Immediate Effects of Fluvastain on Circulating Soluble Endothelial Protein C and Free Tissue Factor Pathway Inhibitor in Acute Coronary Syndromes

Abstract

Treatment with fluvastatin significantly modified key hemostatic factors toward an antithrombotic effect within 6 h. These properties may, in part, explain the early salutary effects of fluvastatin in patients with ACS.

Fluvastatin Upregulates the Expression of Tissue Factor Pathway Inhibitor in Human Umbilical Vein Endothelial Cells

“…Meanwhile, it remains unclear if statins affect TFPI expression. Although some reports, including ours, described the association of statin administration and plasma TFPI concentration [9][10][11] , plasma TFPI does not reflect the amount of TFPI pooled in platelets and on the endothelium. Thus, we considered it beneficial to clarify if statins affect endogenous TFPI production in vitro.…”

Anti-Thrombotic Effects of Statins in Acute Coronary Syndromes: At the Intersection of Thrombosis, Inflammation, and Platelet-Leukocyte Interactions

“…Administration of simvastatin for only 3 days resulted in significant reductions in thrombin formation (baseline 0.258 nmol/L/s vs 0.175 nmol/L/sec at 3 days) and decreased factor Va [19]. In an analysis by Atalar et al [20], high dose fluvastatin (80 mg) administered within 6 hours of ACS presentation, resulted in significantly lower levels of soluble endothelial protein C receptor (EPCR), which would be predicted to reduce thrombin activation. Free tissue factor pathway inhibitor (fTFPI), which can reversibly inhibit Factor Xa, also significantly increased in both groups, although the magnitude of the rise was much greater in the fluvastatin group (450% in fluvastatin group compared to 155% in the placebo group).…”