The role of rivaroxaban in left ventricular thrombi.

Abstract

Left ventricular (LV) thrombus is usually seen in patients with significantly reduced LV systolic function especially those surviving a large ST-elevation myocardial infarction (STEMI). It usually occurs when the STEMI is anterior, anterolateral or anteroseptal with a large area of akinesia or dyskinesia involving the apex. It may occur following an inferior or a posterior STEMI with large akinetic segments in the inferior or posterior walls in rare occasions (1). The main risk associated with LV thrombi is distal systemic embolization that usually occurs during the first 3 - 4 months after infarction (2, 3). The main clinical consequence of thromboembolism is the occurrence of stroke, and the current guidelines do recommend the use of vitamin K antagonists (VKAs) as a preventive measure in patients with LV thrombus. Non-VKA direct oral anticoagulants (DOACs) are currently replacing VKA in several clinical indications, such as in patients with non-valvular atrial fibrillation (AF) where they were found to be either non-inferior or superior to VKAs. However, to our knowledge, there are no robust data on the use of DOACs for the treatment of LV thrombi, and all the available data are limited to individual case reports (4, 5). We present the effect of rivaroxaban, a DOAC, in the dissolution of LV thrombi in a series of patients presenting with acute coronary syndrome (ACS) and receiving dual antiplatelet therapy (DAPT) without valvular heart disease.