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Rosuvastatin use reduces thrombin generation potential in patients with venous thromboembolism: a randomized controlled trial
Author(s) -
Orsi Fernanda A.,
Biedermann Joseph S.,
Kruip Marieke J.H.A.,
Meer Felix J.,
Rosendaal Frits R.,
Hylckama Vlieg Astrid,
Bos Mettine H. A.,
Leebeek Frank W. G.,
Cannegieter Suzanne C.,
Lijfering Willem M.
Publication year - 2019
Publication title -
journal of thrombosis and haemostasis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.947
H-Index - 178
eISSN - 1538-7836
pISSN - 1538-7933
DOI - 10.1111/jth.14364
Subject(s) - rosuvastatin , medicine , hemostasis , statin , randomized controlled trial , thrombin generation , thrombin , rosuvastatin calcium , platelet
Essentials The role of statins in hemostasis and venous thromboembolism ( VTE ) prophylaxis is not clear. This trial assessed whether rosuvastatin use affects thrombin generation in patients with VTE . Endogenous thrombin potential and peak were decreased by 10% and 5% with rosuvastatin therapy. These results provide basis for trials on the efficacy of statins in reducing recurrent VTE risk.Summary Background Statin therapy could form an alternative prophylactic treatment for venous thromboembolism ( VTE ) if statins are proven to downregulate hemostasis and prevent recurrent VTE , without increasing bleeding risk. Objectives The STA tins Reduce Thrombophilia ( START ) trial investigated whether statin affects coagulation in patients with prior VTE . Patients/methods After anticoagulation withdrawal, patients were randomized to rosuvastatin 20 mg day −1 for 4 weeks or no intervention. Plasma samples taken at baseline and at the end of the study were analyzed employing thrombin generation assay. Results and conclusions The study comprised 126 rosuvastatin users and 119 non‐users. Mean age was 58 years, 61% were men, 49% had unprovoked VTE and 75% had cardiovascular (CV) risk factors. Endogenous thrombin potential (ETP) increased from baseline to end of study in non‐statin users (mean 97.22 n m *min; 95% CI, 40.92–153.53) and decreased in rosuvastatin users (mean −24.94 n m *min; 95% CI, −71.81 to 21.93). The mean difference in ETP change between treatments was −120.24 n m *min (95% CI, −192.97 to −47.51), yielding a 10.4% ETP reduction by rosuvastatin. The thrombin peak increased in both non‐statin (mean 20.69 n m ; 95% CI, 9.80–31.58) and rosuvastatin users (mean 8.41 n m ; 95% CI −0.86 to 17.69). The mean difference in peak change between treatments was −11.88 n m (95% CI, −26.11 to 2.35), yielding a 5% peak reduction by rosuvastatin. Other thrombin generation parameters did not change substantially. The reduction in ETP and peak by rosuvastatin was more pronounced in the subgroups of participants with CV risk factors and with unprovoked VTE. We conclude that rosuvastatin reduces thrombin generation potential in patients who had VTE.