Management of metabolic dysfunction and cardiovascular risk in patients with MASLD

Pojsakorn Danpanichkul; Hanna Blaney; Javiera Perelli; Paula Huerta; Francisco Idalsoaga; Marco Arrese; Juan Pablo Arab; Rohit Loomba; Luis Antonio Díaz

doi:10.20517/mtod.2025.32

Management of metabolic dysfunction and cardiovascular risk in patients with MASLD

Journal

Metabolism and Target Organ Damage

ISSN

2769-6375

Date Issued

2026-01-21

Author(s)

Pojsakorn Danpanichkul

Hanna Blaney

Javiera Perelli

Paula Huerta

Facultad de Medicina Clínica Alemana Universidad del Desarrollo

Francisco Idalsoaga

Marco Arrese

Juan Pablo Arab

Rohit Loomba

Luis Antonio Díaz

Type

journal-article

DOI

10.20517/mtod.2025.32

URL

https://hdl.handle.net/123456789/12077

Abstract

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a leading global cause of chronic liver disease and is strongly linked to cardiovascular disease (CVD), which remains the primary cause of death in affected individuals. This narrative review summarizes contemporary evidence on the MASLD–CVD interface and outlines a practical framework for cardiovascular risk assessment and comorbidity management. We discuss how liver disease severity can inform cardiovascular risk stratification beyond traditional scores, including cardiovascular imaging, biomarkers of myocyte injury and stress, inflammation markers, proteomics, lipidomics, and lipid profiles. Lifestyle interventions - dietary optimization, weight loss, and increased physical activity - remain foundational and improve hepatic steatosis and key cardiometabolic parameters. Pharmacotherapies with relevance to MASLD and cardiometabolic disease - including β-selective thyromimetics, incretin-based therapies, sodium–glucose cotransporter 2 inhibitors, and pioglitazone - offer benefits across weight, glycemic control, and metabolic risk, while statins remain the cornerstone of dyslipidemia management and CVD prevention in MASLD. For patients who do not achieve lipid targets or are statin-intolerant, non-statin therapies such as proprotein convertase subtilisin/kexin type 9 inhibitors and bempedoic acid provide additional risk-reduction options. Bariatric surgery can achieve durable weight loss and meaningful improvements in steatohepatitis and fibrosis in carefully selected patients. Finally, we emphasize the need for integrated, multidisciplinary care pathways that coordinate hepatology, cardiology, endocrinology, and primary care to identify high-risk individuals early, tailor intensity of preventive therapies, and address the concurrent liver and CVD burden.