Are current smokers paradoxically protected against atrial fibrillation after cardiac surgery?

The hyperadrenergic condition following surgical stress and inotropic drugs have been identified as leading causes for postoperative atrial fibrillation (AF). Smokers are characterized by higher catecholamine levels and tolerance. We tested the hypothesis that smoking patients are less prone to develop postoperative AF.

A total of 3,245 coronary artery bypass and valvular procedures were reviewed. Predictors of AF and interaction between variables were explored by multivariable logistic regression. AF-predictive scores were created and validated for goodness of fit, and receiver operating characteristic curves were created.

Postoperative AF occurred in 26% of patients. Smokers accounted for 15% of the study population and demonstrated a reduced incidence of postoperative AF compared with nonsmoking individuals (20% vs. 27%, p < .001). Multivariate analysis revealed a significant interaction between smoking status and inotropic support requirement. The AF-protective effect of smoking was confounded by inotropic drugs. However, when we excluded from analysis the patients with inotropic support, smoking conferred a 46% risk reduction of AF (odds ratio [OR] = 0.54, 95% CI = 0.34-0.87, p = .011). In addition, age, valvular surgery, and hypertension were independently associated with AF. Postoperative AF increased the length of hospitalization, without affecting hospital mortality. AF was associated with an increased 1-year mortality (p = .002).

Current smokers are less prone to develop AF after cardiac surgery. Our data support the hypothesis that hyperadrenergic state and catecholamines are key mechanisms in the pathophysiology of postoperative AF.