Why the study?
Coronary plaque in people with HIV presents as a unique phenotype, but little is known about how specific inflammatory pathways contribute to these plaque phenotypes.
Are specific proteomic signatures associated with subclinical coronary artery disease (CAC and plaque) in people with HIV?
Are specific proteomic signatures associated with subclinical coronary artery disease (CAC and plaque) in people with HIV?
Distinct immune and inflammatory proteomic signatures, particularly NRP1, are associated with subclinical coronary artery disease phenotypes in people with HIV.
Answers are grounded in this paper and cite their sources.
Novel inflammatory proteins linked to subclinical CAD in PWH; leaves open targeted interventions pending validation.
BACKGROUND: People with HIV (PWH) have subclinical coronary artery disease (CAD) despite low traditional atherosclerotic cardiovascular disease (ASCVD) risk scores. Coronary plaque in PWH presents as a unique phenotype, but little is known about the contributions of specific inflammatory pathways to plaque phenotypes in PWH. METHODS: The REPRIEVE Mechanistic Substudy enrolled PWH on ART without known cardiovascular disease. We used a targeted discovery proteomics approach to evaluate 246 unique proteins representing cardiovascular, inflammatory, and immune pathways. Proteomic signatures were determined for presence of coronary artery calcium (CAC > 0) and presence of coronary plaque. RESULTS: Data were available for 662 participants (aged 51 [SD 6] years, ASCVD risk score 4.9% [SD 3.1%]). Among 12 proteins associated with both CAC and presence of coronary plaque, independent of ASCVD risk score, the odds ratios were highest for NRP1: 5.1 (95% confidence interval [CI], 2.3-11.4) for CAC and 2.9 (95% CI, 1.4-6.1) for presence of plaque. Proteins uniquely related to presence of plaque were CST3, LTBR, MEPE, PLC, SERPINA5, and TNFSF13B; in contrast, DCN, IL-6RA, OSMR, ST2, and VCAM1 were only related to CAC. CONCLUSIONS: Distinct immune and inflammatory pathways are differentially associated with subclinical CAD phenotypes among PWH. This comprehensive set of targets should be further investigated to reduce atherosclerosis and ASCVD in PWH. CLINICAL TRIALS REGISTRATION: NCT02344290.
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Kolossváry et al. (2022) studied this question.
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