Introduction

Atrial fibrillation (AF) is a multisystemic disorder that is associated with an excess risk of stroke, heart failure and mortality.1 It remains the most common sustained arrhythmia and its significance should not be underestimated. Research focused on unveiling the mechanisms of AF began over a century ago. During this period, several theories have been proposed. More recently, the notion of rotors and spiral waves propagating in the atria was used to address the flaws of prior concepts and enhance our understanding on the development of AF.2 3 Presently, it is believed that the initiation and maintenance of AF is linked to a complex interplay between two crucial components: ‘trigger’ and ‘substrate’. The former refers to one or more ectopic foci that initiate rapid electrical activity resulting in depolarisation of surrounding cardiac myocytes. Maintenance of AF is subsequently dependent on the presence of a suitable substrate in terms of electrophysiological, mechanical and anatomical properties.4 The biggest breakthrough in our understanding of AF occurred two decades ago when Haïssaguerre et al demonstrated the role of pulmonary veins as the most common sites of triggers for the disease.5 This observation serves as the fundamental basis for ablation therapy for AF.

In practice, AF is frequently diagnosed following an incidental finding of uncoordinated atrial activation on a timely surface ECG; subsequent classification of the disease is based on temporal rhythm-based patterns (table 1).6 The latter concept stems from the idea that many patients who develop AF initially suffer from paroxysmal episodes due to triggers that promote …