Abstract 17632: HDL Subclasses are Not All Created Equal: Association of HDL Subclasses and Incident Cardiovascular Events in African Americans from the Jackson Heart Study

Abstract

Background: The relationship between high density lipoprotein cholesterol (HDL-C) subclasses (larger, more buoyant HDL2-C and smaller, denser HDL3-C) and incident coronary heart disease (CHD) in African Americans remains unknown.

Methods: We measured apolipoproteins AI and B (Abbott Diagnostics, Illinois) and cholesterol from lipoprotein subfractions separated by density gradient ultracentrifugation (Atherotech, Birmingham, AL) in 4,722/5,301 participants from the Jackson Heart Study, a prospective, observational study of African Americans. Patients were followed for adjudicated CHD events: CHD death, myocardial infarction (MI), and revascularization. Unadjusted and multivariable adjusted hazard ratios (HR) for HDL-C and subclasses were derived from Cox proportional hazards regression models.

Results: Amongst 4,722 subjects (64% female, 53.9 ± 12.8 yrs), there were 144 CHD events: 27 CHD deaths, 78 MIs, and 39 revascularizations over a median follow up of 5.7 yrs (max 8.2 yrs). Mean HDL-C, HDL2-C, and HDL3-C were 53.5 ± 14.4, 13.5 ± 6.4, and 40 ± 8.8 mg/dL, respectively. Mean apoAI and apoB were 147.5 ± 27.2 and 97.9 ± 24.5 mg/dL, respectively. In a joint model including HDL3-C and HDL2-C that adjusted for both clinical characteristics and apoAI and apoB, HDL3-C was inversely associated with MI (HR=0.56, 0.32-0.96, p=0.034), which drove an inverse association with overall CHD (HR=0.60, 0.40-0.91, p=0.016), while HDL2-C was associated with increased revascularizations (HR=1.74, 1.03-2.95, p=0.04), and a non-significant overall CHD risk (HR=1.25, 0.93-1.69, p=0.145). Total HDL-C was not significantly associated with total CHD events, but was inversely associated with CHD death (HR=0.35, 0.13-0.97, p=0.04).

Conclusions: HDL3-C levels appear inversely related to CHD events in African Americans, while HDL2-C levels may be associated with increased CHD events. HDL3-C subfraction was protective from CHD events independent of apoAI and apoB.