Abstract
Abstract
Objectives
To systematically synthesize evidence on the association between metabolic dysfunction-associated steatotic liver disease (MASLD) and imaging biomarkers of subclinical atherosclerosis and hepatic steatosis/fibrosis, and to quantify the magnitude of these associations across study populations.
Methods
We systematically searched PubMed, Embase, Web of Science Core Collection, and Cochrane Library (January 2000-February 28, 2026) for observational studies enrolling adults with MASLD (or historical NAFLD/MAFLD) that reported atherosclerotic cardiovascular disease (ASCVD)-related imaging outcomes. Primary outcomes were continuous coronary artery calcium (CAC; Agatston units), epicardial adipose tissue (EAT; cm3), controlled attenuation parameter (CAP; dB/m), and liver stiffness measurement (LSM; kPa). Weighted mean differences (WMDs) for continuous outcomes and odds ratios (ORs) for dichotomized thresholds were pooled using random-effects models with restricted maximum likelihood (REML) estimation and Hartung-Knapp adjustment where applicable; heterogeneity was quantified with I2 and τ2.
Results
Sixteen observational studies (n = 34 713; 6 cohorts, 10 cross-sectional) from North America, Asia, and Europe were included. In modality-specific threshold analyses, MASLD was associated with higher odds of subclinical disease: CAC (OR 1.41, 95% CI: 1.32-1.51; I2 = 75.0%), high EAT (OR 1.44, 95% CI: 1.21-1.68; I2 = 0%), high CAP (OR 1.47, 95% CI: 1.35-1.58; I2 = 0%), and high LSM (OR 1.49, 95% CI: 1.31-1.66; I2 = 0%). For continuous outcomes, CAC was higher by 49.2 Agatston units (95% CI: 46.8-51.7; I2 = 75.4%) and LSM was higher by 0.57 kPa (95% CI: 0.46-0.68; I2 = 0%) in MASLD versus comparators. EAT (k = 2; n = 4306): WMD 76.18 cm³ (95% CI: 5.04-147.32; I2 = 98.3%) (exploratory only; not suitable for point estimation). CAP (k = 2; n = 6652): WMD 45.12 dB/m (95% CI: 0.96-89.27; I2 = 98.1%) (exploratory only; not suitable for point estimation).
Conclusions
MASLD is consistently associated with greater calcific coronary burden, pericoronary adiposity, hepatic steatosis, and hepatic stiffness relative to non-MASLD comparators. These findings represent between-group imaging differences and should be interpreted as evidence of concurrent adverse imaging burden rather than formal demonstration of incremental predictive value beyond validated clinical risk engines. Whether these biomarkers improve discrimination, reclassification, or net clinical benefit beyond established scores (Pooled Cohort Equations [PCE], SCORE2, Framingham Risk Score [FRS]) requires prospective validation with pre-specified incremental prediction analyses.
Advances in knowledge
This study provides a comprehensive quantitative, multimodality synthesis demonstrating that MASLD is consistently associated with concurrent adverse changes across 4 key imaging biomarkers spanning subclinical atherosclerosis (CAC, EAT) and hepatic disease burden (CAP, LSM), establishing a critical evidence base to motivate prospective studies on integrating standardized imaging protocols to refine ASCVD risk characterization in MASLD populations.