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Management of left atrium appendage thrombosis in nonvalvular atrial fibrillation patients

We have read with interest a recent article comparing non-vitamin K oral anticoagulants (NOACs) and warfarin for left atrial appendage (LAA) thrombus resolution in nonvalvular atrial fibrillation (AF) or flutter reported by Hussain et al. They concluded that in patients with nonvalvular AF or flutter who were OAC naïve at the time of LA appendage thrombus diagnosis, treatment with NOACs and warfarin for at least 3weeks had similar rates of complete LAappendage thrombus resolution.1 We believe that their study is likely to form a valuable addition to the literature. Despite a thorough study design, in our opinion, some important issues have not been addressed by the authors. AF is the most common sustained cardiac arrhythmia and is associated with increased risk of systemic thromboembolism due to the development of LA and LA appendage thrombus. LAA is the most important site of LA thrombus formation, with more than 90% of thrombus occurring within this anatomical structure.2 Once an LAA thrombus is diagnosed, current guidelines were recommended for effective anticoagulation at least 3 weeks before and 4 weeks after cardioversion (CV).3 In this setting, vitamin K antagonist therapy for 4 weeks with repeated transesophageal echocardiogram (TOE) showed resolution of thrombus in 80-89% patients who were not previously anticoagulated.3 Several randomized trials have demonstrated the efficacy of NOACs to reduce rates of stroke and systemic thromboembolism compared to warfarin; however, data on the use of NOACs in patients with thrombus in LAA are less well established. In the study of Hussain et al, 31 patients who had not received anticoagulant therapy previously underwent TOE before CV. Persistent AF was present in 18 of the patients in the study, but the reason for not receiving anticoagulant therapy prior to these patients was not specified. How do the authors explain this situation? Were there any patients who had previously started anticoagulant therapy and discontinued due to side effects? If so, what should be taken into consideration when starting anticoagulant therapy again? A recent study byWhiteside et al following≥ 4weeks of continuous anticoagulation with apixaban, the prevalence of LAA thrombus and LAAthrombus/dense spontaneousechocardiographic contrastwas3.1 and 6.6%, respectively. In addition, persistent AF, left ventricular ejection fraction<30%, severe LA dilation, and reduced LAA velocity were associated with thrombus formation. Persistent AF and reduced LAA velocity were identified as independent predictors of LAA thrombus.4 However, in this study by Hussain et al, no information was given about whether these parameters were measured or not. In our opinion, if the data on time in therapeutic range for the warfarin group and NOAC treatment administration criteria for patients were specified; more objective and valuable results could be obtained about this study.