Concept of ‘endocardial remodelling’ in fibrillating atria. In accordance to Virchow's triad hypercoagulability, flow abnormalities, and endothelial changes must co-exist to induce thrombogenesis at the atrial endocardium. Molecular studies have revealed substantial endocardial changes in left atrial tissue samples. Prothrombogenic factors (vWF, adhesion molecules like VCAM-1, P-selectin etc; green) are expressed at the surface of endothelial cells causing an increased adhesiveness of platelets and leucocytes to the atrial endocardium. This initiates atrial thrombogenesis at the atrial endocardium. Several clinical factors like diabetes mellitus, heart failure ageing etc. (CHA2DS2VASc Parameters) increase molecular alterations (oxidative stress pathways etc.) within myocytes and endothelial cells, and thereby, increase the expression of prothrombogenic factors. These alterations are not directly related to the presence of absensce of atrial fibrillation in the surface ECG, and therefore, help to explain, why thrombogenesis is increased even during episodes of sinus rhythm.