Objective. To evaluate the association of BNP and CRP with the development of postoperative atrial fibrillation following coronary artery bypass grafting surgery. Methods. The series consists of 125 patients (aged 65 ± 9 years), who underwent isolated CABG-surgery. BNP and CRP levels were measured pre- and 24 hours postoperatively and their correlation to the development of postoperative AF was analyzed. Results. Forty-four patients (35%) developed AF postoperatively. They were significantly older (68 ± 8 versus 63 ± 9, P = 0.01) and predominantly nonsmokers (18% versus 46%, P = 0.004), compared to the non-AF cases. In addition they showed significant higher preoperative mean BNP levels of 629 versus 373？pg/mL (P = 0.019). Postoperative BNP levels were significantly higher in both groups (AF-group: 1032？pg/mL versus non-AF group: 705？pg/mL; ), while there was a trend of more increased postoperative levels in AF-cases (P = 0.065). AF-episodes appeared significantly more frequent in the two highest quartiles of BNP levels with 44% (P = 0.035). On the contrary pre- and postoperative CRP levels were not associated with AF. Multivariable analysis revealed only increased preoperative BNP levels as independent predictor for postoperative AF (P = 0.036). Conclusion. Elevated preoperative BNP serum levels are associated with the development of post-CABG AF, while CRP does not seem to be influential. 1. Introduction Atrial fibrillation (AF) occurs in 25–40%, representing the most common arrhythmia in patients undergoing isolated coronary artery bypass surgery (CABG) [1–3]. Although it is not a life-threatening rhythm disturbance and may present as self-limiting onset, it has major medical and economical implications. It may compromise cardiac function, increase 2- to 3-fold the risk of stroke and thromboembolism, result in iatrogenic complications due to additional treatment efforts, prolong hospitalization duration (by 1–3 days), and elevate treatment cost [3–7]. Numerous studies, mainly retrospective, have been conducted to clarify the pathogenesis of postoperative AF as well to identify predisposing factors. However, the exact etiologic pattern still remains unclear. The proposed contributory factors include inflammation triggered by cardiopulmonary bypass, beta-blocker withdrawal, right coronary artery stenosis, atrial ischemia, inadequate intraoperative cardiac protection, perioperative ischemic injury, postoperative pericarditis, autonomic imbalance, and fluid/electrolyte disturbances during the intra- and postoperative periods [8–14]. Brain natriuretic
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