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The pathogenesis and risk of ischaemic stroke are associated with the inflammatory process that is involved in the development of atherosclerosis. The blood level of C‐reac‐ tive protein (CRP) is a widely used predictor of inflammation. The level of this protein is used for the assessment of risk and prognosis in cardiovascular disorders and stroke. C‐reactive protein level depends on genetic and environmental factors such as genetic polymorphism and statin use. The aim of the study was to assess the potential effects of sim‐ vastatin on the CRP level and lipid profile in stroke in regard to the variant of ‐717A>G CRP gene polymorphism. Materials and methods: There were 125 subjects enrolled in the study, hospitalized with a diagnosis of ischaemic stroke (95 patients in group 1 and 30 patients in group 2). Patients in group 1 were treated with a 40 mg dose of simvastatin from the 1st day; in group 2 simvastatin was not used. Blood CRP level and lipid profile were measured in all patients on day 1 and 10 after admission. The ‐717A>G CRP gene polymorphism status was genotyped in all patients. Results: In both groups there was a significant increase in CRP level, despite simvastatin treatment. No association was found between genotype and levels of both CRP and lipids change from the 1st to the 10th day. Conclusions: Simvastatin does not affect the CRP level in rela‐ tion to any of the ‐717A>G CRP gene polymorphism variants in the acute phase of stroke. Simvastatin significantly changes lipid levels, but it does not depend on ‐717A>G CRP gene polymorphism.

pomeranian journal of life sciences

The effects of simvastatin on the C-reactive protein level and lipid profile in the acute phase of ischaemic stroke in relation to -717A&gt;G CRP gene polymorphism