Atrial fibrillation (AF) is one of the most frequent complications of cardiac surgery, affecting more than one third of patients. The mechanism of this arrhythmia is believed to be reentry. The electrophysiologic substrate may be preexisting or may develop due to heterogeneity of refractoriness after surgery. Multiple perioperative factors have been proposed to contribute to the latter, including operative trauma, inflammation, elevations in atrial pressure (including that due to left ventricular diastolic dysfunction), autonomic nervous system imbalance, metabolic and electrolyte imbalances, or myocardial ischemic damage incurred during the operation. Whether ectopic beats originating in the pulmonary veins explain at least some episodes of postoperative AF, as has been shown for nonsurgical patients with the arrhythmia, is of current interest as such sites could easily be isolated at the time of surgery. The development of postoperative AF is associated with a higher risk of operative morbidity, prolonged hospitalization, and increased hospital cost compared with that in patients remaining in sinus rhythm. Many factors have been identified as being associated with postoperative AF, but the most consistent variable across studies is increasing patient age. It is speculated that age-related pathologic changes in the atrium contribute to arrhythmia susceptibility. An important modifiable risk factor for postoperative AF is the failure to resume therapy with β-adrenergic receptor blockers after surgery. The stratification of patients who are at higher risk for AF would focus preventative strategies on patients who are most likely to benefit from such therapy. Nonetheless, since postoperative AF often develops in patients with comorbidities who are predisposed to other complications and prolonged hospitalization, it is presently unclear whether the prevention of postoperative AF will result in improved patient outcomes, particularly shorter hospitalizations.