Objective
In the general population, lipoprotein(a), Lp(a), has been established as an independent causal risk factor for cardiovascular disease (CVD). Lp(a) levels are to a major extent regulated by a size polymorphism in the apolipoprotein(a), apo(a), gene. The roles of Lp(a)/apo(a) in HIV-related elevated CVD risk remain unclear.
Approach and Results
The associations between total plasma Lp(a) level, allele-specific apo(a) level, an Lp(a) level carried by individual apo(a) alleles, and common carotid artery intima-media thickness (cIMT) were assessed in 150 HIV-infected and 100 HIV-uninfected women in the Women’s Interagency HIV Study. Linear regression analyses with and without adjustments were used. The cohort was young (mean age: ~31 years) with the majority being African-Americans (~70%). The prevalence of a small size apo(a) (≤22 Kringle repeats) or a high Lp(a) level (≥30 mg/dL) was similar by HIV status. Total plasma Lp(a) level (p=0.029) and allele-specific apo(a) level carried by the smaller apo(a) sizes (p=0.022) were significantly associated with cIMT in the HIV-infected women only. After accounting for confounders (age, race, smoking, BMI, blood pressure, HCV co-infection, menopause, plasma lipids, treatment status, CD4+ T-cell count, and HIV/RNA viral load), the association remained significant for both Lp(a) (p=0.035) and allele-specific apo(a) level carried by the smaller apo(a) sizes (p=0.010) in the HIV-infected women. Notably, none of the other lipids/lipoproteins was associated with cIMT.
Conclusions
Lp(a) and allele-specific apo(a) levels predict cIMT in HIV-infected young women. Further research is needed to identify underlying mechanisms of an increased Lp(a) atherogenicity in HIV infection.