부산대학교 도서관

Introduction: Lipoprotein (a) (Lp(a)) has atherogenic effects. Proprotein convertase subtilisin /keksin type 9 (PCSK9) involved in the degradation of LDL-C receptors, increasing LDL-C blood level.Hypothesis: Identify the relationship between Lp(a) and PCSK9 blood levels and major cardiovascular events (unstable angina, myocardial infarction, cardiovascular death) after acute myocardial infarction.Methods: The study included 119 patients with acute myocardial infarction (97 men and 22 women aged 50-70 years). Blood samples were taken on the 2nd day of myocardial infarction. The Lp(a) blood level was determined by immunoturbidimetry (RANDOX), the PCSK9 blood level was determined by ELISA (BioVendor). Primary combined endpoint included hospitalization due to myocardial infarction and unstable angina and cardiovascular death. Patient follow-up was 52 weeks. Statistical analysis methods included Mann-Whitney test and non-parametric correlation by Spearman.Results: In 36 (30.2%) patients with acute myocardial infarction the Lp(a) blood levels were higher than 30 mg/dL. In 83 (69.7%) patients the Lp(a) blood level were below 30 mg/dL. Mean values of Lp(a) blood level was 29.26 ± 2.79 (men 27.71 ± 2.82 mg/dL, women 36.07 ± 8.54 mg/dL, p = 0.797). Mean PCSK9 blood level was 479.7 ± 15.4 ng/ml (males 465.6 ± 16.2ng/ml, females 534.9 ± 38.9 ng/ml, p = 0.122). There was no significant correlation of Lp(a) blood level with total cholesterol, LDL-C, triglycerids and PCSK9 blood levels. No significant correlation was found between Lp(a) and PCSK9 blood levels and cardiovascular events within 12 months. In the group of smoking patients (n = 22) there was found negative correlation between PCSK9 and HDL-C blood levels (-0.45, p = 0.039).Conclusions: Due to the fact that there is no relationship between Lp(a) and PCSK9 blood levels and subsequent cardiovascular events within 52 weeks, the effectiveness of the use of PCSK9 inhibitors after acute myocardial infarction is doubtful.