Statins
Lp(a) tracks with coronary inflammation in men with HIV and undetectable viral load, and statins do not blunt the link, MACS analysis finds (Eur Heart J Imaging Methods Pract 2026)
Original title: Lipoprotein(a) is associated with coronary inflammation in people with HIV and undetectable HIV RNA
This analysis of the Multicenter AIDS Cohort Study measured the perivascular fat attenuation index (FAI), a CT-derived marker of coronary inflammation, in 583 men, including 280 with HIV and undetectable viral load (below 50 copies/mL). In adjusted linear regression, higher log10-Lp(a) was associated with greater left anterior descending FAI specifically in men with undetectable HIV (+1.99 HU, 95% CI 0.38-3.59, P = 0.02), but not in men without HIV or those with detectable virus; the right coronary artery association held only in unadjusted analysis. Statin use was linked to lower LAD inflammation but did not modify the Lp(a)-inflammation relationship. This suggests Lp(a)-driven vascular inflammation contributes to the residual cardiovascular risk seen in virally suppressed people with HIV, independent of statin therapy, though the cross-sectional design cannot establish causation.
Original abstract
Aims: People with HIV (PWH) and undetectable virus experience elevated cardiovascular risk independent of traditional risk factors. Vascular inflammation may contribute to this residual risk. The perivascular fat attenuation index (FAI), derived from coronary computed tomography angiography (CCTA), is a biomarker of coronary inflammation. Lipoprotein(a) [Lp(a)] carries oxidized phospholipids that may promote inflammation. Statins have demonstrated cardiovascular benefit in PWH, including pleiotropic anti-inflammatory effects. This study assessed the associations of Lp(a) and of statin use with coronary inflammation (FAI) in men with HIV (MWH).
Methods And Results: We analysed FAI of the left anterior descending (LAD) and the right coronary arteries (RCA) in 583 men from the Multicenter AIDS Cohort Study, a prospective, multicentre cohort study, including 280 with undetectable HIV RNA, <50 copies/ml. Associations between log10[Lp(a)] and LAD and RCA FAI were assessed using linear regression, adjusting for demographic and cardiovascular risk factors. Log10[Lp(a)] was associated with LAD FAI in MWH with undetectable HIV in adjusted analysis [+1.99 HU (0.38, 3.59); P = 0.02] but not among men without HIV (MWoH) or MWH with detectable HIV. Associations with RCA FAI were only significant in the unadjusted analysis. Statin use was associated with lower FAI, less inflammation in the LAD in MWH with undetectable virus, but did not modify the association between Lp(a) and coronary inflammation.
Conclusion: Lp(a) was associated with increased coronary inflammation, independent of traditional cardiovascular risk factors, in MWH with undetectable virus. Statin therapy did not modify the relationship between coronary inflammation and Lp(a).
Summary written by lp-a.org from the published abstract; figures as published. Page updated 17 August 2026. Methods.