ArticleAnnals of medicine2025
Inflammatory and metabolic markers mediate the association of hepatic steatosis and fibrosis with 10-year ASCVD risk.
Article in Annals of medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Oxidative balance score as a predictor of MASLD-CVD comorbidity risk and mortality: Insights from traditional and machine learning approaches.International journal of cardiology. Cardiovascular risk and prevention · 2026Article
- Clinical clustering identifies MASLD subtypes with distinct longitudinal cardiovascular risks and lipidomic profiles.Hepatology international · 2026Article
- Risk-associated and clinically informative biomarkers for cardiovascular risk stratification in metabolic dysfunction-Associated steatotic liver disease.American journal of preventive cardiology · 2026Article
- Association between triglyceride-glucose index-a body shape index and atherosclerotic cardiovascular disease, and the modification effect of dietary patterns.Frontiers in nutrition · 2026Article
- Circadian rhythms of gut microbiota and plaque vulnerability: mechanisms and chrono-microbiota modulation interventions.Gut microbes · 2025Review
- Letter to editor regarding from family medicine perspective: 'Inflammatory and metabolic markers mediate the association of hepatic steatosis and fibrosis with 10-year ASCVD risk'.Annals of medicine · 2025Article
- Association between fibrosis-4 index and coronary heart disease: a population-based study.BMC cardiovascular disorders · 2025Article
- Metabolic Dysfunction-Associated Steatotic Liver Disease and Liver Fibrosis are Associated with Advanced Cardiovascular-Kidney-Metabolic Syndrome in Chinese and US Populations.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
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Authors and funding
13 authors.
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Abstract
BACKGROUND AND
aimsLiver steatosis and fibrosis increase the predicted 10-year atherosclerotic cardiovascular disease (ASCVD) risk, though the roles of chronic inflammation and metabolic dysregulation remain unclear. This cross-sectional study quantitatively assesses this association and evaluates the mediating effects of metabolic dysregulation and chronic inflammation.
methodsIn this study, we enrolled 6110 adults from ten communities in Canton, China. Hepatic steatosis and fibrosis were assessed using vibration-controlled transient elastography (VCTE) through controlled attenuation parameter (CAP) and liver stiffness measurement (LSM), while predicted 10-year ASCVD risk was calculated using the China-PAR project model. Associations between CAP/LSM values and predicted 10-year ASCVD risk were analyzed. Mediation analysis quantified the effects of high-sensitivity C-reactive protein (hs-CRP), homeostasis model assessment of insulin resistance (HOMA-IR), remnant cholesterol (RC), and non-high-density lipoprotein cholesterol (non-HDL-C). The main statistical methods used included logistic regression, restricted cubic splines (RCS) analysis, interaction calculations, and mediation analysis to examine the relationships and mediators.
resultsThe study population had a mean age of 50.1 years (SD = 9.7), with 3927 females (64.3%) and 2183 males (35.7%). Additionally, 808 participants (13.2%) had type 2 diabetes, and 1911 participants (31.3%) had hypertension. Compared to the first CAP quartile (Q1), higher CAP quartiles showed increased odds ratios (OR) for predicted moderate to high 10-year ASCVD risk: 1.14 (0.89, 1.45), 1.37 (1.08, 1.73), and 2.44 (1.93, 3.10). Mediation analysis showed hs-CRP and HOMA-IR mediated CAP's link to ASCVD risk, with mediation proportions of 15.40% and 27.37%. RC and non-HDL-C mediated this association at 7.12% and 6.26%. Among patients with hepatic steatosis (CAP ≥ 248 dB/m), LSM Q4 participants had a significantly higher predicted 10-year ASCVD risk than those in LSM Q1 (OR 2.22, [1.52, 3.25]), with hs-CRP and HOMA-IR mediating 2.62% and 13.75%, respectively.
conclusionLiver steatosis and fibrosis were associated with the increased predicted ASCVD risk, with mediation effects from hs-CRP, HOMA-IR, RC, and non-HDL-C.
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