BACKGROUND:

Atrial fibrillation is the most prevalent sustained cardiac arrhythmia, affecting over 2 million Americans. Post-operative atrial fibrillation, leading to significant morbidity and to prolongation of hospital stay, complicates 20 to 40% of surgical procedures requiring cardiopulmonary bypass. While recent randomized clinical trials indicate interruption of the renin-angiotensin-aldosterone system by either ACE inhibition or ATi receptor antagonism decreases the incidence of atrial fibrillation following myocardial infarction or cardioversion, the effect of interruption of the renin-angiotensin-aldosterone system on the incidence of post-operative atrial fibrillation has not been investigated in a randomized, prospective study. Studies in both animal models and humans suggest that inflammation-induced atrial remodeling plays an important role in the pathogenesis of this arrhythmia. At the same time, emerging data provide evidence that activation of the renin-angiotensin aldosterone system induces inflammation, myocyte injury, proarrhythmic electrical remodeling and fibrosis through aldosterone.

DESIGN NARRATIVE:

A randomized clinical trial to test the hypothesis that ACE inhibition or aldosterone receptor antagonism will decrease inflammation and atrial fibrillation following cardiopulmonary bypass.