Splenic infarction was likely related to an embolic process, as suggested by the concomitant acute kidney infarctions (case 1) and induced by the particles used for BAE. However, the hypothesis of cholesterol emboli secondary to the arterial catheterization could not be excluded. Nevertheless, our patients did not have eosinophilia, cutaneous lesions, or renal dysfunction during follow-up. Furthermore, the short time between the symptoms onset and the interventional procedure goes against this hypothesis. Last, we cannot exclude that the left ventricular thrombus could have migrated and been source of splenic embolus in case 2. However, the duration of discontinuation of anticoagulation was short. Second, although echocardiography revealed a large akinetic apical segment with no thrombus, the cardiac MRI clearly showed the persistence of the thrombus.