UCLA

The pathogenesis of atherosclerosis in human immunodeficiency virus (HIV)-infected individuals is incompletely understood and appears to be multifactorial. Proatherogenic changes in blood and tissue lipids are associated with an increased risk of cardiovascular disease among HIV-infected subjects, and these changes may be both quantitative (dyslipidemia) and qualitative. In view of the pivotal role of dyslipidemia in the process of atherosclerosis, the increased incidence of dyslipidemia in HIV-infected individuals, and the emerging role of lipid abnormalities in systemic pathophysiologic processes such as immune activation, we review the contributions of dyslipidemia to cardiovascular risk in HIV infection.