This editorial refers to ‘Low disease prevalence and inappropriate implantable cardioverter defibrillator shock rate in Brugada syndrome: a nationwide study’ by A.G. Holst et al ., on page 1025 Brugada syndrome is an entity associated with premature sudden cardiac death, familial aggregation, and specific electrocardiographic abnormalities in the right precordial leads known as the coved-type or type 1 Brugada syndrome electrocardiogram (ECG). Importantly, the type 1 ECG requires at least a 2 mm elevation of the J point with a coved aspect followed by a negative T wave in two or more right precordial leads (V1, V2, or V3; often also V1 and V2 in the third intercostal space are included).1 This ECG pattern is not specific for Brugada syndrome alone but can also occur in other conditions such as myocardial infarction, severe electrolyte disturbances, or mediastinal tumours.1 Therefore, the diagnosis of Brugada syndrome requires at least one other criterion suggestive of arrhythmias or familial occurrence, namely documented ventricular tachycardia or fibrillation (VT/VF), a family history of sudden cardiac death <45 years of age, coved-type ECGs in family members, inducibility of VT/VF during electrophysiological study, unexplained syncope, or nocturnal agonal respiration. Hence, there is a difference between the Brugada ECG pattern and Brugada syndrome. Since its first description as a separate entity in the early 1990s, there have been many patients around the world who appeared to have this peculiar type 1 Brugada ECG pattern. In the last decade it also became clear that most of these patients had in fact a silent phenotype, they did not have and did not develop symptoms. Moreover, their type 1 ECG could only be uncovered through provocation with potent sodium channel blockers such as ajmaline, flecainide, or pilsicainide. However, because of early reports on …