Background: Atrial fibrillation is the most common complication after cardiac surgery. Postoperative atrial fibrillation (PAF) has been shown to increase length of stay, morbidity, and mortality. Because the clinical behavior of PAF parallels that of inflammation following surgery, we investigated the effect of the inflammatory mediator arachidonic acid on the electrical behavior of normal atrial tissue in vitro and assessed the efficacy of the topical application of anti-inflammatory drugs at suppressing PAF in an animal model.

Methods: To study changes in electrical behavior from inflammation, the conduction properties of six normal canine right atrial appendages were quantified as a function of the direction of impulse propagation with and without 80 mum arachidonic acid. To study the effect of topical anti-inflammatory drugs, 24 adult mongrel dogs were prepared according to the model of sterile talc pericarditis. Nine dogs received talc alone (T), seven received talc combined with 600 mg ibuprofen (T + I), and eight received talc combined with 10 mg methylprednisolone (T + M). Three days following preparation, programmed electrical stimulation was performed to quantify conduction characteristics and to attempt the induction of atrial fibrillation (AF).

Results: In vitro, arachidonic acid produced an anisotropic and rapidly reversible 36.1 +/- 3.4% (P = 0.01) decrease in conduction velocity transverse to the long axis only. In vivo, both ibuprofen and methylprednisolone significantly reduced the incidence of sustained AF (from 56 to 0% T + I and 12% T + M, respectively, P = 0.02). No differences in conduction velocities or refractory periods were seen during sinus rhythm among the groups.

Conclusions: Acute inflammation as mimicked by arachidonic acid slows conduction anisotropically, mainly transverse to the long axis of the atrial myocardial fibers. This may set the stage for reentry. Preventing inflammation in vivo by the topical application of anti-inflammatory drugs supports this hypothesis, suggesting a possible role for inflammation in the genesis of postoperative atrial fibrillation and shedding light on the mechanism underlying PAF.