A pilot study evaluating the effect of rivaroxaban versus warfarin on the outcome of deep venous thrombosis patients

Abstract

Deep vein thrombosis (DVT) and acute pulmonary embolism (PE) are two manifestations of the same disorder, venous thromboembolism (VTE) (Prandoni, Prins et al., 2015). Venous thromboembolism affects 1 to 2 adults per 1000 annually and is the third most common cause of vascular death after myocardial infarction and stroke (Oger, 2000). Although its exact incidence is unknown, nearly 1 million cases of it (incident or recurrent, fatal and nonfatal events) occur in the United States each year (Heit, 2008). A major theory delineating the pathogenesis of venous thromboembolism (VTE), often called Virchow's triad (Dickson, 2004; Bagot and Arya, 2008), proposes that VTE occurs as a result of: alterations in blood flow (i.e., stasis), vascular endothelial injury and alterations in the constituents of the blood (i.e., inherited or acquired hypercoagulable state). A thrombus in the deep venous system of the leg is not dangerous in itself. The situation becomes life-threatening when a piece of the thrombus breaks off, travels downstream through the heart into the pulmonary circulation system, and becomes lodged in the lung leading to PE. Therefore, diagnosis and treatment of a deep venous thrombosis (DVT) is meant to prevent pulmonary embolism (Goldhaber, Visani et al., 1999). Also post-phlebitic syndrome can occur after a deep vein thrombosis (the affected leg can become chronically swollen and painful with skin color changes and ulcer formation around the foot and ankle)(Kahn and Ginsberg, 2004). 112 Summary  117 Given that VTE can be debilitating or fatal, it is important to treat it quickly and aggressively (Wells, Anderson et al., 2000). Conversely, because major bleeding induced by antithrombotic drugs can be equally harmful, it is important to avoid treatment when the diagnosis is not reasonable certainty. The current standard treatment for many patients with deep venous thrombosis is rapidly acting parenteral anticoagulants (low molecular weight heparin, unfractionated heparin or fondaparinux) for 5 to 7 days overlapped with at least 3 months of treatment with a vitamin K antagonist (warfarin) ( Guyatt, Gordon et al., 2012). Warfarin has been