The natural history of HIV infection in many patients has been dramatically altered through the use of highly-active antiretroviral therapy (HAART). However, this treatment paradigm of chronic chemotherapy may not be sustainable given the short and long-term toxicities of these medications. Among the more concerning are the development of atherogenic lipoprotein abnormalities and a state of relative insulin resistance. Logically, there has been concern that such metabolic disturbances may predispose towards cardiovascular morbidity and mortality. Although these therapies have only been in widespread use for a short period of time, a growing body of evidence from case reports and cohort studies has suggested that HIV-infected patients on HAART may experience premature coronary artery disease. The explanation of this phenomenon is most likely multifactorial. In terms of pathophysiology, the relative contributions of HIV viral replication, host immune response, and the use of antiretroviral agents remains unknown. HIV-1 could possibly have a direct effect on the endothelium as has been suggested for other infectious agents such as chlamydia, herpes simplex, and cytomegalovirus. One could postulate that the virus might have some capacity to effect the production of nitric oxide (NO), as a pathogenic mechanism. It is unknown whether the medications have direct toxicities or whether the common underlying mechanism is drug-induced abnormalities in lipid and/or glucose metabolism. Furthermore, intervention with therapeutics that reverse these metabolic disturbances might ameliorate these risk factors, normalize endothelial function, and thus decrease the risk of cardiovascular disease among this patient population. Even if such patients are at no higher risk than HIV-negative patients with similar metabolic profiles, attention must be paid to modifiable risk factors as patients are living longer. This protocol aims to assess endothelial function among a group of HIV-infected patients with varying degrees of virologic control and levels of immune function on a variety of different HAART regimens. These patients will then be administered medications with known effects on lipid and glucose metabolism to determine if they might serve a role in improving these parameters and thus endothelial function. The results of this study will hopefully yield effective strategies to maintain the efficacy of HAART therapy while minimizing or reversing toxicities. Understanding the factors important to causing endothelial dysfunction will help better characterize the relative risks/benefits of early vs. late and continuous vs. intermittent HAART therapy. Additionally, it will hopefully offer some insights as to the underlying pathophysiology of the phenomenon of premature cardiovascular disease among HIV-infected patients on HAART that could then be more thoroughly investigated in subsequent clinical trials. We may ultimately learn that either the virus or antiretroviral drugs or the consequent lipid and insulin abnormalities they induce alters NO function at the level of the endothelium.