S2592 Association Between MASLD and Atherosclerotic Cardiovascular Disease Risk Among US Adults

Introduction: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a growing public health concern due to its implications for cardiovascular (CV) risk. What is less clear are the individual roles of steatosis and fibrosis in conferring CV risk. Using a nationally representative sample, we evaluated the association between MASLD and estimated 10-year atherosclerotic cardiovascular disease (ASCVD) risk among U.S. adults. Methods: We conducted a cross-sectional analysis of U.S. adults aged 40–79 years from NHANES 2017–2020 with complete vibration-controlled transient elastography (VCTE), cardiometabolic, and laboratory data. Exclusion criteria included pregnancy, viral hepatitis (HBsAg-positive or HCV RNA-positive), excessive alcohol use (>30 g/day for men, >20 g/day for women), known liver disease, and prior cardiovascular events. Participants with missing data required to calculate ASCVD risk scores were excluded. MASLD was defined as a Controlled Attenuation Parameter (CAP) ≥288 dB/m plus ≥1 cardiometabolic risk factor. Significant fibrosis was defined as liver stiffness measurement ≥8.0 kPa. A 4-category composite exposure variable was created as follows: MASLD - /Fibrosis -, MASLD +/Fibrosis-, MASLD-/Fibrosis+, and MASLD+/Fibrosis+. The primary outcome was elevated 10-year ASCVD risk (≥7.5%) calculated using pooled cohort equations. Survey-weighted logistic regression models adjusted for sociodemographic variable, physical activity, statin use and log-transformed CRP. Sensitivity analyses examined continuous ASCVD risk score and stratified by obesity and sex. Results: A total of 1,336 participants met inclusion criteria for ASCVD risk estimation. The weighted MASLD prevalence was 39.8%. Among participants with MASLD, 50.6% had elevated ASCVD risk (≥7.5%), compared to 34.5% among those without MASLD (P = 0.0023). After adjustment, MASLD+/Fibrosis+ conferred the greatest odds (aOR: 2.19; 95% CI: 1.13–4.00; P = 0.018), followed by MASLD without fibrosis (aOR: 1.70; 95% CI: 1.03–2.40; P = 0.038). Fibrosis alone showed no significant association. Conclusion: Our findings demonstrate that MASLD especially with concomitant fibrosis, is independently associated with elevated 10-year ASCVD risk. Interestingly, fibrosis alone, does not increase CV risk, suggesting that interventions to reduce steatosis may mitigate CV risk prior to fibrosis improvement. These findings underscore the importance of CVD risk stratification in MASLD management, even among those without obesity or established CVD.