Effect of dexamethasone on atrial fibrillation after cardiac surgery: prospective, randomized, double-blind, placebo-controlled trial.

2007 
Objective: The purpose of this study was to assess the effect of preoperative dexamethasone (DEX) on the occurrence of postoperative atrial fibrillation (AF). Design: Prospective, randomized, double-blind, placebo-controlled clinical trial. Setting: Tertiary referral center. Participants: Seventy-eight adult patients undergoing combined valve and coronary artery bypass graft (CABG) surgery were randomized to receive either DEX or placebo. Interventions: The DEX group received dexamethasone, 0.6 mg/kg, after induction of anesthesia, and the placebo group received an equal volume of normal saline. Interleukin (IL)-6, -8, and -10; tumor necrosis factor α; and endothelin (ET)-1 were measured preoperatively and on postoperative days (POD) 1, 2, and 3. Complement (C-4) and C-reactive protein (CRP) were measured preoperatively and on POD 2. Exhaled nitric oxide (NO) was measured preoperatively, 15 minutes after aortic unclamping, and 1 hour after intensive care unit admission. Measurements and Main Results: No significant difference in the incidence of AF was found between the placebo (41%) and DEX groups (30%) (95% confidence interval [−11%, 34%); p = 0.31). DEX significantly reduced at least 1 postoperative level of IL-6, IL-8, IL-10, CRP, and exhaled NO. DEX did not affect ET-1 or C-4 levels. IL-10 on POD 3 was positively correlated with postoperative hospital length of stay ( r = 0.30, p = 0.01). Increased levels of IL-8 and IL-10 on POD 1 were positively correlated with the intubation time ( r = 0.31, p = 0.01; r = 0.30, p = 0.01, respectively). Conversely, C-4 on POD 2 was negatively correlated with the intubation time and intensive care unit length of stay ( r = −0.32, p = 0.006; r = −0.30, p = 0.01, respectively). Conclusions: DEX did not affect the incidence of AF in patients undergoing combined CABG and valve surgery. However, it did modulate the release of several inflammatory and acute-phase response mediators that are associated with adverse outcomes.
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