Abstract 17805: Association of LpPLA2 with Lipoprotein Subclasses, Inflammation, Atherosclerosis & Endothelial Dysfunction in a Web-Based Lifestyle Intervention Study: Baptist Employee Healthy Heart Study (BEHHS)
INTRODUCTION: A recent meta-analysis demonstrated that Lipoprotein-associated phospholipase A2 (LpPLA2) activity is associated with CVD events. However, the mechanisms which mediate this risk are poorly established. This study aims to assess the cross-sectional association between LpPLA2 and components of an advanced lipid panel, subclinical CVD and markers of inflammation.
METHODS: The Baptist Employee Healthy Heart Study (BEHHS) is an ongoing study examining the effect of web-based interventions on reducing CVD risk in individuals with metabolic syndrome & type II diabetes mellitus. Cardio IQ™ Ion Mobility lipoprotein fractionation was utilized for advanced lipid subclass measurement resulting in direct quantification of particles in each lipoprotein sub-class fraction. Endothelial function was assessed using endoPAT2000 (Itamar, Israel) and individuals older than 35 years had CT scan for coronary artery calcium (CAC). LpPLA2 was measured by Enzyme-linked Immunosorbent Assay (ELISA).
RESULTS: The population consisted of 182 individuals, 74% female with a mean age of 51±10 years (range 25 - 72). Overall the median plasma LpPLA2 level was 199 ng/mL. In univariate analyses, there was a significant association with several lipid subclasses and with hs-CRP. After adjusting for risk factors, LpPLA2 was independently associated with LDL-c and LDL particle size, Large LDL subclass A, small IDL, small, medium and large VLDL, and with hs-CRP. On the other hand there was no association between LpPLA2 mass and HOMA-IR, reactive hyperemia index or presence of CAC.
CONCLUSIONS: LpPLA2 is significantly associated with several lipoprotein sub-classes and with systemic inflammation without affecting vascular endothelial function or atherosclerosis. Further studies are required to determine if lifestyle interventions affect LpPLA2 and how this may translate to reduced systemic inflammation and an improvement in cardiometabolic profile.
Author Disclosures: O. Jamal: None. E. Aneni: None. L. Roberson: None. S. Shaharyar: None. A. Younus: None. S.S. Ali: None. B. Rosell: None. E. Oni: None. H. Guzman: None. C. Ye: None. C. Ye: None. R. Malik: None. M. Aziz: None. J. Post: None. R. Cury: None. J. Fialkow: None. M. Ozner: None. T. Feldman: None. A. Agatston: None. E. Veledar: None. K. Nasir: None.
- © 2014 by American Heart Association, Inc.