Indexed on: 20 Dec '18Published on: 20 Dec '18Published in: Journal of Thrombosis and Haemostasis
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. The STAtins Reduce Thrombophilia (START) trial investigated whether statin affects coagulation in patients with prior VTE. After anticoagulation withdrawal, patients were randomized to rosuvastatin 20mg/day for 4 weeks or no intervention. Plasma samples taken at baseline and at the end of the study were analyzed employing thrombin generation assay. 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 97.22nM*min; 95%CI 40.92 to 153.53) and decreased in rosuvastatin users (mean -24.94nM*min; 95%CI -71.81 to 21.93). The mean difference in ETP change between treatments was -120.24nM*min (95%CI -192.97 to -47.51), yielding a 10.4% ETP reduction by rosuvastatin. Thrombin peak increased in both non-statin (mean 20.69nM; 95%CI 9.80 to 31.58) and rosuvastatin users (mean 8.41nM; 95%CI -0.86 to 17.69). The mean difference in peak change between treatments was -11.88nM (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. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.