Is Increased Coronary Inflammation Driving Higher Cardiovascular Risk in People with HIV?

In a baseline analysis of 727 participants from the randomized trial to prevent vascular events in HIV (REPRIEVE) mechanistic substudy, researchers found that pericoronary adipose tissue (PCAT) density was associated with coronary plaque, including noncalcified plaque, coronary artery calcium (CAC), vulnerable plaque, and higher coronary artery disease (CAD) burden in people with HIV. These findings suggest a link between increased coronary inflammation and plaque development in this population.

There is evidence that PCAT, through inflammatory mechanisms, may contribute to plaque formation and progression in the coronary arteries. Understanding this relationship is critical for people with HIV, who are at increased risk for cardiovascular disease (CVD) despite advancements in HIV treatment. Prior studies have indicated a higher burden of atherosclerosis in people with HIV, and this research aimed to explore how pericoronary inflammation might contribute to their elevated CVD risk.

In this study, PCAT density was assessed via computed tomography (CT) imaging and related to various coronary plaque characteristics using multivariable logistic regression. The researchers evaluated the presence of coronary plaque, the extent of CAD, noncalcified plaque, CAC, and features of vulnerable plaque. Additionally, PCAT density was compared between people with HIV in the REPRIEVE cohort and a matched control group from the Framingham Heart Study (N = 464).

The study found an association between increased PCAT density and the presence of coronary plaque, with an adjusted odds ratio (OR) of 1.44 per 10 Hounsfield Units (HU) increase in density (95% confidence interval [CI], 1.22–1.70; P < .001), independent of established cardiovascular risk factors, BMI, and systemic immune or inflammatory markers. Additionally, PCAT density was associated with the presence of coronary artery calcium (CAC > 0, P = .002), noncalcified plaque (P < .001), vulnerable plaque (P = .001), and a higher coronary artery disease burden (Leaman score > 5, P = .002). When compared with the matched control group from the Framingham Heart Study, individuals with HIV exhibited higher PCAT density (-88.2 ± 0.5 HU vs -90.6 ± 0.4 HU; P < .001), indicating greater pericoronary inflammation in this population.

A major limitation of this study is its cross-sectional design, which limits the ability to infer causality between increased PCAT density and plaque development. Additionally, while the study controlled for several clinical covariates, residual confounding factors related to HIV infection and treatment may still influence the findings.

“Among people with HIV 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,” the study authors concluded.

Reference

Foldyna B, Mayrhofer T, Zanni MV, et al. Pericoronary adipose tissue density, inflammation, and subclinical coronary artery disease among people with HIV in the REPRIEVE cohort. Clin Infect Dis. 2023;77(12):1676-1686. doi:10.1093/cid/ciad419.