Rosuvastatin use increases plasma fibrinolytic potential: a randomised clinical trial. (16th April 2020)

• Record Type: Journal Article
• Authors: Schol‐Gelok, Suzanne; de Maat, Moniek P. M.; Biedermann, Joseph S.; van Gelder, Teun; Leebeek, Frank W. G.; Lijfering, Willem M.; van der Meer, Felix J. M.; Rijken, Dingeman C.; Versmissen, Jorie; Kruip, Marieke J. H. A.
• Is Part Of: British journal of haematology. Volume 190:Number 6(2020)
• Page Start: 916
• Page End: 922
• Publication Date: 2020-04-16
• Subjects: venous thromboembolism -- fibrinolysis -- blood coagulation tests -- fibrin clot lysis time -- HMG‐CoA reductase inhibitors; Hematology -- Periodicals; Blood -- Diseases -- Periodicals; 616.15
• DOI: 10.1111/bjh.16648
• Languages: English
• ISSNs: 0007-1048

Abstract

Abstract: We conducted a study to assess the effect of rosuvastatin use on fibrinolysis in patients with previous venous thromboembolism (VTE). This was a post hoc analysis within the STAtins Reduce Thrombophilia (START) study (NCT01613794). Plasma fibrinolytic potential, fibrinogen, plasmin inhibitor, plasminogen activator inhibitor‐1 (PAI‐1) and thrombin‐activatable fibrinolysis inhibitor (TAFI) were measured before and after four weeks of rosuvastatin or no treatment in participants with prior confirmed VTE, after ending anticoagulant therapy. In the non‐rosuvastatin group ( n = 121), plasma fibrinolytic potential and individual fibrinolysis parameters did not change at the end of the study versus the baseline, whereas in the rosuvastatin group ( n = 126), plasma fibrinolytic potential increased: the mean clot lysis time decreased by 8·75 min (95% CI −13·8 to −3·72), and plasmin inhibitor levels and TAFI activity were lower at the end of the study (−0·05 U/ml; 95% CI −0·07 to −0·02 and −4·77%; 95% CI −6·81 to −2·73, respectively). PAI‐1 levels did not change and fibrinogen levels were 0·17 g/l (95% CI 0·04–0·29) higher. In participants with prior VTE, rosuvastatin use led to an increased fibrinolytic potential compared with non‐statin use. Our findings support the need for further studies on the possible role for statins in the secondary prevention of VTE.