Human immunodeficiency virus (HIV) and stroke: targets for intervention

Abstract

Human immunodeficiency virus (HIV) infection causes stroke through several mechanisms. Stroke results from opportunistic infection and neoplasia, HIV induced cardiac disease, HIV associated cerebral vasculopathy, and perhaps of HIV induced facilitation of some forms of systemic vasculitis and prothrombotic haematological conditions. HIV causes more ischaemic stroke than cerebral haemorrhage. Although stroke is currently a relatively infrequent manifestation of HIV infection, the incidence of stroke in HIV infected individuals is likely to increase with current combination antiretroviral therapy. HIV infection per se induces endothelial activation and dyslipidaemia, predisposing to accelerated atherosclerosis. Antiretroviral therapy, which increases life expectancy and therefore inherently increases ischaemic stroke risk with advancing age and length of exposure to traditional risk factors, also causes pro-atherosclerotic metabolic and endothelial dysfunction. Antiretroviral induced vascular dysfunction together with pre-existing HIV induced vascular disease has the potential to increase atherosclerotic causes of ischaemic stroke. New antiretroviral agents should ideally eradicate the human immunodeficiency virus thereby reducing vascular risk and HIV related causes of stroke without inducing metabolic or endothelial dysfunction. Future studies of vascular disease in HIV infected individuals, particularly studies investigating the impact of current and future antiretroviral agents, should ideally assess stroke as a specific outcome, and provide data by pathological stroke type and ischaemic stroke subtype, to clarify the mechanisms of stroke and guide the approach to treatment and prevention of stroke.