Cardiovascular Disease, Statins, and HIV

Abstract

Human immunodeficiency virus (HIV)-infected patients are at an increased risk of serious, non-AIDS-defining comorbidities, even in the setting of viral suppression with combination antiretroviral therapy. This increased risk is due in part to immune dysfunction and heightened inflammation and immune activation associated with chronic HIV infection. Statins have wide-reaching immunomodulatory effects, and their use in the HIV-infected population may be of particular benefit. In this article, we review the pathogenesis of increased inflammation during HIV infection and how it contributes to the risk of cardiovascular disease among HIV-infected individuals. We then we review the immunomodulatory effects of statins and how they may attenuate the risk of cardiovascular disease and other comorbidities in this unique patient population.

Keywords: HIV; cardiovascular disease; hydroxy-3-methylglutaryl coenzyme A reductase inhibitors; immune activation; inflammation; statins.

Figure 1.

Cholesterol biosynthesis pathway highlighting the biologically active metabolites and pleotropic activities. Statins have wide-reaching immunomodulatory properties that are mainly driven by inhibition of the isoprenoids geranylgeranyl pyrophosphate (GGPP) and farnesyl pyrophosphate (FPP) to perform protein prenylation (ie, isoprenylation), which is a downstream effect of inhibiting hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase in the mevalonate pathway for the synthesis of cholesterol. Abbreviation: GPP, geranyl pyrophosphate.