Rosuvastatin significantly reduced the occurrence of symptomatic venous thromboembolism compared to placebo (0.18 vs 0.32 events per 100 person-years; HR 0.57; 95% CI 0.37-0.86; P=0.007).
RCT (n=17,802)
Does rosuvastatin 20 mg per day reduce the first occurrence of pulmonary embolism or deep-vein thrombosis in apparently healthy men and women with LDL < 130 mg/dL and hsCRP >= 2.0 mg/L?
In apparently healthy individuals with elevated hsCRP and normal LDL cholesterol, rosuvastatin 20 mg daily significantly reduces the risk of symptomatic venous thromboembolism.
Hazard Ratio: 0.57 (95% CI 0.37–0.86)
Absolute Event Rate: 0.18% vs 0.32%
p-value: p=0.007
BACKGROUND: Controversy persists regarding the extent of shared pathways between arterial and venous thrombosis and whether treatments of known efficacy for one disease process have consistent benefits for the other. Observational studies have yielded variable estimates of the effect of statin therapy on the risk of venous thromboembolism, and evidence from randomized trials is lacking. METHODS: We randomly assigned 17,802 apparently healthy men and women with both low-density lipoprotein (LDL) cholesterol levels of less than 130 mg per deciliter (3.4 mmol per liter) and high-sensitivity C-reactive protein levels of 2.0 mg per liter or higher to receive rosuvastatin, 20 mg per day, or placebo. We followed participants for the first occurrence of pulmonary embolism or deep-vein thrombosis and performed analyses of the data on an intention-to-treat basis. RESULTS: During a median follow-up period of 1.9 years (maximum, 5.0), symptomatic venous thromboembolism occurred in 94 participants: 34 in the rosuvastatin group and 60 in the placebo group. The rates of venous thromboembolism were 0.18 and 0.32 event per 100 person-years of follow-up in the rosuvastatin and placebo groups, respectively (hazard ratio with rosuvastatin, 0.57; 95% confidence interval CI, 0.37 to 0.86; P=0.007); the corresponding rates for unprovoked venous thromboembolism (i.e., occurring in the absence of a known malignant condition, trauma, hospitalization, or surgery) were 0.10 and 0.17 (hazard ratio, 0.61; 95% CI, 0.35 to 1.09; P=0.09) and for provoked venous thromboembolism (i.e., occurring in patients with cancer or during or shortly after trauma, hospitalization, or surgery), 0.08 and 0.16 (hazard ratio, 0.52; 95% CI, 0.28 to 0.96; P=0.03). The rates of pulmonary embolism were 0.09 in the rosuvastatin group and 0.12 in the placebo group (hazard ratio, 0.77; 95% CI, 0.41 to 1.45; P=0.42), whereas the rates of deep-vein thrombosis only were 0.09 and 0.20, respectively (hazard ratio, 0.45; 95% CI, 0.25 to 0.79; P=0.004). Consistent effects were observed in all the subgroups examined. No significant differences were seen between treatment groups in the rates of bleeding episodes. CONCLUSIONS: In this trial of apparently healthy persons, rosuvastatin significantly reduced the occurrence of symptomatic venous thromboembolism. (ClinicalTrials.gov number, NCT00239681.)
Glynn et al. (2009) conducted an RCT in Venous Thromboembolism (n=17,802). Rosuvastatin vs. Placebo was evaluated on First occurrence of pulmonary embolism or deep-vein thrombosis (symptomatic venous thromboembolism) (HR 0.57, 95% CI 0.37 to 0.86, p=0.007). Rosuvastatin significantly reduced the occurrence of symptomatic venous thromboembolism compared to placebo (0.18 vs 0.32 events per 100 person-years; HR 0.57; 95% CI 0.37-0.86; P=0.007).