“…Current evidence from TEE studies: Studies in AFl and AF performed in the last decade using TEE, although conflictual, have established some crucial points: 1) AFl in patients with a history of AF should be treated exactly as AF, since thromboembolic risk is in this case superimposable, leaving treatment uncertainties only for "pure" Afl [1,2], 2) Compared to AF, pAFl has a lower thromboembolic risk and less atrial stunning [13], 3) Risk of cardioembolic stroke and consequent opportunity for antithrombotic treatment builds from well established risk factors, consistently reported across the studies, among which cardiac rhythm is only one, together with: previous stroke, mitral stenosis, LV dysfunction, absence of MR, diabetes, hypertension, LA diameter, LASEC, LAAeV and LA thrombus, [3][4][5][6][7]9,14] 4) There is evidence from large TEE studies in patients with recent stroke that LAA function (namely emptying velocity) is the most powerful determinant of thrombus formation, independently of the underlying rhythm (sinus rhythm, AFl, or AF) [15]. 5) The simplistic paradigm that cardioembolic stroke occurs after CV because of a pre-existing cardiac thrombus moving peripherically should be reassessed since: a) TEE studies in AF/AFl CV offered strong arguments against it, one among many being the finding that most of post-CV embolic strokes both in AF and AFl occur in patients being cardioverted after a normal TEE, suggesting that if a cardiac thrombus is culprit, either it can not be ruled out by normal TEE at the time of CV or (more probably) it is generated after CV [1,16,17], b) the recent demonstration of safety of CV after 4-week anticoagulation in AF patients with thrombus detected at previous TEE, without repeat TEE, whereas echocardiographers know from their practice that a substantial proportion of thrombi take more time, even 3-4 months, to dissolve [17].…”