HFpEF Beyond the Heart: Exploring the Heart–Liver–Pancreas Axis

Figures

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  Figure 1. Proposed model illustrating heart–liver axis in patients with heart failure including congestive hepatopathy, acute cardiogenic liver injury, and cardiac cirrhosis. Resultant cardiac cirrhosis can exacerbate heart failure causing cirrhotic cardiomyopathy. Created in BioRender. Rahal, O. (2025) https://BioRender.com/u3cv6z8

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  Figure 2. Diagram illustrating the pathogenesis of acute pancreatitis and how spill-over of inflammatory cytokines causes SIRS resulting cardiovascular manifestations. After a strong immune response such as SIRS, a compensatory anti-inflammatory response increases the risk of developing infected pancreatic necrosis which can potentially lead to sepsis and worsening of multi-organ disturbances. Created in BioRender. Rahal, O. (2025) https://BioRender.com/c6zymrb

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  Figure 3. Proposed model of the heart–liver–pancreatic exocrine insufficiency axis in heart failure. Heart failure causes systemic inflammation, autonomic dysfunction, pancreatic hypoperfusion, and congestion all of which contribute to the pathogenesis of pancreatic exocrine insufficiency. Pancreatic exocrine insufficiency causes malabsorption of micronutrients worsening the cachexia and metabolic decline which may worsen heart failure. Created in BioRender. Rahal, O. (2025) https://BioRender.com/07qhwc9

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  Figure 4. Proposed integrated heart–liver–pancreas inflammation axis. Acute pancreatitis has a unidirectional inflammatory relationship with heart failure with preserved ejection fraction and pancreatic exocrine insufficiency, while the latter two form a vicious loop with continuing deconditioning of both organs. Metabolic dysfunction-associated steatotic liver disease underlying metabolic interaction further contributes to the development of heart failure with preserved ejection fraction and indirectly exerts deleterious effects on the pancreas