Abstract 15057: Omega-3-Acid Ethyl Esters to Treat Dyslipidemia in Patients with Hiv: A Multi-Center Randomized Placebo-Controlled Trial

Abstract

Background The advent of antiretroviral therapy has resulted in increased life expectancy of patients with HIV, however cardiovascular disease is an increasing cause of death in these patients. Validating novel strategies for managing risk in HIV-infected patients is of paramount importance. Hence, we performed a randomized placebo-controlled trial of omega-3-acid (O3A) ethyl esters (Lovaza®) in dyslipidemic patients with HIV, hypothesizing that omega-3-acid ethyl esters would improve dyslipidemia and systemic inflammation. Methods HIV-infected patients (N=48 recruited at three sites) with CD4 count > 200 cells/mm3, suppressed viral load, and triglycerides > 200 mg/dL receiving stable retroviral therapy were randomized to placebo or 3.6 g/d of O3A. Fasting lipid profiles, soluble TNF receptors 1 and 2 and the Omega-3 Index (O3I; EPA+DHA as a proportion of total red blood cell membrane fatty acids) were assessed at baseline and after 8 weeks of treatment. Results Baseline HIV status and cardiovascular risk factors were similar between groups; 66% of patients were taking other lipid-lowering therapy (64% taking statins, 34% fibrates, 4% niacin, and 9% ezetimibe). The baseline total cholesterol was 202 ± 54, HDL 40 ± 12, and triglycerides 355 ± 166 mg/dL and baseline O3I was 5.2 ± 1.4% with no significant differences between groups. The triglyceride levels in patients receiving O3A decreased by 76 ± 126 mg/dL and increased 28 ± 149 mg/dL in patients receiving placebo (p = 0.016). The O3I increased by 3.2 ± 0.6 % in patients receiving O3A and was unchanged in patients receiving placebo (p<0.0001). There were no effects of treatment (vs placebo) on total cholesterol (C), HDL-C, non-HDL-C or soluble-TNF receptors 1 and 2. There were no significant adverse events reported. Conclusions Omega-3-acid ethyl esters decreased triglycerides and increased the O3I in dyslipidemic patients with well-controlled HIV but had no effect on other lipid measurements or markers of systemic inflammation. Large clinical trials with defined cardiovascular endpoints are needed to further clarify the role of O3A in reducing risk for cardiovascular disease in patients with HIV. GlaxoSmithKline supported this investigator-initiated study, providing drug and funding.