Key result
Higher Lp(a) is linked to ~2 HU greater LAD coronary inflammation in men with undetectable HIV.
Why the study?
People with HIV and undetectable virus have elevated cardiovascular risk independent of traditional risk factors, and vascular inflammation may contribute to this residual risk.
Does elevated Lipoprotein(a) increase coronary inflammation in men with HIV and undetectable HIV RNA?
Does elevated Lipoprotein(a) increase coronary inflammation in men with HIV and undetectable HIV RNA?
Elevated Lipoprotein(a) is associated with increased coronary inflammation in men with well-controlled HIV, and this relationship is not modified by statin therapy.
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Supports Lp(a) measurement to identify residual inflammation risk in well-controlled HIV; extends prior evidence and leaves open therapeutic benefit.
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 We analyzed FAI of the left anterior descending (LAD) and the right coronary arteries (RCA) in 583 men from the Multicenter AIDS Cohort Study, a prospective, multicenter 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. Results 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 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. Conclusions 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).
Nasrallah et al. (2026) studied this question. In men with HIV and undetectable virus, each log₁₀ increase in Lp(a) was linked to a 1.99 HU rise in LAD coronary inflammation (FAI), independent of risk factors.
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