Venous thromboembolism (VTE) is a frequent clinical condition and a common cause of potentially preventable mortality, morbidity, and increased medical costs. Risk-appropriate prophylaxis can prevent most VTE events; however, it is often underutilized in clinical practice.1 Preventing VTE is the target of many researches. Many risk factors have been related to the development of VTE including, surprisingly, lipids. Besides their effects on atherogenesis, it has been suggested that lipids and lipoproteins could contribute to the development of VTE. This association has been investigated in a few observational studies with conflicting results.2,3 Moreover, there is a need to find an anticoagulant with minimum risk of bleeding. As a result, many trials were done trying to explore the role of statins in the prevention of VTE.
Then JUPITER (Justification for the Use of Statins in Prevention: an Intervention Trial Evaluating Rosuvastatin) came along and confirmed the statin role in VTE.4 However, just before we start selling statins for this new role, Rahimi and colleagues asked us to think again. They reported a meta-analysis5 of 29 randomized controlled trials (RCTs) investigating the effect of statins on the occurrence of venous thrombosis. Of the 29 RCTs with primary end points other than VTE, there were 22 trials comparing statin use to no statin (105,759 participants), and seven trials comparing intensive versus a standard dose statin regimen (40,594 participants). VTE events were reported as adverse effect, and most of the results were unpublished but data were made available to the authors.
The meta-analysis showed that there was no statistically significant reduction in VTE events in the statin group (0.9% versus 1%, odds ratio [OR] 0.89, 95% CI 0.72 to 1.01, P=0.08) in the 22 trials comparing statin use to no statin use, and also higher doses of statins did not reduce the VTE events compared to standard dose statin (1% versus 1%, OR 0.98, 95% CI 0.80 to 1.20, P=0.87). When they excluded JUPITER trial (which had the most positive results for the powerful preventive role of statin), the findings of VTE events did not change (431 [0.9%] versus 461 [1.0%], OR = 0.93 [95% CI 0.82–1.07], p = 0.32 among the other 21 trials). The effect of statin use (or higher doses of statin) on deep vein thrombosis (DVT) and pulmonary embolism (PE) was examined individually. They found no benefit for either statin therapy or higher dose regimen in reducing the risk or either DVT (266 versus 311, OR 0.85, 95% Confidence Interval [CI] 0.72–1.01) or PE (205 versus 222, OR 0.92, 95% CI 0.76–1.12). They concluded that the protective effect of statin (or higher doses) on VTE is modest (up to 1-fifth) at best.
Many beneficial effects, beyond the lipid lowering effect, had been attributed to statins. However, one should be cautious before rushing to use them for VTE prevention.
1. Streiff MB, Carolan HT, Hobson DB, et al. Lessons from the Johns ...