Resolution of giant left atrial appendage thrombus with rivaroxaban

doi:10.1160/TH12-11-0821 Thromb Haemost 2013; 109: 583–584 A 64-year-old man was transferred to our hospital for external cardioversion (ECV) of symptomatic persistent atrial fibrillation (AF). At the time of hospital admission the patient presented with functional NYHA class III; he had a clinical history of symptomatic coronary artery disease, ischaemic cardiomyopathy with severely impaired left ventricular function, and chronic kidney disease stage 3B to 4 (creatinine clearance CrCL 29 ml/minute). Pretreatment with the vitamin-K antagonist (VKA) phenprocoumon was instituted in 2006 due to a high AF related thromboembolic risk with an actual CHA2DS2VASc score of 6. Since the international normalised ratio (INR) was not well controlled before elective ECV we performed a transesophageal echocardiography (TEE), which revealed a small thrombus formation (11 x 12 mm) in the apex of the left atrial appendage (LAA) (▶ Figure 1 A). Therefore, ECV was deferred for six weeks under closely controlled VKA therapy with levels of INR ranging between 2.5 – 3.5 (mean 3.2 ± 0.7, range 2.4 to 4.2). Interestingly, repeated TEE (▶ Figure 1 B) showed a markedly increased giant thrombus mass (12 x 45mm) now protruding into the left atrium. In general VKAs have a slow onset of action and their indirect anticoagulant activity depends on clearance of the vitamin K–dependent clotting proteins and replacement with functionally impaired factors (1). In contrast to current guidelines, there is increasing evidence that VKAs have a poor capability to resolve large intracardiac thrombi. Therefore, we decided to switch oral anticoagulation (OAC) to the direct factor Xa (FXa) inhibitor rivaroxaban dosed with 15 mg once daily. After four weeks of rivaroxaban treatment TEE showed a relevantly decreased thrombus size (▶ Figure 1 C) and a complete thrombus resolution was achieved after six weeks of anticoagulant therapy with the FXa inhibitor (▶ Figure 1 D). Finally, ECV was performed successfully without clinical signs of cardiac embolism and the patient was discharged in good medical conditions under continued anticoagulant treatment with rivaroxaban. To the best of our knowledge this is the first documented case of LAA thrombus resolution under rivaroxaban therapy and illustrates some clinically important characteristics of the new direct acting FXa inhibitor. First, in contrast to indirect acting VKAs, FXa inhibitors have the potential to (a) prevent de novo thrombus formation and more importantly (b) to resolve established thrombi by direct inhibition of free and thrombusassociated FXa. Thereby they reduce clot-induced fibrinopeptide A generation to a similar extent as hirudin, a potent inhibitor of thrombin (2).