Background: Chronic inflammation may play role in the development of atherosclerosis and its complications. In hypercholesterolemia, the evidences of chronic inflammation such as the stimulation of chemokines and cytokines, increase in endothelial adhesion molecules, and the immune reactions against oxidants on lipoproteins are detected. It was shown that statins had some beneficial effects on lipids, thrombosis, endothelial dysfunction, and smooth muscle proliferation.
Aim: To investigate the effects of atorvastatin on hematological and inflammatory parameters in prospective study.
Material and methods: Forty patients (14 male and 26 female) with primary hypercholesterolemia were treated with 20 mg/day atorvastatin for 12 weeks, according to Adult Treatment Panel for Third Report of National Cholesterol Education Program. All patients received a detailed description of this study and signed consent prior to enrollment. National and local ethical committees approved this study. The exclusion criteria were secondary hypercholesterolemia, acute coronary syndromes, liver and renal dysfunctions, diabetes mellitus, acute/chronic infection and inflammatory diseases, pregnancy, lactation, malignancy, and tendency to bleeding. At baseline, and 12th weeks, lipid levels such as low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), very-low-density lipoprotein cholesterol (VLDL-C), triglycerides (TGs), and hematological parameters such as whole blood cell counts, hemoglobin and fibrinogen levels, CD3, CD4, CD5, CD8, CD14, CD16, CD19, CD40, CD45 using flow-cytometry, inflammatory parameters such as interleukin-1 (IL-1), IL-6, IL-18, tumor necrosis factor-alpha (TNF-a), interferon-gamma, soluble CD-40, intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1, high-sensitive CRP, sedimentation rate, and enzymes including CK, AST, ALT were evaluated. The results were compared with two-paired student’s-t test.
Results: At the end of study, atorvastatin decreased TC (p<0.001), LDL-C (p<0.001), TGs (p=0.006), VLDL-C (p=0.012), and HDL-C (p<0.001). While absolute lymphocyte (p=0.003) and platelet counts (p=0.001) were decreased with atorvastatin treatment, absolute monocyte count increased (p=0.002). On flow-cytometric examination, the expressions of CD14 (p=0.015) and CD19 (p=0.039) on lymphocytes were decreased with atorvastatin. Moreover, atorvastatin decreased the levels of TNF-a (p<0.001), sCD40 (p<0.001), ICAM-1 (p<0.001), and IL-18 (p=0.024). ALT increased at the end of treatment (p=0.041). But important adverse events were not seen in the patients.
Conclusion: The anti-platelet and anti-inflammatory effects of atorvastatin, independent from lipid-lowering effects, may play an important role on the prevention of atherosclerosis, in addition to its beneficial effects on lipid parameters.
Disclosures: No relevant conflicts of interest to declare.