Abstract 11918: Lipoprotein(a) Predicts Subclinical Atherosclerosis in HIV-infected Young Women in the Women’s Interagency HIV Study
Background/Objectives: Lipoprotein(a), Lp(a), is an independent causal risk factor for cardiovascular disease (CVD), where levels are regulated by the apolipoprotein(a), apo(a), gene. HIV-infected individuals are at significantly elevated CVD risk compared to HIV-uninfected individuals. The role of Lp(a) in HIV-related CVD remains unclear. We investigated the association between Lp(a) level, apo(a) size polymorphism and subclinical atherosclerosis in HIV-infected and HIV-uninfected women in the Women’s Interagency HIV Study.
Methods: Lp(a) level, apo(a) size polymorphism and common carotid artery intima-media thickness (cIMT) were determined in 150 HIV-infected and 100 HIV-uninfected women. Lp(a) levels were square-root transformed to achieve normality. Linear regression models were used to evaluate the association of Lp(a) with cIMT adjusting for confounders.
Results: The mean ages for the HIV+ and HIV- groups were 31 ± 4 and 30 ± 4 years, respectively. The majority of women were African-Americans (69% and 76% in the HIV+ and HIV- group, respectively). HDL-cholesterol, triglyceride and Lp(a) levels were significantly lower in the HIV+ vs. HIV- group. Prevalence of atherogenic small size apo(a) (<22 Kringles) was ~20% in both groups. Notably, Lp(a) level was predictive of cIMT in the HIV+ group [β = 0.00541, 95% CI = (0.000608, 0.010212), p=0.029], but not in the HIV- group [β = 0.00175, 95% CI = (-0.0045024, 0.0080024), p=0.584]. After accounting for confounders (age, race, smoking, BMI, blood pressure, HCV co-infection, menopause, blood lipids, treatment status, CD4+ T-cell count, and HIV/RNA viral load), the association remained significant [β = 0.00532, 95% CI = (0.0000672, 0.0105728), p=0.049] in the HIV+ group.
Conclusions: Lp(a) level is associated with subclinical atherosclerosis in young HIV-infected women. Further research is needed to identify mechanisms underlying Lp(a)-associated increased CVD risk in HIV-infected individuals.
Author Disclosures: B. Enkhmaa: None. E. Anuurad: None. W. Zhang: None. C. Li: None. R. Kaplan: None. J. Lazar: None. D. Merenstein: Expert Witness; Modest; for probiotic legal cases. R. Karim: None. B. Aouizerat: None. M. Cohen: None. K. Butler: None. S. Pahwa: None. I. Ofotokun: None. A.A. Adimora: None. E. Golub: None. L. Berglund: None.
- © 2016 by American Heart Association, Inc.