Repolarization abnormalities after catheter ablation (cardiac memory) are not always benign and may significantly increase the risk of proarrhythmia when QT-prolonging antiarrhythmics are administered.
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Post-ablation cardiac memory may amplify sotalol proarrhythmia risk; case report leaves open need for delayed initiation or enhanced monitoring.
Radiofrequency catheter ablation of a right septal accessory pathway was performed in a 66-year-old patient with incessant orthodromic atrioventricular reentrant tachycardia. Intravenous administration of flecainide, ajmaline, verapamil, and d,l-sotalol had been ineffective in controlling the tachycardia. After the ablation procedure, precordial T-wave inversion was observed during sinus rhythm. These repolarization abnormalities persisted and were suggested to represent "cardiac memory." Three days later, atrial fibrillation with a fast ventricular response developed and oral d,l-sotalol, which had been well tolerated previously on a long-term basis, was started again. However, at this time, and in the presence of the persisting repolarization abnormalities, the T waves became deeper and broader within a few hours after the introduction of d,l-sotalol. Marked QT prolongation that was paralleled by the occurrence of repeated episodes of torsade de pointes developed. Serum electrolytes were normal. Direct current cardioversion was necessary due to the degeneration of torsade de pointes into ventricular fibrillation. Further sustained arrhythmia episodes were suppressed by temporary endocardial ventricular pacing. The patient recovered without any sequela. This case demonstrates that repolarization abnormalities after catheter ablation, which may be due, at least in part, to the "cardiac memory," are not always benign but may contribute significantly to proarrhythmia.
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Haverkamp et al. (1998) studied this question.
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