We Can Improve the Treatment of Patients with Atrial Fibrillation

Abstract & Commentary

Synopsis: Angiotensin-converting enzyme inhibitors decreased the number of defibrillation attempts needed and reduced hospitalization in patients with atrial fibrillation.

Source: Zaman A G et al. Am Heart J. 2004;147:823-827.

Atrial fibrillation (AF) is the most common cardiac arrhythmia and is associated with a high risk of thromboembolism. A recent Framingham study demonstrated that men and women, at age 40, had a 1 in 4 lifetime risk for developing AF.1 The best therapy for AF is still uncertain. Rate-controlled therapy when compared to rhythm-controlled therapy has recently been shown to decrease mortality.2 Little is known about the long term outcome of nonpharmacologic therapies such as atrioventricular nodal ablation, pacemakers and atrial defibrillators.3

Zaman and colleagues have noted that withdrawal of angiotensin-converting enzyme inhibitors (ACEI) was associated with AF in patients undergoing coronary artery bypass surgery. As a result of this finding they set out to establish whether ACEI could reduce atrial arrhythmogenicity.

The study was a 1 year, prospective, follow-up, comprised 47 patients with persistent AF undergoing electrical cardioversion. Patients receiving ACEI were compared with those receiving other medications. The study end point was the number of defibrillation attempts required for atrial defibrillation and the number of hospital admissions. A secondary end point was change in signal-averaged P-wave duration (SAPD) 1 year after successful electrical cardioversion. (Signal-averaged electrocardiography reflects conduction abnormalities in the perinodal atrial muscle. Remodeling of the atrial myocardium may be detected by prolongation of the atrial impulses).4

Of those admitted and requiring defibrillation, the number of defibrillation attempts required for successful cardioversion was significantly less in the ACEI group. The incidence rate ratio for admissions, comparing recipients of ACEI with those not receiving ACEI, was 0.14. Patients receiving ACEI therapy had significantly lower SAPD at 1 year when compared with the no-ACEI group.

The use of long-term ACEI therapy facilitated electrical defibrillation in patients with persistent AF. ACEI therapy also reduced SAPD, suggesting amelioration of the arrhythmogenic substrate. Furthermore, they confirmed that SAPD is prolonged in patients with persistent AF.

Comment by Ralph R. Hall, MD, FACP

Zaman et al point out that the observational nature of this study and the small number of patients are potential limitations. Also the majority of the patients in this study were hypertensive so the study might not apply to those with normal blood pressure. They also note that the non-randomized nature of this study led to differences in the medication the 2 groups were receiving. However, there is no evidence to suggest that beta blockers or calcium antagonists affect AF. The study did not include measurements of diastolic dysfunction. This is another factor which should be examined. AF occurs in a high percentage of patients with diastolic dysfunction.

Consider the patient who has had 5 bouts of AF, all of short duration. All episodes occurred while on decongestants and all were more than a year apart. Repeated 48 hour monitoring did not identify asymptomatic AF. Will he eventually have more protracted episodes? Will taking ACEI prevent recurrence?

There is a need for more and improved trials for patients with AF. Treatment for AF is often unsatisfactory and many of the patients we see do not fit the profiles of those in previous trials. Therefore, despite the limitations of this study, it identifies the need for randomized trials to examine the role of ACEI in the management and perhaps prevention of atrial fibrillation.

Dr. Hall, Emeritus Professor of Medicine University of Missouri-Kansas City School of Medicine, is Associate Editor of Internal Medicine Alert.


1. Lloyd-Jones DM et al. Circulation. 2004;110:1042-1046.

2. Wyse DG, et al. N Engl J Med. 2002;347:1825-1833.

3. Al-Khatib SM. Am Heart J. 2004; 147: 751-752.

4. Yamada T, et al. Am Heart J. 2001; 142: 286-293.