The physiology of the autonomic innervation of the heart is intriguing. Bradycardia and tachycardia promote their own automaticity, not necessarily related to the ANS [
33]. The sinus node, the atria and the AV node are controlled by the vagal and adrenergic nervous system. Apart from its effects on heart rate, the ANS contributes to inhomogeneous activation of the atria, and has effects on conduction and repolarisation creating or maintaining the arrhythmia. Coumel made a very clear and didactic distinction between vagally induced and adrenergic mediated forms of AF [
16]; the first occurred in the setting of a normal heart, at rest, while the second typically occurred during exercise, and suggested the presence of a more pathological and damaged substrate. The first type of AF was not to be treated with beta-blockers, while this was considered to be the perfect therapy for the second type. From a clinical point of view, only a minority of AF patients seem to correspond to these prototypes, and many are mixed [
34]. Is the role of the ANS then only marginal? In specific situations, the influence of the ANS can be more pronounced, as in postoperative situations, where vagal withdrawal, with sudden adrenergic changes, can provoke AF [
35]. Epicardial fat pad ablation was found to be successful to prevent AF after coronary bypass [
36]. According to some, PVI should be completed by additional ablation of the autonomic ganglia, while a recent surgical trial was negative [
37]. It cannot be excluded that the success of large circumferential ablation (as opposed to segmental PVI) is due to modulation of the antra, where many of these structures are situated [
38]. Furthermore, beta-blocking agents are the only drugs withstanding the scrutiny of the Cochrane review of antiarrhythmic drugs, with a significant reduction of AF recurrence, and a low incidence of side effects [
39]. Therefore, I feel that the influence of the ANS should still be assessed in all patients, even when this is limited to a simple Holter recording.