EFFICACY OF ROSUVASTATIN IN DYSLIPIDEMIA CORRECTION IN PATIENTS AFTER Q-WAVE MYOCARDIAL INFARCTION

Aim. To study the efficacy of rosuvastatin in dyslipidemia correction in patients after Q-wave myocardial infarction (Q-MI).Material and methods. 40 patients (aged 52.7±9.4 years old) were included into the study after 10-14 days of the acute Q-MI onset. Determination of blood lipids profile, alanine and asparagine transaminase levels was included into the initial examination. Rosuvastatin in a fixed dose of 20 mg/day was prescribed to the patients as a part of the standard therapy. Depending on the dynamics of the investigated parameters the individual doses of rosuvastatin were adjusted from 10 to 40 mg/day after 1 month of therapy. Final evaluation of blood lipids profile and transaminase levels was performed in the next 2 months of therapy.Results. Rosuvastatin 20 mg/day for 1 month in patients with an acute Q-MI provides a significant decrease in low-density lipoprotein (LDL) cholesterol level by 21.4%, and achievement of target levels of this parameter in 59.5% of patients. Rosuvastatin dose adjustment was required in 48.6% of patients after 1 month of therapy. Individually adjusted rosuvastatin doses provided the achievement of LDL cholesterol target levels by the end of the third month of treatment in 91% of patients. Elevated liver transaminase levels were observed in 7.5% of patients after 1 month of treatment. There were no new cases of adverse events after 3 months of therapy.Conclusion. Rosuvastatin 10-40 mg/day is effective and safe medicine for the treatment of dyslipidemia in patients after acute Q-MI

Oxidation-specific epitopes restrain bone formation

Atherosclerosis and osteoporosis are epidemiologically linked and oxidation specific epitopes (OSEs), such as phosphocholine (PC) of oxidized phospholipids (PC-OxPL) and malondialdehyde (MDA), are pathogenic in both. The proatherogenic effects of OSEs are opposed by innate immune antibodies. Here we show that high-fat diet (HFD)-induced bone loss is attenuated in mice expressing a single chain variable region fragment of the IgM E06 (E06-scFv) that neutralizes PC-OxPL, by increasing osteoblast number and stimulating bone formation. Similarly, HFD-induced bone loss is attenuated in mice expressing IK17-scFv, which neutralizes MDA. Notably, E06-scFv also increases bone mass in mice fed a normal diet. Moreover, the levels of anti-PC IgM decrease in aged mice. We conclude that OSEs, whether produced chronically or increased by HFD, restrain bone formation, and that diminished defense against OSEs may contribute to age-related bone loss. Anti-OSEs, therefore, may represent a novel therapeutic approach against osteoporosis and atherosclerosis simultaneously