Coronary Inflammation is Associated with Plaque Progression in Men with HIV
Abstract
Background People with HIV (PWH) are at elevated risk for atherosclerotic cardiovascular disease despite viral suppression, suggesting contributions from nontraditional mechanisms. Coronary vascular inflammation may play a role, but its relationship to plaque progression remains incompletely defined. The perivascular fat attenuation index (FAI) Score, derived from coronary computed tomography angiography (CCTA), is associated with vascular inflammation. We evaluated whether coronary inflammation is associated with the incidence and progression of coronary plaque and whether these relationships differ by HIV status. Methods A total of 504 men (n=292 HIV; n=212 without HIV) from the Multicenter AIDS Cohort Study underwent CCTA over a median 4.5 years [3.8–4.9]. FAI measurements were performed on baseline scans. Changes in noncalcified, calcified, and total plaque volumes were categorized into tertiles of progression. Associations were estimated using multinomial logistic regression adjusted for interscan time and cardiovascular risk factors. Modified Poisson regression estimated incident plaque. Results Higher FAI Scores in the LAD and LCx were associated with greater odds of belonging to the highest tertile of noncalcified [LAD OR 1.83 (1.27, 2.64); LCx OR 2.55 (1.66, 3.91)], calcified [LAD OR 2.62 (1.64, 4.18); LCx OR 3.92 (2.36, 6.51)], and total plaque progression [LAD OR 1.81 (1.25, 2.62); LCx OR 2.65 (1.71, 4.10)] among men with HIV (MWH), per standard deviation increase in FAI Score after adjusting for cardiovascular risk factors, and remained significant after adjustment for baseline plaque. Higher LAD FAI Score was associated with incident calcified plaque in MWH [RR 1.21 (1.01, 1.46)]. Associations for noncalcified and calcified plaque progression were stronger in MWH than in MWoH. Conclusions Coronary inflammation, assessed by FAI, is independently associated with incident and progressive coronary plaque in MWH. These findings support a role for vascular inflammation in accelerated atherosclerosis in PWH and highlight FAI as a potential biomarker for risk stratification.