Clinical lecturer in Cardiology, Academic Department of Cardiology, Castle Hill Hospital, University of Hull, Kingston-upon-Hull, UK
Received August 16, 2004; revised August 16, 2004; accepted August 19, 2004 * Corresponding author. Tel.: +44 1482624073; fax: +44 7092 840055 (E-mail: rhidianshelton{at}btopenworld.com).
To the Editor,
I read with interest the recent publication on the use of sotalol, quinidine and verapamil in the prevention of atrial fibrillation (AF) following electrical cardioversion.1 I was, however, surprised to see no mention of the several recent randomised trials favouring a rate control strategy in the management of AF. Nevertheless my principal concern lies with the choice of antiarrythmic agent following cardioversion.
AF is common in ageing patients with ischaemic and structural heart disease. Data from this study suggests 20% of patients suffer angina (some of who had suffered a previous MI) and 42% have NYHA class II or above heart failure symptoms. The use of verapamil, quinidine and sotalol in such patients is not without significant risk.
Safety and efficacy are important considerations in choosing an antiarrythmic drug for the treatment of AF. In patients with cardiac failure amiodarone, digoxin and dofetilide are the only drugs with studies demonstrating a neutral effect on survival. The SWORD trial established that d-sotalol was associated with increased mortality in patients with left ventricular dysfunction or previous MI.2 A different study comparing sotalol to bisoprolol in preventing AF recurrence showed equivocal efficacy but a superior safety profile (less pro-arrhythmic events) for bisoprolol.3 The current study describes 10 episodes (one fatal) of torsade de pointes tachycardia, all associated with sotalol use.
The concern regarding quinidine ('quinidine syncope') stems mainly from a meta-analysis of quinidine trials which demonstrated more deaths in patients receiving quinidine for maintenance of sinus rhythm than placebo.4 The vagolytic action of quinidine and its inherent risk of accelerated arrhythmias necessitate its use with AV nodal blocking agents; in this case verapamil. Based on the Cardiac Arrhythmia Suppression Trial data, class I agents should probably be avoided in post-MI patients.
The Canadian Trial of Atrial Fibrillation (CTAF) together with the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) substudy have shown amiodarone's superiority to sotalol and class I anti-arrythmics, although side-effects were once again common.
As regards alternatives to anti-arrythmic drugs in 'high risk' populations; there is growing evidence for the prevention of occurrence and recurrence of AF in patients with systolic dysfunction, by the use of 'up-stream' therapy. Both angiotensin converting enzyme (ACE) inhibitors and angiotensin-receptor blockers (ARB's) can lead to regression of atrial remodelling and restoration of atrial effective refractory periods (ERPs). Chronic beta-blockade is also associated with prolongation of action potentials and ERPs in human atrial cells. Evidence from clinical trials, albeit mainly retrospective data, indicates a decrease in the incidence of AF with ACE-inhibitors,5 ARBs,6 and beta-blockers.7 Therefore, aggressive treatment of heart failure is likely to result in a reduction in the incidence of AF, and a reduction in the recurrence rate of AF following restoration of sinus rhythm.
If anti-arrythmic agents are required for maintenance of sinus rhythm, their safety profile, together with individual patient characteristics, should be of utmost concern.
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