Atrial fibrillation (AF) is common after cardiac surgery, occurring in 11% to 40% of patients after coronary artery bypass grafting (CABG)1-8 and in more than 50% of patients after valvular heart surgery.
Atrial fibrillation (AF) is common after cardiac surgery, occurring in 11% to 40% of patients after coronary artery bypass grafting (CABG)1-8 and in more than 50% of patients after valvular heart surgery.2 A recent meta-analysis of 8 trials that included a total of 17,748 patients undergoing isolated CABG demonstrated an overall incidence of postoperative AF of 25%.9 Risk factors for postoperative AF have been clearly delineated and include age, concomitant valvular heart surgery, hypertension, a history of previous AF, and male sex.10 Although postoperative AF rarely persists for more than 4 to 6 weeks after surgery, it has a strong negative impact on patient recovery in the early postoperative period. AF is more frequent in patients readmitted to the intensive care unit,11 those requiring reintubation,11,12 and those with pneumonia, perioperative myocardial infarction, congestive heart failure, cardiac arrest, and renal failure. Overall, mortality is higher at 30 days and 6 months in patients with AF after cardiac surgery than in those without AF.11
Several mechanisms have been proposed to explain the high incidence of AF after cardiac surgery, including sympathetic activation induced by the postoperative state, altered atrial electrophysiological properties, and systemic inflammation. Prophylaxis with beta blockers and amiodarone target the first 2 mechanisms, respectively. Treatment with either agent is effective for preventing AF,13-15 but prophylactic amiodarone is rarely employed due to concerns about toxic side effects. Although it is now well recognized that cardiopulmonary bypass is associated with a systemic inflammatory response,16,17 less investigative effort has focused on strategies to reduce inflammation in order to prevent postoperative AF. In
the present study
, Halonen et al conducted a randomized, double-blind, placebo-controlled study of 241 patients that evaluated the efficacy of hydrocortisone for preventing postoperative AF.18 The hydrocortisone was administered starting on the evening of the operative day, then 100 mg every 8 hours for the ensuing 3 days. The primary end point was the incidence of postoperative AF, which was defined as an AF episode lasting longer than 5 minutes. The incidence of AF was significantly lower in the hydrocortisone group than in the placebo group (30% vs 48%, hazard ratio 0.54, P = .004). Importantly, the investigators did not observe an increased incidence of superficial or deep wound infections in the hydrocortisone group.
There are some important limitations of this study that militate against recommending prophylactic hydrocortisone for this indication at the present time. The definition of AF (episodes lasting 5 minutes or greater) likely resulted in the inclusion of many episodes of brief AF that may not have required treatment or affected clinical outcomes. No data was presented regarding the duration of AF episodes that qualified as end point events. In addition, nearly two thirds of the patients who were screened for the study were excluded from participation, which suggests that the study population may not be representative of most patients who undergo cardiac surgery. While the exclusion criteria are specified, the breakdown of the precise reasons why these patients were excluded was not provided. These data are important for clinicians who need to determine if the results of this study can be generalized to patients who are encountered in routine clinical practice. Future studies that investigate the use of corticosteroids for the prevention of postoperative AF should be large, adequately powered to test efficacy and detect important toxic side effects, and utilize a clinically meaningful definition of postoperative AF.