Abstract 12679: Circulating High-Density Lipoprotein Particle Profiles Are Independently Associated With Heart Failure With Preserved Ejection Fraction and Predict Adverse Clinical Outcomes
Introduction: High-density lipoprotein particle concentration (HDL-P) and size (HDL-Sz) impact atherogenesis and inflammation, both of which are implicated in the pathobiology of heart failure with preserved ejection fraction (HFpEF). However, the role of HDL in HFpEF has not been well evaluated. We characterized HDL particle characteristics in a large cardiovascular cohort to determine association with HFpEF and prognostic capability in this growing patient population.
Methods: HFpEF cases (N=1004), HFrEF controls (N=782), and No-HF controls (N=4742) were identified in the CATHGEN biorepository of sequential patients undergoing cardiac catheterization. HFpEF was defined by left ventricular EF (LVEF) ≥45% and history of HF; HFrEF was defined similarly, except for LVEF <45%; No-HF had LVEF ≥45%, and no history of HF. NMR-based lipoprotein profiling was performed on frozen fasting plasma obtained at catheterization. Multivariable analysis of variance was used to compare HDL profiles among groups; proportional hazards modeling evaluated associations among HDL profiles and time-to all-cause mortality and major adverse cardiac events.
Results: HDL-Sz, large HDL-P, and small HDL-P differed significantly across groups (all P≤0.006). Mean HDL-Sz was higher in HFrEF than HFpEF, both of which were higher than No-HF (all two-way P<0.0001). Large HDL-P was greater in HFrEF than HFpEF (P=0.007); by contrast, small HDL-P was lower in HFrEF than HFpEF, which were both lower than No-HF (all P≤0.0002). Greater HDL-Sz and large HDL-P were associated with increased risk of adverse events; whereas, greater small HDL-P was associated with decreased risk (Table).
Conclusions: In the largest analysis of HDL profiles in HFpEF, we identified derangements in HDL-P and HDL-Sz independently associated with adverse events. These findings suggest that HDL profiling may be helpful in identifying high-risk HFpEF subtypes, and could provide new insights into HFpEF pathophysiology.
Author Disclosures: W.G. Hunter: None. R.W. McGarrah: None. J.P. Kelly: Research Grant; Significant; JPK is supported by grant 5T32 HL 7101-39 from the National Institutes of Health. C. Haynes: None. D.M. Craig: None. E.J. Velazquez: Research Grant; Modest; Abbott, Medtronic, Alnylam, Amgen, Pfizer, and Novartis. Consultant/Advisory Board; Modest; Amgen, Merck, and Novartis, lecture fees from Novartis and Spire Learning. W.E. Kraus: Research Grant; Modest; Liposcience Inc.. S.H. Shah: None.
- © 2016 by American Heart Association, Inc.