Abstract 17959: Paradoxical Association of LDL Measures With the Risk of Incident Atrial Fibrillation
Background: LDL cholesterol (LDL-C) is a strong risk factor for atherosclerosis but has an inverse (paradoxical) association with atrial fibrillation (AF). Cholesterol has stabilizing effects on cell membranes; however, it is unknown whether the paradoxical association of LDL-C with AF is due to the cholesterol component of the LDL particle.
Methods: To provide insight into the paradoxical association of LDL-C with AF, we prospectively evaluated several LDL measures in relation to incident AF in 23,738 women free of AF and CVD at baseline. The number of LDL particles (total, small, and large) and average LDL size were measured by nuclear magnetic resonance spectroscopy. Apolipoprotein B, the major protein of the LDL particle, was measured by immunoassay. Subsequent AF events were confirmed by medical record review. Cox models were used to estimate the relative risks (95% CIs) adjusting for age, AF risk factors, inflammatory, hemostatic, and dysglycemic biomarkers.
Results: Over a median follow-up of 16.4 years, 795 women developed AF. In unadjusted analyses, several LDL measures were positively associated with AF, including apolipoprotein B and the number of total LDL particles, in particular small cholesterol-poor LDL particles (Table). However, after multivariable adjustment, the associations of LDL-C, apolipoprotein B, and the number of total and small cholesterol-poor LDL particles with AF all became inverse. By contrast, large cholesterol-rich LDL and average LDL size were not associated with AF in multivariable models.
Conclusion: While LDL-C was paradoxically associated with incident AF, so were apolipoprotein B, the number of total LDL particles, and small cholesterol-poor LDL particles, but not the larger cholesterol-rich LDL particles. These findings suggest that the paradoxical association of LDL-C with AF may not be only related to the cholesterol component of LDL. Future studies are needed to determine the underlying mechanisms of these associations.
- © 2013 by American Heart Association, Inc.