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Purpose of Review <p>Metabolic Dysfunction–Associated Steatotic Liver Disease (MASLD) and atherosclerotic cardiovascular disease (ASCVD) are familiar co-attendants, while two-way pathophysiological relationships between them are incompletely determined. Mechanisms—insulin resistance, dyslipidemia, inflammation, and endothelial dysfunction—that underlie MASLD-induced atherogenesis are discussed in the narrative. Ascertainment of tools for the risk stratification of ASCVD in the population is also made.</p> Recent Findings <p>In the last five years, the findings of the cohort studies show MASLD severity is related to subclinical atherosclerosis and future cardiovascular events. New biomarkers (e.g., apolipoprotein B, adipokines) and imaging techniques (e.g., coronary CT angiography) enhance the prediction of risk over the traditional factors. New treatments—GLP-1 receptor agonists and SGLT2 inhibitors—appear to decrease the hepatic steatosis and endpoints of ASCVD, but the use of statins is suboptimal due to the perceived safety issue of the liver.</p> Summary <p>MASLD is a marker and mediator of the risk of ASCVD and thus warrants joint screening and management strategies. Incorporating MASLD-related biomarkers within cardiovascular risk models may be helpful for early detection. High priority for the future is large-scale, randomly controlled clinical studies of combined metabolic therapies to gain dual optimal benefits for the liver and the heart.</p>

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Metabolic Dysfunction-Associated Steatotic Liver Disease and Cardiovascular Disease- A Growing Threat Beyond the Liver

  • 期刊论文

  • 发表日期：

    2025年10月30日

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  • Mohammad Dawar Zahid,
  • Abhishek Lal,
  • Aysha Almas,
  • Om Parkash

摘要

Purpose of Review

Metabolic Dysfunction–Associated Steatotic Liver Disease (MASLD) and atherosclerotic cardiovascular disease (ASCVD) are familiar co-attendants, while two-way pathophysiological relationships between them are incompletely determined. Mechanisms—insulin resistance, dyslipidemia, inflammation, and endothelial dysfunction—that underlie MASLD-induced atherogenesis are discussed in the narrative. Ascertainment of tools for the risk stratification of ASCVD in the population is also made.

Recent Findings

In the last five years, the findings of the cohort studies show MASLD severity is related to subclinical atherosclerosis and future cardiovascular events. New biomarkers (e.g., apolipoprotein B, adipokines) and imaging techniques (e.g., coronary CT angiography) enhance the prediction of risk over the traditional factors. New treatments—GLP-1 receptor agonists and SGLT2 inhibitors—appear to decrease the hepatic steatosis and endpoints of ASCVD, but the use of statins is suboptimal due to the perceived safety issue of the liver.

Summary

MASLD is a marker and mediator of the risk of ASCVD and thus warrants joint screening and management strategies. Incorporating MASLD-related biomarkers within cardiovascular risk models may be helpful for early detection. High priority for the future is large-scale, randomly controlled clinical studies of combined metabolic therapies to gain dual optimal benefits for the liver and the heart.