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.
Aim: The study aims to explore the relationship between objectively measured physical
Methods: Data were obtained from the UK Biobank, a population-based prospective cohort study. From February 2013 to December 2015, the PA of the participants was objectively measured by continuously wearing an accelerometer for 7 days. CVD was defined through the International Classification of Diseases (10th Revision) codes by linking to national hospitalization data. Death data was obtained through the National Health Service Information Center. K-means cluster analysis was used to cluster patients with similar temporal activity patterns.
Results: Among 3,143 adults with T2DM (mean age 65.9 years; 62.0% men), followed for a median of 7.82 years, 13.91% developed CVD, 13.53% died from cardiovascular causes, and 9.61% died from any cause. A Cox proportional hazards regression model showed that higher hourly PA was associated with lower CVD and cardiovascular mortality risk, particularly for activity accumulated between 8 am and 4 pm. Lower ACM risk was observed for activity performed throughout the day and evening, whereas elevated early-morning activity, most notably around 3 am, was linked to higher CVD and mortality risk. Cluster analysis identified three PAtiming profiles. Compared with participants exhibiting evenly distributed daytime activity (Cluster 1), those with morning activity peaks at 8-9 am (Cluster 2) or 11-12 am (Cluster 3) had substantially reduced CVD incidence {hazard ratio (HR) 0.449 [95% confidence interval (CI), 0.318-0.634] and 0.493 (95%CI: 0.363-0.670), respectively}. The ACM risk was similarly lower in clusters 2 [HR 0.625 (95%CI: 0.448-0.873)] and 3 [HR 0.548 (95%CI: 0.403-0.746)]. These associations were independent of overall PA intensity.
Conclusion: Engaging in PA in the late morning or at noon is associated with a lower risk of CVD and ACM in patients with T2DM. Time-dependent PA interventions may constitute an additional benefit for managing cardiovascular and mortality risks in these patients.