We thank Dr. El Muayed for his letter and interest about our study (1). The mechanisms by which angiotensin-converting enzyme (ACE) inhibition exerts its protective effect against development of atrial fibrillation in the setting of hypertension or heart failure (2) are not completely understood. We have discussed several possible contributing mechanisms in our study. In patients with congestive heart failure, neurohormonal activation, left ventricular remodeling, elevated left atrial pressure, and atrial fibrosis probably interact to provide a pathophysiologic substrate for atrial fibrillation, which can be, at least partially, reversible with ACE inhibition (3- 4). Some of these beneficial effects of ACE inhibitors may also be relevant for the prevention of atrial fibrillation in patients with hypertension (1).

In addition to its favorable role in atrial structural remodeling, inhibition of angiotensin II also has favorable effects on electrophysiologic remodeling by preventing atrial effective refractory period shortening and loss of atrial effective refractory period rate adaptation during rapid pacing (5). Reduction of angiotensin-mediated norepinephrine release from atrial sympathetic fibers (6) may contribute, along with other preventive effects on structural and electrophysiologic remodeling, to the reduced occurrence of atrial fibrillation with ACE inhibitor therapy.