Inflammation
Lp(a) is linked to greater peri-coronary inflammation in people with HIV compared to those without, in a study of 79 participants (J Clin Lipidol 2024)
Original title: Association of Lipoprotein(a) with peri-coronary inflammation in persons with and without HIV infection
In a study of 58 people with HIV (PWH) and 21 people without HIV (PWoH), free of cardiovascular disease, coronary CT-derived fat attenuation index (FAI) was used to assess peri-coronary inflammation. Lp(a) was associated with greater peri-coronary inflammation in the right coronary artery among PWH compared to PWoH (beta=1.73, P=0.019) in adjusted models. Lp(a) also correlated with systemic inflammatory markers, including TNF receptor-I (P<0.001), TNF receptor-II (P=0.002), and high-sensitivity C-reactive protein (P=0.028), as well as with specific monocyte and T-cell activation markers. The findings suggest Lp(a) may interact with HIV-related immune activation to promote coronary inflammation, a novel mechanistic link warranting further study in this high cardiovascular-risk population.
Original abstract
Background: Persons with human immunodeficiency virus (HIV) (PWH) have an increased risk of developing cardiovascular disease (CVD) compared to persons without HIV (PWoH). Lipoprotein(a) [Lp(a)] is a known atherosclerotic risk factor in PWoH, but there are no studies investigating Lp(a) and peri-coronary inflammation.
Objective: To investigate whether Lp(a) is associated with peri-coronary inflammation as assessed by the fat attenuation index (FAI) and activated monocytes and T lymphocytes in PWH and PWoH.
Methods: We measured plasma levels of Lp(a) at study entry in 58 PWH and 21 PWoH without CVD and who had FAI measurements. Associations of Lp(a) with FAI values of the right coronary artery (RCA) and left anterior descending artery were evaluated using multivariable regression models adjusted for potential confounders. Correlations between Lp(a) levels and systemic inflammatory markers and immune cell subsets were examined.
Results: Lp(a) was associated with greater peri-coronary inflammation among PWH compared to PWoH (β=1.73, P=0.019) in the RCA, in adjusted models. Significant correlations were observed with certain inflammatory markers (tumor necrosis factor receptor [TNFR]-I, b=0.295, P<0.001; TNFR-II, b=0.270, P=0.002; high-sensitivity C-reactive protein, b=0.195, P=0.028). Significant correlations were found between Lp(a) levels and several markers of monocyte activation: CD16 -CD163+ (b= -0.199, P=0.024), and CD16 -DR+ MFI (b= -0.179, P=0.042) and T cell subset CD38+CD4+ TEMRA (b= 0.177, P= 0.044).
Conclusions: Lp(a) was associated with greater peri-coronary inflammation in the RCA in PWH compared to PWoH, as well as with select systemic inflammatory markers and specific subsets of immune cells in peripheral circulation.
Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.