Abstract Body (Do not enter title and authors here): Background
People with HIV (PWH) remain at elevated risk for cardiovascular disease despite control of traditional risk factors and effective antiretroviral therapy. Vascular inflammation is a proposed contributor to this residual risk. Perivascular fat attenuation index (FAI), derived from coronary computed tomography angiography (CCTA), is a validated imaging biomarker of coronary inflammation. Lipoprotein(a) [Lp(a)], elevated in PWH, carries oxidized phospholipids that may drive this residual risk. This study assessed the association of Lp(a) and statin use on coronary inflammation (FAI) in PWH with undetectable HIV RNA.

Research Questions
In PWH with undetectable HIV RNA, is Lp(a) associated with coronary inflammation (FAI)? Does statin use mitigate this association?

Methods
We evaluated 299 men with HIV (MWH) with undetectable HIV RNA (<50 copies/mL) from the Multicenter AIDS Cohort Study who underwent CCTA with FAI measurement. Lp(a) concentrations and other laboratory measures were obtained from the study visit closest to imaging. Associations were assessed using unadjusted and adjusted linear regression models with bootstrap 95% confidence intervals derived from 1000 replicates. Adjustments included age, race, statin use, BMI, diabetes, hypertension, and smoking history.

Results
The median age was 52 [47-57] years; 61.7% White individuals, and 29.7% Black individuals. The median Lp(a) was 26 [9-75] nmol/L and 34% were on statin therapy. 98% were receiving antiretroviral therapy (Table 1).
Among men with undetectable HIV, log[Lp(a)] was associated with LAD FAI in unadjusted (+3.21 HU; 95% CI: 1.60, 4.92; p=0.002) and adjusted models (+2.68 HU; 95% CI: 0.99, 4.48; p=0.008) (Table 2).
Statin use was associated with lower LAD FAI regardless of Lp(a) (-2.89 HU; 95% CI:-4.57, -1.11; p<0.001) and remained significant after further adjustment for age, race, and cardiovascular risk factors (-1.89 HU; 95% CI: -3.62, -0.30; p=0.024) (Figure 1).

Conclusion
These findings offer important insights regarding an inflammatory driver of residual cardiovascular risk in PWH. Coronary inflammation was present and associated with Lp(a), in individuals with undetectable HIV, independent of age, race, statin use, and cardiovascular risk factors. Statin use was associated with a lower LAD FAI regardless of Lp(a). These results highlight Lp(a) as a potential therapeutic target to reduce vascular inflammation and cardiovascular risk in PWH.