Adiponectin-dependent effects of pitavastatin on platelet-derived microparticles, soluble CD40 ligand and MCP-1 in hyperlipidemic patients
Abstract number: PP-WE-781
Inami1 N., Nomura2 S., Shouzu3 A., Omoto1 S., Shimazu4 T., Satoh1 D., Kajiura1 T., Yamada1 K., Iwasaka1 T.
11Second Department of Internal Medicine, Kansai Medical University, Moriguchi 22Division of Hematology, Kishiwada City Hospital, Kishiwada 33Department of Internal Medicine, Saiseikai Izuo Hospital 44Second Department of Internal Medicine, Kansai Medical University, Osaka, Japan
How-to-cite Inami N, Nomura S, Shouzu A, Omoto S, Shimazu T, Satoh D, Kajiura T, Yamada K, Iwasaka T. Adiponectin-dependent effects of pitavastatin on platelet-derived microparticles, soluble CD40 ligand and MCP-1 in hyperlipidemic patients. Journal of Thrombosis and Haemostasis 2009; Volume 7, Supplement 2: Abstract PP-WE-781
The effects of statins on platelet activation markers, chemokines and adiponectin were investigated in 135 patients with hyperlipidemia. Of the 135 hyperlipidemic patients, 63 were allocated to the simvastatin group, treated with simvastatin at the dose of 10 mg daily, and the remaining 72 were allocated to the pitavastatin group, treated with pitavastatin at the dose of 2 mg daily. Plasma levels of platelet-derived microparticles (PDMP), cell adhesion molecules (sCD40L and sP-selectin), chemokines (MCP-1 and RANTES) and adiponectin were measured at the baseline and after 6 months’ treatment in both the group. In addition, we carried out a basic study to investigate the induction by MCP-1 of tissue factor expression on cells of the monocytic lineage (THP-1). The plasma levels of PDMP, sCD40L, sP-selectin, RANTES and MCP-1 were higher, while those of adiponectin were lower, in the hyperlipidemic patients than in the normolipidemic controls. Plasma PDMP and sCD40L were positively correlated, while plasma adiponectin was negatively correlated, with the plasma levels of MCP-1. No significant differences in the plasma levels of PDMP, sCD40L, sP-selectin, RANTES and MCP-1 measured before and after treatment were observed in either the simvastatin or pitavastatin group. Significant increase of the plasma adiponectin levels was observed after 6 months’ treatment with pitavastatin, but not after an equal duration of treatment with simvastatin. When pitavastatin-treated patients were divided into two groups accorting to the adiponectin response to pitavastatin treatment, significant decreases of the plasma MCP-1, PDMP and sCD40L were onserved after pitavastatin treatment in the responder group. In the aforementioned basic study, MCP-1 by itself did not induce the expression of tissue factor on the THP-1 cells. However, the recombinant sCD40L-induced expression of tissue factor on THP-1 was enhanced by the addition of MCP-1.These findings suggest that PDMP, sCD40L and MCP-1 may participate in the development of atherothrombosis in patients with hyperlipidemia, and that pitavastatin may exert an adiponectin-dependent anti-atherothrombotic effect in hyperlipidemic patients.
Disclosure of interest: none declared.
