Preventing Postoperative Atrial Fibrillation: A Stimulating New Approach.

Abstract

Postoperative atrial fibrillation (POAF) occurs in up to 50% of patients undergoing open-heart surgery and is associated with worse outcomes, including stroke, mortality, increased length of hospital stay, and increased health care costs.1 AF typically occurs within one week after cardiac surgery and 70% of patients who have AF after coronary artery bypass surgery have episodes within the first 3 days.2 POAF is no longer considered a transient one-off event, as it highlights an increased long term vulnerability to the development of AF.3 Therefore, the consequences of POAF are more substantial and sustained than may first appear. The mechanism(s) of POAF (Figure) is a combination of postoperative pro-fibrillatory milieu consisting of pericarditis, atrial injury, heightened sympathetic tone, ischemia-reperfusion, hemodynamic and metabolic derangements, superimposed on preexisting electrophysiological and structural atrial abnormalities.4,5 An imbalance, specifically, overactivity in both sympathetic and parasympathetic activities of the cardiac autonomic nervous system (CANS), plays a crucial role in promoting AF, including postoperative AF.6–8 Current guidelines recommend medical therapy for AF after cardiac and thoracic surgery, but do not include any nonpharmacological interventions for treatment or prevention of AF.1 To treat postoperative AF, beta blockers are recommended as first-line therapy, followed by nondihydropyridine calcium channel blockers if adequate rate control is not achieved with beta blockers. For prevention of postoperative AF in high-risk patients undergoing cardiac surgery, preoperative amiodarone can be used to reduce the incidence of AF (Class IIA recommendation). There is also data to support using sotalol or colchicine to reduce the risk of postoperative AF (Class IIB recommendation). However, pharmacological preventative measures and treatments can be limited by medication side effects, including hypotension and bradycardia. In the current issue, Andreas et al9 present pilot data on the use of noninvasive low level transcutaneous electrical stimulation (LLTS) of the greater auricular nerve to reduce the risk of postoperative AF.9 Their hypothesis is that LLTS modulates activity of an imbalanced CANS triggered by the postoperative insult, leading to protection against POAF. In this single-center, randomized, double-blind study, 40 patients were randomized to LLTS treatment (n=20) or sham group (n=20). After cardiac surgery, patients in the treatment group received stimulation applied via electrodes in the triangular fossa of the ear for 40-minute increments followed by a 20-minute break for up to 2 weeks. All patients had continuous ECG monitoring as well as inflammatory markers including C-reactive protein and interleukin-6 measured immediately postsurgery and day 2 and 7 postsurgery. The key finding was that patients receiving LLTS had a significantly lower incidence of POAF EDITORIAL