Accumulating evidence suggests that HIV-infected individuals have an increased risk of cardiovascular events. This risk seems to be at least partially mediated by dyslipidaemia, which is related to the use of highly active antiretroviral therapy (HAART). As HIV-infected individuals live longer due to HAART, their cardiovascular risk will invariably increase. Because HAART is likely to be used indefinitely, HAART-related dyslipidaemia has emerged as a major cardiovascular concern. This article summarises the evaluation of dyslipidaemia and cardiovascular risk in HIV-infected individuals, the potential pathophysiological and genetic mechanisms involved in HAART-related dyslipidaemia and the current treatment approaches. In general, dyslipidaemia is evaluated and treated as in HIV-negative persons. The first step is cardiovascular risk assessment and the determination of target lipid levels. A healthier lifestyle and, in particular, smoking cessation should be promoted. Lowering levels of low-density lipoprotein cholesterol (or, in the setting of significant hypertriglyceridaemia, non-high-density lipoprotein cholesterol) is the primary target of intervention. Switching HAART to a more lipid-favourable regimen should be considered if this does not jeopardise virological control. Many patients will need lipid-lowering drug therapy. Appropriate low-density lipoprotein cholesterol target levels may be more difficult to reach than in the HIV-negative population, and the potential for drug interactions when using lipid-lowering agents together with HAART needs to be considered. The identification of HAART strategies with no or minimal metabolic toxicity, and the identification of the safest and most efficacious lipid-lowering therapies for HIV-infected individuals with dyslipidaemia are important research goals.