Fibrosis-Driven Cardiovascular Risk in Metabolic Dysfunction-Associated Steatotic Liver Disease: Emerging Links With Atherosclerotic Cardiovascular Disease.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly recognized as a multisystem cardiometabolic disorder with major implications for atherosclerotic cardiovascular disease (ASCVD). Although hepatic steatosis has traditionally been considered the hallmark of MASLD, emerging evidence suggests that hepatic fibrosis severity rather than steatosis alone appears to be an important prognostic marker of adverse cardiovascular outcomes. These observations have prompted growing interest in incorporating fibrosis assessment into cardiovascular risk stratification and integrated cardio-hepatic care. This narrative review explores the evolving concept of the "fibrotic cardio-hepatic axis", highlighting the potential mechanistic pathways linking hepatic fibrosis with vascular injury and atherogenesis. Key mechanisms include chronic systemic inflammation, endothelial dysfunction, oxidative stress, proatherogenic lipid alterations, gut-liver-vascular interactions, and prothrombotic states. The review further discusses the expanding role of noninvasive fibrosis assessment tools, including the fibrosis-4 index, enhanced liver fibrosis score, and transient elastography, as emerging cardiovascular risk stratification instruments. Recent imaging studies linking fibrosis severity with coronary artery calcium progression, carotid atherosclerosis, coronary plaque burden, and myocardial remodeling are also examined. Additionally, contemporary therapeutic approaches including glucagon-like peptide-1 receptor agonists, sodium-glucose cotransporter-2 inhibitors, and novel anti-fibrotic agents are reviewed for their potential to simultaneously improve hepatic fibrosis and reduce ASCVD burden. Finally, future directions involving fibrosis-integrated cardiovascular risk models, precision medicine, artificial intelligence, and multidisciplinary cardio-hepatology care pathways are discussed. Recognition of fibrosis as an important cardiovascular risk marker may refine risk assessment and therapeutic strategies in MASLD.