The ability of lipoprotein (a) level to predict early carotid atherosclerosis is impaired in patients with advanced liver fibrosis related to metabolic associated fatty liver disease

Abstract

Background: 

Hepatic fibrosis reduces the serum level of lipoprotein (a) [Lp(a)] and may affect its accuracy in cardiovascular disease prediction of metabolic-associated fatty liver disease (MAFLD). We aimed to estimate the association between Lp(a) levels and the risk of carotid atherosclerosis in MAFLD patients with advanced fibrosis.

Methods and Materials: 

This was a cross-sectional study enrolling 4348 consecutive subjects (1346 MAFLD and 3002 non-MAFLD patients) who were admitted to the First Affiliated Hospital, Sun Yat-sen University and underwent abdominal and carotid ultrasonography from 2015 to 2021. Lp(a) levels, liver biochemical markers, metabolic indices and anthropometric parameters were measured. Liver fat content (LFC) and fibrosis severity were assessed by MRI-PDFF, using the NAFLD fibrosis score (NFS) and liver stiffness measurement (LSM) of 2D-shear wave elastography (SWE), respectively.

Result: 

There was an L-shaped relationship between Lp(a) levels and LSM in MAFLD patients, and Lp(a) levels had the different relationship with LFC in MAFLD patients with F1-2 versus those with F3-4. Non-MAFLD patients had higher levels of Lp(a) than MAFLD patients with or without advanced fibrosis (both p<0.05). Lp(a) levels and degree of liver fibrosis were both positively correlated with carotid atherosclerosis in MAFLD patients. Lp(a) levels performed well on carotid atherosclerosis risk prediction for non-MAFLD patients with an AUC of 0.819, which was significantly better than the carotid atherosclerosis risk prediction for MAFLD patients with NFS≤-1.836 (AUC: 0.781), NFS>-1.836 (AUC: 0.692) and LSM≥9.0 kPa (AUC: 0.635) (all p<0.05).

Conclusion: 

Advanced liver fibrosis significantly reduces the predictive value of Lp(a) levels for the risk of carotid atherosclerosis in MAFLD patients.