Abstract
In the mid-1990s, case reports of myocardial infarction (MI) in young patients infected with human immunodeficiency virus (HIV) sparked interest in the relationship between HIV infection and cardiovascular disease (CVD).1,2 Although the initial focus was primarily on the relationship between dyslipidemia associated with antiretroviral therapy (ART) and cardiovascular risk, a broader appreciation of the complex interplay between traditional risk factors for CVD and HIV infection has emerged more recently. Several groups of investigators have designed studies to examine various aspects of the relationship between HIV infection, traditional cardiovascular risk factors, ART, and short- and longer-term cardiovascular risk3–11 (see also Working Group 1). Studies have included both clinical end points (MI, hospitalization for MI or angina, and revascularization) and surrogate markers of atherosclerosis (endothelial function or carotid intima-media thickness). Successive studies have generally improved in quality, with inclusion of data on traditional risk factors, longer follow-up, and more diverse patient populations. HIV and ART can contribute to an altered risk of CVD in 3 principal ways: (1) HIV may serve as a marker to identify a subgroup of the general population with an altered prevalence of traditional cardiovascular risk factors, unrelated to HIV or ART (eg, HIV-infected patients may have higher smoking rates); (2) HIV or ART may affect the risk of developing a traditional cardiovascular risk factor (eg, HIV or ART may worsen dyslipidemia); and (3) HIV or ART may affect the pathogenetic process that leads to CVD in ways other than via an effect on traditional risk factors (eg, through effects on inflammation or endothelial function). Importantly, there is substantial evidence to suggest that all 3 mechanisms are in operation and affect the risk of CVD in patients infected with HIV. All 3 factors should be considered in epidemiological studies assessing the relationship between CVD and HIV …
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