Treated HIV infection is not associated with carotid vascular inflammation or plaque progression as assessed by dynamic contrast magnetic resonance imaging.

Abstract

Background: Inflammation and immune dysregulation are thought to drive residual cardiovascular disease risk among persons living with human immunodeficiency virus (HIV) (PLWH) despite effective viral suppression with antiretroviral therapy (ART).

Methods: We investigated differences in carotid inflammation and atherosclerosis in a longitudinal cohort of virally suppressed PLWH (N = 50; on stable ART with CD4 > 250 cells/mm³, viral load < 200 copies/mL for > 6 months) and HIV-uninfected controls (N = 51) matched for age, sex, hypertension, diabetes, smoking, hyperlipidemia, and family history of premature coronary artery disease (CAD). Participants were ≥ 40 years old at enrollment. Measures of carotid vascular inflammation (K^trans), neovascularization (V_p), and wall thickness were assessed at baseline, 1 year, and change over 1 year by dynamic contrast-enhanced magnetic resonance imaging (MRI).

Results: Among 101 participants, 8% were women, 42% had hypertension, 52% had hyperlipidemia, 16% had diabetes, and 48% had a family history of CAD. Both PLWH and control participants demonstrated a reduction in systolic and diastolic blood pressures and total cholesterol over 1 year; however, the difference was not significant by HIV status. PLWH had a significant reduction in triglycerides compared with controls (-48.8 vs 12.8 mg/dL, p = 0.026). HIV was not associated with baseline, follow up, or change in markers of systemic inflammation assessed by plasma cytokines, nor vascular inflammation as assessed by K^trans, V_p, carotid wall thickness, or percent wall volume (a measure of plaque burden).

Conclusion: In contrast to other studies of treated and virally suppressed PLWH, HIV infection was not associated with carotid inflammation or plaque in our hypothesis-generating study.