NEUROHUMORAL MECHANISMS IN PATIENTS WITH HEART FAILURE ASSOCIATED WITH METABOLIC DYSFUNCTION-ASSOCIATED FATTY LIVER DISEASE
Keywords:
heart failure, MASLD, metabolic dysfunction-associated steatotic liver disease, neurohumoral activation, sympathetic nervous system, renin–angiotensin–aldosterone system, natriuretic peptides, insulin resistance, inflammation, hepatic fibrosis.Abstract
The coexistence of heart failure (HF) and metabolic dysfunction-associated steatotic liver disease (MASLD) represents an important interdisciplinary problem in contemporary cardiology and hepatology. These conditions share several metabolic, inflammatory, hemodynamic, and neurohumoral mechanisms. Particular importance is attributed to activation of the sympathetic nervous system and the renin–angiotensin–aldosterone system (RAAS), increased circulating catecholamines, vasopressin and endothelin-1, and alterations in the natriuretic peptide system.\
MASLD should not be considered solely a hepatic disorder. It is increasingly recognized as a systemic cardiometabolic condition associated with insulin resistance, visceral adiposity, dyslipidemia, chronic low-grade inflammation, endothelial dysfunction, oxidative stress, and cardiovascular remodeling. Current evidence indicates a close relationship between MASLD and heart failure, particularly heart failure with preserved ejection fraction (HFpEF). The cardiovascular risk appears to increase with progression of hepatic fibrosis.
The aim of this review is to summarize current concepts regarding the neurohumoral mechanisms involved in the development and progression of heart failure in patients with MASLD and to discuss potential approaches to the integrated diagnosis and management of this comorbid condition.
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