{'fraction_non_alphanumeric': 0.03160667251975417, 'fraction_numerical': 0.016681299385425813, 'mean_word_length': 5.927051671732523, 'pattern_counts': {'":': 0, '<': 1, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Phenytoin in the Treatment of Inducible Ventricular Tachycardia: Results of Electrophysiologic Testing and Long‐Term FoUow‐Up

Phenytoin treatment of inducible ventricular tachyarrhythmias was assessed by serial electrophysiologic studies (EPS) in 64 patients with spontaneous ventricular tachycardia, cardiac arrest, or symptoms compatible with a ventricular tachyarrhythmia. Coronary artery disease was the primary cardiac disease in 75% of the patients. All subjects had either inducible ventricular tachycardia (≥10 repetitive beats) or ventricular fibrillation at electrophysiologic study. Phenytoin was administered Intravenously in 38 studies and orally in 31 studies. The mean serum phenytoin level was 19.5 ± 4.7 mcg/ml. Only seven patients (11%) had a negative electrophysiologic study (≥10 repetitive beats) after the administration of phenytoin and were classified as phenytoin responders (group I). The remaining 54 patients (89%) were classified as nonresponders (group II). For the nonresponders. phenytoin increased the cycle length of identical monomurphic ventricular tachycardias from a mean of 301 ms to a mean of 327 ms(p < 0.001). For the four patients tested receiving both intravenous and oral phenytoin, the intravenous response always predicted the oral response. For the seven patients in whom electrophysiologic study indicated phenytoin efficacy, two are alive and arrhythmia‐event free, two had sudden death when the regimen was changed (one case, quinidine added; one case, subtherapeutic serum level), and three died from nonarrhythmic causes. For the 10 patients treated empirically with phenytoin, either alone (seven patients) or in combination with another antiarrhythmic agent (three patients), four died secondary to an arrhythmic event. These data indicate that: (1) phenytoin is infrequently an effective antiarrhythmic agent for the treatment of ventricular tachyarrhythmias as judged by response to electrophysiologic testing; (2) for phenytoin responders, when phenytoin is maintained at effective serum levels established during electrophysiologic testing, the incidence of subsequent arrhythmic events may be reduced; and (3) empiric use of phenytoin therapy for treatment of ventricular tachyarrhythmias is infrequently efficacious.