Lipoprotein(a) levels and isoforms and fibrinolytic activity in postmenopause - Influence of hormone replacement therapy

Epidemiological studies suggest that hormone replacement therapy (HRT) decr eases the risk of cardiovascular disease in postmenopausal women via severa l mechanisms, including modifications in the fibrinolytic system and lipopr otein(a) [Lp(a)] levels. The aim of this study was to examine the influence of the levels and isoforms of Lp(a) on fibrinolytic activity in 91 postmen opausal women in comparison with premenopause and analyze the effect of HRT on those parameters. In postmenopause, an increase in plasma Lp(a) and pla sminogen activator inhibitor-1 (PAI-1) levels was found. A significant inve rse correlation was observed between Lp(a) or PAI-I levels and plasmin gene ration. Plasma samples with low molecular weight (MW) apo(a) isoforms showe d higher plasmin inhibition than plasmas with high MW apo(a) isoforms and s imilar levels of total Lp(a) and PAI-1. HRT induced a significant decrease in Lp(a) and PAI-I levels and an increase in estradiol levels, as well as a n increase in fibrinolytic activity. A significant correlation was found be tween the percentages of variation in Lp(a) levels and in plasmin generatio n and between the percentages of variation in PAI-1 levels and in the euglo bulin lysis time under HRT. In conclusion, the increase in fibrinolytic act ivity observed in women under HRT could be explained by two independent mec hanisms: (a) the decrease in PAI-1 and (b) the decrease in the inhibition o f plasmin generation due to the decrease in Lp(a) levels.