Pericoronary Adipose Tissue Density, Inflammation, and Subclinical Coronary Artery Disease Among People with HIV in the REPRIEVE Cohort
Abstract
Background Pericoronary adipose tissue (PCAT) may influence plaque development through inflammatory mechanisms. We assessed PCAT density, as a measure of pericoronary inflammation, in relationship to coronary plaque among people with HIV (PWH) and to a matched control population.
Methods In this baseline analysis of 727 participants of the Randomized Trial to Prevent Vascular Events in HIV (REPRIEVE) Mechanistic Substudy, we related CT-derived PCAT density to presence and extent (Leaman score) of CAD, non-calcified plaque, coronary artery calcium (CAC), and vulnerable plaque (VP) features using multivariable logistic regression analyses. We further compared the PCAT density between PWH and age, sex, body mass index (BMI), CAC score, and statin use-matched controls from the community-based Framingham Heart Study (FHS) (N=464), adjusting for relevant clinical covariates.
Results Among 727 REPRIEVE participants (age 50.8±5.8 years; 83.6% [608/727] male), PCAT density was higher in those with (vs. without) coronary plaque, non-calcified plaque, CAC>0, vulnerable plaque, and high CAD burden (Leaman score >5) (p<0.001 for each comparison). PCAT density related to prevalent coronary plaque (aOR [per 10 HU]: 1.44; 95%CI: 1.22–1.70; p<0.001), adjusted for clinical cardiovascular risk factors, BMI, and systemic immune/inflammatory biomarkers. Similarly, PCAT density related to CAC>0, non-calcified plaque, vulnerable plaque, and Leaman score >5 (all p≤0.002). PCAT density was greater among REPRIEVE participants vs. FHS (-88.2±0.5 HU vs. -90.6±0.4 HU; p<0.001).
Conclusion Among PWH in REPRIEVE, a large primary cardiovascular disease prevention cohort, increased PCAT density independently associated with prevalence and severity of coronary plaque, linking increased coronary inflammation to CAD in PWH.