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This case illustrates a toxic effect of flecainide in widening the QRS complex and inducing repolarisation abnormalities on exercise testing in a 67 year old woman, who had presented breathless in atrial fibrillation. Neither history nor examination revealed underlying cardiac abnormality; thyroid function and echocardiography were normal. The figure illustrates the electrocardiographic anterior chest leads during Bruce exercise tests. In the left half, the dose was 150 mg twice daily: the first panel shows the pre-exercise trace, and the second panel stage II, heart rate 115 beats per minute. A dramatic widening of the QRS complex, increase in T wave amplitude, and prolongation of the QT interval occurred. This suggested pro-arrhythmic potential, and the dose was reduced to 50 mg twice daily. The right half shows re-exercise, illustrating lack of the previous abnormalities (at a very similar exercise heart rate).
Flecainide caus es pronounced inhibition of the fast sodium channel, depressing the upstroke slope of the action potential, widening the QRS complex. Exercise augments the toxic effects of flecainide. The cardiac arrhythmia suppression trial (CAST) highlighted proarrhythmia, when patients post-myocardial infarction with ventricular ectopic beats treated with flecainide suffered greater mortality than placebo treated patients. The interaction of ischaemia and flecainide may be important in the mechanism for such increased mortality. There is general acceptance that flecainide is contraindicated in coronary patients, especially those with heart failure. Our case reminds us of these dangers, and suggests that exercise may assist in the assessment of proarrhythmic risk in patients treated with flecainide.
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