63 Managing Cardiovascular Risk and Lipid Disorders Esteban Martinez Hosp Clin Univ of Barcelona, Spain

Background: Although the relative risk associated with specific antiretroviral drugs or classes and the potential benefit of metabolic interventions on the development of cardiovascular disease (CVD) in treated HIV-infected patients have not been demonstrated, antiretroviral drugs have shown differences in their lipid profiles and interventions in the general population have proved to be useful.

Aims: To discuss data about the known factors associated with metabolic abnormalities in HIV-infected patients, and about the impact of changes in antiretroviral therapy and therapeutic interventions on lipid disorders.

Results: Lipid disorders are more prevalent in HIV-infected patients than in age-matched non-HIV-infected people. Although lipid derangements have been related to HIV infection itself, they are far more common and severe in association with combination antiretroviral therapy (cART). Increases in lipid parameters are expected after the initiation of cART irrespective of the drugs used. Ritonavir-boosted protease inhibitors (PIs) or stavudine induce more lipid abnormalities than non-boosted PIs or nucleoside reverse transcriptase inhibitors (NRTIs) other than stavudine, respectively. Among PIs, ritonavir has the strongest hyperlipidemic effect while atazanavir appears to have little if any. Even with similar cART, lipid disorders are more common in antiretroviral-experienced patients, with prior history of hyperlipidemia, or with clinically evident body fat changes. Diet has not been consistently related to lipid abnormalities in HIV-infected patients. Physical exercise may improve hypertriglyceridemia. Switching from PIs to non-NRTIs or abacavir or atazanavir, as well as from stavudine to tenofovir may improve lipid abnormalities, but potential adverse effects and virological failure may arise. Dosage reductions in boosted PIs or stavudine and therapy interruptions may affect lipid parameters positively but their impact on the control of HIV infection is not clear. Fibrates, statins (pravastatin or atorvastatin, to avoid interactions with cytochrome P450), or both may be used but their lipid-lowering effects are usually lower than in the general population.

Conclusions: In the absence of definitive data, it seems reasonable to evaluate lipid disorders in HIV-infected patients according to the same criteria used in the general population. The impact of individual antiretroviral drugs on lipid parameters should be included among the factors to be considered on prescribing cART.