Simvastatin Effects on Inflammation and Platelet Activation Markers in Hypercholesterolemia

• Published in: BioMed research international 2018-01, Vol.2018 (2018), p.1-11
• Main Authors: Cavalot, Franco, Senkeev, Rouslan, Frascaroli, Chiara, Barale, Cristina, Russo, Isabella
• Format: Article
• Language: English
• Subjects: Activation; Adenosine diphosphate; Adult; Advanced glycosylation end products; Aged; Agglomeration; Arachidonic acid; Arteriosclerosis; Aspirin; Atherosclerosis; Biomarkers - blood; Biosynthesis; Blood cholesterol; Blood platelets; Cardiovascular disease; Care and treatment; Cholesterol; Collagen; Cytokines - blood; Deoxyguanosine; Development and progression; Diabetes; Diet; Drug dosages; E-selectin; E-Selectin - blood; Endothelium; Eotaxin; Family medical history; Female; Humans; Hypercholesterolemia; Hypercholesterolemia - blood; Hypercholesterolemia - drug therapy; Inflammation; Inflammation - blood; Inflammation - drug therapy; Insulin; Interleukin 10; Interleukin 13; Interleukin 6; IP-10 protein; Lipids; Low density lipoprotein; Low density lipoproteins; Male; Markers; Middle Aged; Monocyte chemoattractant protein 1; Oxidative stress; P-Selectin - blood; Platelet Activation - drug effects; Platelet aggregation; Platelet-derived growth factor; Platelet-derived growth factor BB; Reduction; Regression analysis; Simvastatin; Simvastatin - administration & dosage; Statins; Thrombosis; Transcription factors; Unsaturated fatty acids; Vascular endothelial growth factor; γ-Interferon
• ISSN: 2314-6133; 2314-6141
• DOI: 10.1155/2018/6508709

Background. Beside the lipid-lowering effect, statins slow the progression of atherosclerosis by exerting anti-inflammatory and platelet inhibiting effects. We investigated whether platelet inhibition by simvastatin correlates with the statin effects on lipid lowering, inflammation, oxidative stress, and endothelial and platelet activation. Methods. In hypercholesterolemic patients allocated to diet (n=20) or a 2-month treatment with diet plus 40 mg simvastatin (n=25), we evaluated platelet aggregating responses to ADP, collagen, and arachidonic acid (AA), the effect of aspirin on AA-induced aggregation, pro- and anti-inflammatory and atherogenic mediators (IL-1β, -5, -6, -7, -8, -9, -10, -12, and -13, IFN-γ, IP-10, Eotaxin, and sRAGE), markers of endothelium (sE-selectin, VEGF, and MCP-1) and platelet activation (sP-selectin, sCD-40L, RANTES, and PDGF-bb), and oxidative stress (8-OH-2’-deoxyguanosine). Results. After treatment, beside the improvement of lipid profile, we observed the following: a reduction of platelet aggregation to ADP (p=0.0001), collagen (p=0.0001), AA (p=0.003); an increased antiaggregating effect of aspirin in the presence of AA (p=0.0001); a reduction of circulating levels of IL-6 (p=0.0034), IL-13 (p