ESC Congress 2026 Abstract · Oct 26, 2026
Higher liver fat content is associated with lower lipoprotein(a) concentrations in men and postmenopausal women
By Markus MRP, de Souza JG, Ittermann T et al.
Background: Higher lipoprotein(a) (Lp[a]) levels are considered a cardiovascular risk factor1 and are accepted to be genetically determined,2 to remain generally stable throughout life, except in postmenopausal females,3 and to be less affected by age, sex, or body weight.4 On the other hand, the liver synthesizes the Lp(a). It is possible that damage to this organ, caused by metabolic dysfunction conditions, compromises this production. The association between hepatic steatosis (HS) and plasma lipoprotein(a) (Lp[a]) levels remains controversial, with no sex- or menopausal status-stratified analyses. Purpose: The purpose of the present study was to analyze the sex- and menopausal status-specific associations of HS and serum transaminases with Lp(a) concentrations in the United Kingdom (UK) Biobank study. Methods: We analysed cross-sectional data from 28,711 individuals (15,024 women) aged 40 to 70 years from the UK Biobank study. We examined sex- and menopausal status-specific associations of HS and liver fat content (LFC), determined by magnetic resonance imaging, and serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma-glutamyltransferase (GGT) with serum log-transformed Lp(a) concentrations using linear regression models adjusted for age, body mass index, hemoglobin A1c, glucose-lowering medication use, hypertension, smoking, and alcohol consumption. HS was defined as LFC ≥ 5%. The results of the regression analyses were presented as geometric mean (GM) ratio with 95% confidence intervals. Results: In the UK Biobank study, men with HS had a 9% (95% confidence interval [CI]: 5% to 13%; p<0.001) lower log-transformed Lp(a) concentrations than those without HS in UK Biobank. Moreover, a 5% higher LFC was associated with a 5% (95% CI: 3% to 7%; p<0.001) lower log-transformed Lp(a) concentrations. Additionally, a 1 µkatal/L higher ALT, and AST level was associated with a 15% (95% CI: 5% to 25%; p=0.005) and a 20% (95% CI: 5% to 34%; p=0.012) lower log-transformed Lp(a) concentrations. There was no association with GGT levels. Higher LFC was also associated with lower Lp(a) concentrations in women, but HS and serum liver enzymes were not (Table 1). After stratification by menopausal status, higher LFC was associated with lower log-transformed Lp(a) concentrations in postmenopausal women, but not in premenopausal women. Specifically, a 5% higher LFC was associated with a 4% (95% CI: 1% to 7%; p=0.018) lower log-transformed Lp(a) concentrations in postmenopausal women (Table 2). Conclusions: Our findings from a large community-based study indicate that HS and higher LFC, ALT and AST were independently associated with lower Lp(a) concentrations in men. Additionally, LFC was also associated with lower Lp(a) concentrations in postmenopausal women. Future studies should analyze how to evaluate the increased cardiovascular risk of patients with metabolic dysfunction conditions when Lp(a) levels are reduced.