Abstract
An established relationship exists between human immunodeficiency virus (HIV) and the vascular system, which is characterised by clinical expressions of aneurysmal and occlusive disease that emanate from a common pathological process. The exact pathogenesis is currently unknown; attempts to implicate opportunistic pathogens have been futile. Theories converge on leucocytoclastic vasculitis with the vaso vasora as the vasculopathic epicentre. It is thought that the virus itself or viral proteins trigger the release of inflammatory mediators that cause endothelial dysfunction and smooth muscle proliferation leading to vascular injury and thrombosis. The beneficial effects of highly active anti-retroviral therapy alter the natural history of the disease profile and promote longevity but are negated by cardiovascular complications. Atherosclerosis is an emerging challenge. Presently patients are managed by standard surgical protocols because of non-existent universal surgical interventional guidelines. Clinical response to treatment is variable and often compounded by complications of graft occlusion, sepsis and poor wound healing. The clinical, imaging and pathological observations position HIV-associated large-vessel vasculopathy as a unique entity. This review highlights the spectrum of HIV-associated large-vessel aneurysmal, occlusive and atherosclerotic disease in vascular surgical practice.
Highlights
An established relationship exists between human immunodeficiency virus (HIV) and the vascular system, which is characterised by clinical expressions of aneurysmal and occlusive disease that emanate from a common pathological process
It is thought that the virus itself or viral proteins trigger the release of inflammatory mediators that cause endothelial dysfunction and smooth muscle proliferation leading to vascular injury and thrombosis
The theoretical basis of this includes continuing viral infection and associated viral protein toxicity leading to vascular wall injury, an increase in viral load associated with the release of interleukin 1 (IL1), interleukin 6 (IL6), interleukin 8 (IL8) and tumour necrosis factor-α (TNF-α), in conjunction with immune activation and immune reconstitution as a result of highly active anti-retroviral therapy (HAART).[14]
Summary
The hallmark pathological feature common to aneurysmal and occlusive disease is an HIV-associated vasculitic process, the exact mechanism of which is poorly understood (Fig. 1A, B).[13,14]. HIV-related endothelial dysfunction, incorporating a complex interplay between cytokines and inflammatory components, has been proposed.[14] The theoretical basis of this includes continuing viral infection and associated viral protein toxicity leading to vascular wall injury, an increase in viral load associated with the release of interleukin 1 (IL1), interleukin 6 (IL6), interleukin 8 (IL8) and tumour necrosis factor-α (TNF-α), in conjunction with immune activation and immune reconstitution as a result of HAART.[14] This has been observed by Nieuwhof et al.[15] who postulated increased T-cell numbers associated with elevated CD25-positive receptors in the setting of cerebral vasculitis. A viral envelope glycoprotein component (gp120) is a catalyst that stimulates production of pro-inflammatory mediators, which target endothelial cells.[14,16,17] Evidence from studies on flow-mediated vasodilatation demonstrates that HIV-associated endothelial dysfunction is catalysed by these cytokines and the inflammatory process.[13,14,17]
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