This article refers to 'Systemic embolism in amyloid transthyretin cardiomyopathy' by S. Vilches et al., published in this issue on pages 1387-1396.Transthyretin amyloidosis (ATTR) is a progressive cardiomyopathy in which amyloid fibrils accumulate in the myocardial interstitial space leading to expanding extracellular volume, tissue disruption and eventually progressive heart failure. 1 The amyloid fibrils deposit in all parts of the heart including ventricles, atria, and cardiac valves, and have been demonstrated in up to 13% of patients with heart failure with preserved ejection fraction 2 and 8.4% of patients with severe aortic stenosis. 3 The haemodynamic consequence of ATTR is restrictive physiology characterized by impaired inotropic reserve and elevated right and left ventricular filling pressure which is very pronounced during exercise. 4 The atrial and ventricular amyloid deposition with altered haemodynamics leads to structural changes in the cardiac chambers with most often significantly bi-atrial dilatation which increases the risk of development of atrial fibrillation (AF). Actually, AF is very frequently reported in ATTR patients with a prevalence of 40-60% at the time of ATTR diagnosis. 5,6 Furthermore, several studies in patients suffering from cardiac amyloidosis have demonstrated a high risk of cardiac thrombus diagnosed by either cardiac magnetic resonance, 7 transoesophageal echocardiography 8,9 or in autopsy data. 10 Despite the numbers of patients with ATTR, especially wild-type ATTR, is increasingly diagnosed, little evidence exists on AF management, risk of systemic embolism (SE) and indication for oral anticoagulation (OAC) in ATTR patients. As such, research unravelling details of SE, effect of OAC and clinical management of AF in ATTR is highly appreciated. In this editorial, we shall focus on the identification of ATTR patients at increased risk of SE, risk modification of SE by OAC in ATTR patients and clinical management of AF in ATTR patients.