BACKGROUND AND AIMS: Metabolic dysfunction-associated steatotic liver disease (MASLD) has recently replaced non-alcoholic fatty liver disease (NAFLD) as the preferred nomenclature, reflecting a shift toward inclusion-based diagnostic criteria rooted in metabolic dysfunction. Beyond its hepatic implications, MASLD has emerged as an independent, modifiable driver of cardiovascular disease (CVD).
METHODS: This review summarizes and synthesizes robust epidemiological and mechanistic evidence linking MASLD to cardiovascular outcomes.
RESULTS: MASLD is associated with increased risk of coronary artery disease, myocardial infarction, atrial fibrillation, stroke, and heart failure-particularly heart failure with preserved ejection fraction (HFpEF). Shared pathophysiological mechanisms include insulin resistance, chronic inflammation, oxidative stress, endothelial dysfunction, and atherogenic dyslipidemia, which collectively contribute to both hepatic fibrogenesis and vascular injury. Fibrosis stage, the strongest predictor of hepatic outcomes, also correlates with subclinical atherosclerosis and cardiovascular mortality, yet remains unaccounted for in current CVD risk models. Non-invasive fibrosis markers such as FIB-4 and elastography, originally developed for hepatology, are gaining traction in cardiovascular risk stratification. Furthermore, pharmacologic agents such as GLP-1 receptor agonists and SGLT2 inhibitors demonstrate dual efficacy in improving hepatic, metabolic, and cardiovascular outcomes.
CONCLUSIONS: This review provides an updated synthesis for cardiologists, outlining the evolution of MASLD nomenclature, its systemic pathophysiology, and its clinical implications-underscoring the urgent need for integrated, multidisciplinary management of this underrecognized cardiometabolic disease.
