arrhythmia through injury and systemic inflammatory response syndrome (SIRS), an inflammatory process mediated by the cytokines released during the injury process. Recognition of this hepato–pancreato–cardiac axis offers a paradigm shift toward integrated management of HFpEF, emphasizing anti-inflammatory, metabolic, and hemodynamic interventions. Future research integrating multi-organ imaging, inflammatory biomarkers, and therapeutic trials such as GLP-1 receptor agonists, SGLT2 inhibitors, and cytokine blockers will be critical to disrupt this tri-organ inflammatory circuit and improve outcomes in HFpEF.
Tun et al. (Thu,) conducted a review in Heart failure with a preserved ejection fraction (HFpEF). Heart failure with preserved ejection fraction is increasingly recognized as a systemic disorder driven by inflammation, congestion, and metabolic dysbiosis along a hepato-pancreato-cardiac axis.