BACKGROUND: In observational studies, patients with HIV have higher levels of soluble ST2 (sST2), galectin-3, and growth differentiation factor-15 (GDF-15) than non-HIV controls. As statins exert pleiotropic immunomodulatory effects that may affect markers of myocardial fibrosis, the objective of the current study is to determine whether biomarkers of myocardial fibrosis reflecting subclinical pathology may be modified by statin therapy in patients with HIV. SETTING AND METHODS: Forty HIV+ men and women participated in a single center 12-month randomized, double-blind placebo-controlled trial of atorvastatin 40 mg every day vs. placebo. At baseline and 12-months, sST2, GDF-15, galectin-3 were measured. RESULTS: The changes in sST2 were -0.310 (-4.195, 2.075) vs. 1.163 (0.624, 4.715) ng/mL, median (interquartile range) atorvastatin vs. placebo (P = 0.04). The change in sST2 was significantly related to changes in monocyte activation marker sCD14 (r = 0.63, P < 0.0001) and MCP (r = 0.52, P = 0.0009), markers of generalized inflammation hs-IL-6 (r = 0.58, P = 0.0002), oxLDL (r = 0.49, P = 0.002), and GDF-15 (r = 0.54, P = 0.0008). CONCLUSIONS: sST2, a member of the IL-1 receptor family and a marker of fibrosis and inflammation increases over time among patients with HIV and this increase is attenuated by statin therapy in HIV. This effect may relate to immunomodulatory mechanisms of statins.
RCT Entities:
BACKGROUND: In observational studies, patients with HIV have higher levels of soluble ST2 (sST2), galectin-3, and growth differentiation factor-15 (GDF-15) than non-HIV controls. As statins exert pleiotropic immunomodulatory effects that may affect markers of myocardial fibrosis, the objective of the current study is to determine whether biomarkers of myocardial fibrosis reflecting subclinical pathology may be modified by statin therapy in patients with HIV. SETTING AND METHODS: Forty HIV+ men and women participated in a single center 12-month randomized, double-blind placebo-controlled trial of atorvastatin 40 mg every day vs. placebo. At baseline and 12-months, sST2, GDF-15, galectin-3 were measured. RESULTS: The changes in sST2 were -0.310 (-4.195, 2.075) vs. 1.163 (0.624, 4.715) ng/mL, median (interquartile range) atorvastatin vs. placebo (P = 0.04). The change in sST2 was significantly related to changes in monocyte activation marker sCD14 (r = 0.63, P < 0.0001) and MCP (r = 0.52, P = 0.0009), markers of generalized inflammation hs-IL-6 (r = 0.58, P = 0.0002), oxLDL (r = 0.49, P = 0.002), and GDF-15 (r = 0.54, P = 0.0008). CONCLUSIONS: sST2, a member of the IL-1 receptor family and a marker of fibrosis and inflammation increases over time among patients with HIV and this increase is attenuated by statin therapy in HIV. This effect may relate to immunomodulatory mechanisms of statins.
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