Impact of Metabolic Dysfunction-associated Steatotic Liver Disease on Cardiovascular Structure, Function, and the Risk of Heart Failure Article

Full Text via DOI: 10.1016/j.cjca.2025.04.012 Web of Science: 001583152300007

Cited authors

  • Bansal B, Lajeunesse-Trempe F, Keshvani N, Lavie CJ, Pandey A

Abstract

  • Mounting evidence has established metabolic dysfunction-associated steatotic liver disease (MASLD) as an independent risk factor for heart failure (HF), particularly HF with preserved ejection fraction (HFpEF). In this narrative review we explore the impact of MASLD on cardiovascular structure and function. We summarize findings from multiple cohort studies demonstrating that MASLD is associated with distinct patterns of adverse cardiac remodeling, including increased left ventricular concentricity and impaired diastolic function. These subclinical changes in cardiac structure and function often precede overt HF development and appear to occur in the context of multiple interconnected pathways involving metabolic dysfunction, systemic inflammation, adipose tissue dysregulation, vascular dysfunction, and altered hepatic hemodynamics. Early identification of cardiac structural and functional abnormalities through systematic screening may enable timely intervention in this high-risk population. Lifestyle modifications remain foundational, but achieving and maintaining signifi-cant weight loss is challenging. Recent clinical trials have shown promising results with cardiometabolic agents, particularly glucagonlike protein 1 receptor agonists, which demonstrate significant weight loss and hepatic and cardiovascular benefits. Despite these advances, key knowledge gaps remain regarding optimal screening strategies, mechanisms linking MASLD to HF, and targeted therapeutic approaches. Addressing these gaps will be essential for developing effective prevention and treatment strategies in this high-risk population.

Authors

Publication date

  • 2025

Published in

International Standard Serial Number (ISSN)

  • 0828-282X

Number of pages

  • 17

Start page

  • 1777

End page

  • 1793

Volume

  • 41

Issue

  • 9