The vagus nerve wanders from the brainstem throughout the chest and abdomen innervating the heart, lungs and intestines. It is part of the autonomic nervous system and its cardiac action is to slow the heart. For some patients increased vagal activity is associated with the initiation of atrial fibrillation. So called vagal AF is enigmatic but should be more recognised. This is important because it needs to be managed differently from other more common types of atrial fibrillation.
When to suspect vagal AF: If the arrhythmia occurs at rest, after meals or during sleep then it is more likely to be vagal stimulated. Commonly this type of AF stops in the morning or during periods of exercise and can be precipitated by cough, nausea, after eating, swallowing and ingestion of cold foods and drinks. Vagal AF is more frequently seen in younger patients (30-50 years old), typically men and usually the heart is structurally normal on echocardiography. If the patient participates in endurance sports such as cycling, marathon running or cross country skiing then AF is also more common. ECG recordings often show a combination of atrial flutter alternating with atrial fibrillation. When a 24h ECG monitor is performed sinus bradycardia usually occurs before the onset of the AF. The ventricular rate during the AF is generally not fast. It is possible to measure the activity of the autonomic nervous system but it is difficult. One way is to assess heart rate variability which can assess the balance between the sympathetic and parasympathetic or vagal tone. Vagal stimulation shortens atrial effective refractory period and augments the ability of a single atrial premature beats to induce AF.
How should vagal AF be managed? Anticoagulation as per the underlying stroke risk predicted by CHAD2VASC score should be considered. With respect to reducing vagal AF episodes there are only anecdotal data about the best way to manage this. Drugs which block the sympathetic nervous system commonly used in the management of AF such as beta blockers and digoxin should be avoided. Alternative drugs such as those which reduce vagal tone should theoretically be effective. These drugs include flecainide, quinidine, and disopyramide. The pulmonary veins are a well-recognised source of AF in many patients and ablation can be effective in reducing paroxysmal AF. In contrast there are no specific studies reporting the success of ablation in vagal AF. One recent development is the awareness of increased activity of the If channels which raises the possibility that blockade of these channels with ivabradine might have an anti-arrhythmic in vagal AF patients. This is still an area for research and further information will be needed before this can be used routinely in the clinic.