Copyright © 2004 by the European Society of Cardiology.
Letter to the Editor
Cardioversion threshold, IRAF and beyond
Department of Cardiology, University Hospital Maastricht, P.O. Box 5800, 6202 AZ Maastricht, The Netherlands
* Tel.: +31-433-875-093; fax: +31-433-875-104
E-mail address: hcri{at}cardio.azm.nl
We read with great interest the report of De Simone et al. in the August 2003 issue of the journal.1 The main finding of their study was that verapamil, added to flecainide or amiodarone reduced recurrences of atrial fibrillation after cardioversion. They also report that patients on flecainide required less shocks and had a lower mean cumulative energy to defibrillate than patients on amiodarone. They state that this illustrates the favourable effect of flecainide on defibrillation energy requirements. However, on the basis of their definition of successful cardioversion (i.e. at least three beats of sinus rhythm, probably indicating 3 or more atrial complexes irrespective of the site of origin in the atria) it is impossible to correctly determine and compare defibrillation thresholds in the treatment groups. In stead, absence of electrical activity in the atria immediately after a shock should have been used. The definition of De Simone et al. gauges cardioversion threshold, resumption of sinus rhythm and suppression of hyperacute immediate recurrence of atrial fibrillation (IRAF), all at the same time. In other words, the higher `cardioversion threshold' may in fact have been due to a more marked depressing effect of amiodarone on atrial pacemaker activity compared to flecainide. Such an effect may impede resumption of normal sinus rhythm and facilitate IRAF. Considering the above, the authors could have taken the opportunity to report the effects of various drug combinations on threshold as well as on IRAF, i.e. recurrences occurring within 1–2 min after cardioversion.2 The fact that verapamil added to amiodarone was not associated with increased energy requirements is not discussed, but suggests a favorable effect due to reduction of IRAF.3 We feel it is important to dissect the different drug effects on threshold, resumption of normal pacemaker activity and IRAF.4 Considering the meticulous monitoring of the heart rhythm around the cardioversion, the study by De Simone et al. could have added valuable information in this respect. Such information may enhance a targeted use of antiarrhythmic drugs in the suppression of consecutive recurrence mechanisms in patients undergoing cardioversion of persistent atrial fibrillation.
References
- De Simone A, De Pasquale M, De Matteis C et al. Verapamil plus antiarrhythmic drugs reduce atrial fibrillation recurrences after an electrical cardioversion (VEPARAF Study). Eur. Heart J. 2003;24(15):1425–1429.
[Abstract/Free Full Text] - Fuster V, Ryden LE, Asinger RW et al. American College of Cardiology/American Heart Association Task Force on Practice Guidelines; European Society of Cardiology Committee for Practice Guidelines and Policy Conferences (Committee to Develop Guidelines for the Management of Patients With Atrial Fibrillation); North American Society of Pacing and Electrophysiology. ACC/AHA/ESC Guidelines for the management of Patients With Atrial Fibrillation: Executive Summary. Eur. Heart J. 2001;20:1852–1923.
- Daoud EG, Hummel JD, Augostini R et al. Effect of verapamil on immediate recurrence of atrial fibrillation. J. Cardiovasc. Electrophysiol. 2000;11:1231–1237.[CrossRef][ISI][Medline]
- Crijns HJ, van Noord T, van Gelder IC. Recurrence of atrial fibrillation and the need for new definitions. Eur. Heart J. 2001;19:1769–1771.
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