Association between serum apolipoprotein A1 and atrial fibrillation in the Chinese population: a case-control study

Xia Zhong1, Jie Yu2, Dongsheng Zhao1

  • 1Department of First Clinical Medical College, Shandong University of Traditional Chinese Medicine, Jinan, Shandong, PR China.

Insights

Low serum apolipoprotein A1 (APOA1) is linked to atrial fibrillation (AF) in the Chinese population. This finding suggests APOA1 may serve as a potential biomarker for AF risk and progression.

Area of Science:

  • Cardiovascular Research
  • Biomarker Discovery
  • Epidemiology

Background:

  • The association between serum apolipoprotein A1 (APOA1) and atrial fibrillation (AF) remains largely unexplored.
  • Understanding this relationship is crucial for identifying novel risk factors and therapeutic targets for AF.

Purpose of the Study:

  • To investigate the association between serum APOA1 levels and the risk of developing AF in the Chinese population.
  • To explore the correlation between APOA1 and lipid profiles and its predictive performance for AF.

Main Methods:

  • A case-control study involving 950 AF patients and matched controls in China.
  • Pearson correlation analysis for APOA1 and lipid profiles; multivariate regression for AF association.
  • Receiver operator characteristic (ROC) curve analysis to determine predictive cut-off values for APOA1.

Main Results:

  • Low serum APOA1 was significantly associated with AF in both men and women (OR = 0.261, P < 0.001).
  • APOA1 showed positive correlations with total cholesterol, LDL-C, HDL-C, and APOB.
  • Optimal cut-off values for APOA1 predicting AF were identified as 1.105 g/L for males and 1.205 g/L for females.

Conclusions:

  • Low serum APOA1 is a significant risk factor for AF in the Chinese population, particularly in non-statin users.
  • APOA1 may serve as a potential biomarker for AF, potentially contributing to its pathological progression alongside lipid profiles.
  • Further research is warranted to elucidate the underlying mechanisms connecting APOA1, lipid profiles, and AF pathogenesis.
Abstract