Aggravation of induced arrhythmias with antiarrhythmic drugs during electrophysiological testing

There is evidence that antiarrhythmic drugs can worsen ventricular arrhythmias in patients. In a previous study ventricular arrhythmias worsened 11% when noninvasive monitoring and exercise tests were performed to evaluate drug effect. How frequently this complication occurs when patients undergo electrophysiologic studies is not known. Electrophysiologic (EP) tests were carried out in 63 patients who had a history of malignant, sustained ventricular tachyarrhythmias. Monitoring and exercise tests showed low-frequency or nonreproducible ventricular arrhythmia. Criteria for definite drug-induced aggravation of arrhythmia included (1) conversion of nonsustained ventricular tachycardia to a sustained ventricular arrhythmia and (2) provocation of the end point with one extrastimulus when three were required during control. Aggravation was deemed possible when, as compared to a control group, the end point resulted with the use of one less extrastimulus and sustained tachycardia with a more rapid rate was provoked. A total of 216 single drug studies were performed (3.4/patient). In general, definite or possible aggravation occurred in 35 tests (16%). In 28 cases (12.9%) aggravation was categorized as definite, while in 7 cases (3.2%) the induced arrhythmia was deemed as possibly related to the use of the antiarrhythmic drugs. Drug tests with multiple agents caused aggravation of arrhythmia in 19 patients (30%). Therefore, exacerbation of arrhythmia by antiarrhythmic drugs also occurs during electrophysiologic study. The incidence approximates that reported when monitoring and exercise tests are used for evaluating drug efficacy

Daily reproducibility of electrophysiologic testing in patients with malignant ventricular arrhythmia

The reproducibility of electrophysiologic testing on successive days was assessed in the absence of antiarrhythmic drug treatment. Forty-two patients, 17 with compromising ventricular tachycardia and 25 with ventricular fibrillation unrelated to myocardial infarction, underwent 2 baseline studies. During the first electrophysiologic study, arrhythmia was induced in 32 of 42 patients (76%); however, during the second study a similar endpoint was reached in only 22 patients (52%)(\u3c72 = 5.12, p <0.05). Only 18 of the 32 patients (56%) with induced arrhythmia during the first study had a reproducible result. Reproducibility was not related to presence of coronary artery disease, nature of presenting arrhythmia, or endpoint achieved (sustained or nonsustained ventricular tachycardia) during electrophysiologic study. Hence, reproducibility of endpoint during electrophysiologic investigation should be ascertained in each patient before initiating serial drug studies

Fatal ventricular tachycardia in association with propafenone, a new class IC antiarrhythmic agent.

A man with a past history of malignant ventricular arrhythmias occurring late after myocardial infarction was admitted for assessment. Monitoring revealed frequent ventricular premature beats and occasional non-sustained runs of ventricular tachycardia. Other drugs having failed, he was started on oral propafenone which is a new Vaughan Williams class IC antiarrhythmic agent. Several hours after starting this drug he had incessant ventricular tachycardia and subsequently died. Other class IC agents have been shown to have a high incidence of proarrhythmic effects, and particular care should be taken with these potent new drugs