Chiale P A, Franco D A, Selva H O, Militello C A, Elizari M V
Division of Cardiology, Ramos Mejía Hospital and Instituto Sacre Coeur, Buenos Aires, Argentina.
J Am Coll Cardiol. 2000 Nov 1;36(5):1637-45. doi: 10.1016/s0735-1097(00)00906-2.
The goal of this study was to report a variety of atrial tachycardia that might be caused by an unusual electrophysiologic substrate.
The mechanism of atrial tachycardias is attributed to re-entry, abnormal automaticity or triggered activity, based on their electropharmacological responses. A rate-related and lidocaine-sensitive atrial tachycardia has not been reported.
Eight patients (3 women and 5 men, aged 14 to 60 years) with repetitive, uniform atrial tachycardias were studied. In six patients the arrhythmia had been refractory to at least three antiarrhythmic agents (class 1A and C sodium channel blockers, amiodarone, beta-adrenergic blocking agents, verapamil, digoxin). Conventional electrocardiograms, Holter recordings and B mode echocardiograms were performed in each patient. Intravenous lidocaine and verapamil were tested in the eight patients. Six patients underwent an electrophysiologic study.
The baseline electrocardiogram showed nearly incessant runs of atrial tachycardia in all patients. The mean atrial ectopic cycle length ranged from 376 to 502 ms. In seven patients a progressive prolongation of the cycle length from the beginning to the end of the salvos was documented. The arrhythmia was suppressed by increments of sinus node rate and by atrial pacing at cycle lengths longer than that of the atrial tachycardia. In all patients the arrhythmia was abolished by intravenous lidocaine, whereas intravenous verapamil was ineffective. Four symptomatic patients were successfully treated with radiofrequency ablation of the ectopic focus, and two patients were treated with oral mexiletine.
The peculiar electropharmacological responses of this arrhythmia suggest an uncommon underlying mechanism that remains to be elucidated.
