Blood vessels at the crossroads: angiogenesis in the intersection of HIV and atherosclerosis.

BACKGROUND

The increased risk of cardiovascular disease (CVD) in people living with HIV (PLWH) remains a significant concern. The process of atherosclerosis in PLWH is accelerated and is believed to be independent of traditional CVD risk factors, as well as being present despite the use of combination antiretroviral therapy.

OBJECTIVES

This review is focused on the vasa vasorum (VV) in HIV-associated atherosclerosis and how the inflammation and immune dysregulation inherent to HIV infection contribute to atheroma formation and instability through VV-dependent pathways.

SOURCES: We conducted a structured literature review using PubMed exploring all relevant literature to HIV infection, atherosclerosis, VV angiogenesis, plaque vulnerability, and noninvasive vascular imaging.

CONTENT: The VV contributes to atherogenesis in PLWH through several mechanisms, including the promotion of inflammation, angiogenesis, lipid deposition, and infiltration by monocytes and other inflammatory cells, leading to the formation of highly unstable, lipid-laden lesions. These prone-to-erosion lesions are associated with high-grade inflammatory vascular disease (i.e. HIV-induced endothelial dysfunction and chronic vascular inflammation), which predisposes PLWH to exaggerated VV angiogenesis and impaired vascular function, increasing the risk of acute cardiac and cerebral events. Information on VV angiogenesis and plaque vulnerability can be obtained noninvasively using, for example, contrast-enhanced ultrasound and high-resolution magnetic resonance imaging. The possibility of improving atherosclerotic vascular disease in PLWH through therapeutic antiangiogenic and anti-inflammatory approaches is also an area for further investigation and better elucidation of what vasculature interventions are optimal in PLWH.

IMPLICATIONS: New-generation imaging techniques and the identification of new biomarkers associated with VV-related vascular risk may facilitate earlier identification of VV-related vascular risk and more tailored strategies to manage cardiovascular risk in PLWH. This will enhance the impact of VV assessment on CVD prevention in this at-risk population.