
Torsade de Pointes Secondary to d, I‐Sotalol after Catheter Ablation of Incessant Atrioventricular Reentrant Tachycardia—Evidence for a Significant Contribution of the “Cardiac Memory”
Author(s) -
Haverkamp W.,
Hördt M.,
Breithardt G.,
Borggrefe M.
Publication year - 1998
Publication title -
clinical cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.263
H-Index - 72
eISSN - 1932-8737
pISSN - 0160-9289
DOI - 10.1002/clc.4960210111
Subject(s) - medicine , sotalol , cardiology , atrioventricular reentrant tachycardia , tachycardia , radiofrequency catheter ablation , catheter ablation , ablation , anesthesia , reentry , accessory pathway , atrial fibrillation
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 prolongatio that was paralleled by the occurrence of repeated episodes of torsade de pointes developed. Serum electrolytes were nomal. 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 replarization 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.