Prevention of atrial fibrillation in cardiac surgery: time to consider a multimodality pharmacological approach

Abstract

Atrial fibrillation (AF) is very common within the first 5 days of cardiac surgery. It is associated with significant morbidity including stroke, ventricular arrhythmias, myocardial infarction, heart failure, acute kidney injury, prolonged hospital stay, and also short- and long-term mortality. The underlying mechanisms of developing AF after cardiac surgery are multifactorial; risk factors may include advanced age, withdrawal of beta-blockers and angiotensin-converting-enzyme inhibitors, valve surgery, obesity, increased left atrial size, and diastolic dysfunction. There are many pharmacological options in preventing AF, but none of them are effective for all patients and they all have significant limitations. Beta-blockers may reduce the incidence of AF by more than a third, but bradycardia, hypotension, or exacerbation of heart failure often limit their utility postoperatively. Recent evidence suggests that class III antiarrhythmic drugs, sotalol and amiodarone, are more effective than beta-blockers, but they both share similar hemodynamic side effects of beta-blockers. Magnesium, antiinflammatory drugs such as statins, omega fatty acids, and low-dose corticosteroids also have some efficacy and they have the advantages of not causing significant hemodynamic side effects. Data on effectiveness of calcium channel blockers, digoxin, alpha-2 agonists, sodium nitroprusside, and N-acetylcysteine are more limited. Because the pathogenesis of AF is multifactorial, a combination of drugs with different pharmacological actions may have additive or synergistic effect in preventing AF after cardiac surgery. Randomized controlled trials evaluating the effectiveness of a multimodality pharmacological approach in patients at high-risk of AF after cardiac surgery are needed.