LAUSR

This is the case of a 65-year-old male with permanent atrial fibrillation (AF), CHA2DS2VASc of 7, and previous history of intracranial hemorrhage (ICH) under oral anticoagulation. The patient underwent left atrial appendage occlusion (LAAO) with the implant of a 25-mm Amulet device without complications. Device implantation was slightly deep, and pulmonary ridge was not covered by the device disc (Fig. 1a). The patient was discharged under dual antiplatelet treatment (DAPT). At 3 months, TEE showed a small thrombus below the pulmonary ridge (Fig. 1b). Considering the small size of the thrombus and previous history of ICH, DAPT was continued. A new TEE after 2 months showed a giant central protruding thrombus (25 × 23 mm) (Fig. 1c). DAPT was therefore substituted by apixaban 2.5 mg/12 h (adjusted for renal function). After 3 months, the size of the thrombus was clearly smaller (11 × 10 mm) (Fig. 1d), and apixaban was continued. Six months later, TEE showed complete DRT resolution (Fig. 1e). Aspirin was therefore started, and an additional TEEs showed no novel thrombus (Fig. 1f). The patient did not experience any symptom that could suggest an embolic event during the clinical follow-up. Device related thrombosis (DRT) is currently one of the most concerning topics in the LAAO field. A central thrombus is defined as the one that is originated around the central pin or screw in the disc of the device. In previous series, this central location was described as the most frequent site for DRT [1]. Recently, it has been shown that the area below the pulmonary ridge is the most common location for DRT [2]. Other described DRT patterns are the ones that cover the entire disc in a diffuse and thin manner [3]. Some potential risk factors for DRT have been described: permanent AF, large LAA, prior stroke, higher CHA2DS2-VASc and HAS-BLED scores, chronic kidney disease, older age, and reduced ejection fraction [4–6]. Our patient presented a higher CHA2DS2VASc score, chronic kidney disease, and older age as potential risk factors for DRT. Among others, the absence of pulmonary ridge coverage may also represent a risk factor as it might generate areas of flow-turbulence and low-blood velocities [2, 7]. The present case highlights the fact that a central thrombus not always reflects a central origin. In this case, the coagulation cascade that was enhanced after the initial thrombus formation was probably the trigger for this giant central DRT. In our case, it is possible that oral anticoagulation had work better than antiplatelet therapy in the resolution of the thrombus, as DRT may imply a low flow situation such as observed in large veins or at r ia l /cardiac chambers . In fac t , anticoagulation has been shown to be superior to antiplatelet agents for stroke/thromboembolic prevention in AF [8]. More studies will be necessary to evaluate if not only upper DRT but also central thrombus are linked to the absence of pulmonary ridge coverage.