OBJECTIVE: Despite improved perioperative management, atrial fibrillation (AF) 
after coronary artery bypass grafting (CABG) remains a relevant clinical 
problem, whose pathogenetic mechanisms remain incompletely explained. A reduced 
incidence of postoperative AF has been described in CABG patients receiving IV 
tri-iodothyronine (T3). This study was designed to define the role of thyroid 
metabolism on the genesis of postoperative AF.
METHODS AND RESULTS: Free T3 (fT3), free thyroxine (fT4), and thyroid 
stimulating hormone were assayed at admission in 107 consecutive patients 
undergoing isolated CABG surgery. Patients with thyroid disease or taking drugs 
known to interfere with thyroid function were excluded. A preoperative rhythm 
other than sinus rhythm was considered an exclusion criterion. Thirty-three 
patients (30.8%) had postoperative AF. An older age (P=0.03), no therapy with 
beta-blockers (P=0.08), chronic obstructive pulmonary disease (P=0.08), lower 
left ventricle ejection fraction (P=0.09) and lower fT3 concentration (P=0.001), 
were univariate predictors of postoperative AF. On multivariate analysis, low 
fT3 concentration and lack of beta-blocking therapy were independently related 
with the development of postoperative AF (odds ratio, OR, 4.425; 95% confidence 
interval, CI, 1.745-11.235; P=0.001 and OR 3.107; 95% CI 1.087-8.875; P=0.03, 
respectively). Postoperative AF significantly prolonged postoperative hospital 
stay (P=0.002).
CONCLUSIONS: Low basal fT3 concentration can reliably predict the occurrence of 
postoperative AF in CABG patients.