Key result
High inflammation profile linked to ~2.4-fold higher odds of obstructive CAD in HIV.
Why the study?
People with HIV have high risk of coronary and peripheral artery disease independent of traditional risk factors, and single immune-inflammatory biomarkers provide limited insight into disease risk and phenotypes.
Does a high immune-inflammatory profile associate with increased severity of coronary and peripheral artery disease in people with HIV?
Cross-Sectional (n=651)
Does a high immune-inflammatory profile associate with increased severity of coronary and peripheral artery disease in people with HIV?
Odds Ratio: 2.42 (95% CI 1.06–5.33)
An immune-inflammatory profile characterized by T cell senescence, inflammation, and endothelial dysfunction is associated with high-risk CAD severity and peripheral artery disease in people with well-controlled HIV.
Background and Aims People with HIV (PWH) have high risk of coronary (CAD) and peripheral (PAD) artery disease independent of traditional risk factors. Single immune-inflammatory biomarkers provide limited insight into disease risk and phenotypes, whereas integrative profiling may reveal novel mechanisms. Here we investigated associations between immune-inflammatory profiles, CAD, and PAD in PWH. Methods We included PWH from the Copenhagen Comorbidity in HIV Infection (COCOMO) Study with undetectable HIV RNA and measurements of 25 immune-inflammatory biomarkers. Participants underwent coronary computed tomography angiography and ankle-brachial index (ABI) measurements to assess for CAD and PAD. Unsupervised hierarchical clustering on principal components grouped participants by immune-inflammatory clusters, and we assessed their associations with CAD and PAD. Results Among 651 PWH, we identified three immune-inflammatory clusters: one with low senescent T cell proportions; one with low concentrations of inflammation, innate activation, and endothelial dysfunction markers (reference cluster); and one with high senescent T cell proportions and concentrations of inflammation, innate activation, and endothelial dysfunction markers (high inflammation cluster). The high inflammation cluster was associated with obstructive CAD (adjusted OR 2.42 [95% CI: 1.06;5.33]), higher lipid-rich plaque volumes (adjusted β = 8.47 [95% 0.84;16.1] μL), and lower ABI (adjusted β = -0.07 [95% CI: -0.13;-0.01]) among those with PAD compared to the reference cluster, after adjustment for age, sex, smoking, hypertension, diabetes, and dyslipidaemia. Conclusions An immune-inflammatory profile characterised by T cell senescence, inflammation, innate activation, and endothelial dysfunction was associated with high-risk CAD severity, highlighting immunopathogenic pathways associated with atherosclerosis in PWH.
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Suarez‐Zdunek et al. (2026) conducted a cross-sectional in HIV (n=651). High inflammation cluster vs. Reference cluster (low inflammation) was evaluated on Obstructive CAD (OR 2.42, 95% CI 1.06-5.33). A high inflammation profile was associated with obstructive coronary artery disease in people with HIV compared to a reference profile (adjusted OR 2.42; 95% CI 1.06-5.33).
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