title: Antiarrhythmic drug exacerbation of ventricular tachycardia inducibility during electrophysiologic study.
abstract: Most studies examining antiarrhythmic drug exacerbation of ventricular arrhythmias have been performed in patients in whom clinical proarrhythmia developed. The clinical significance and predictors of antiarrhythmic drug exacerbation of inducible ventricular arrhythmias during electrophysiologic study have received less attention. Accordingly, a consecutive number of patients undergoing electrophysiologic study for evaluation of ventricular arrhythmias (but who had no history of clinical proarrhythmia) were prospectively examined. Drug-induced exacerbation was defined as no inducible ventricular tachycardia in the baseline drug-free state that increased to inducible nonsustained or sustained ventricular tachycardia, or inducible nonsustained ventricular tachycardia at baseline that increased to inducible sustained ventricular tachycardia. After administration of primarily type IA antiarrhythmic agents (procainamide and quinidine in 97% of the patients), patients were considered drug test negative (n = 80) when they had no increase in inducible ventricular tachycardia, and patients were considered drug test positive (n = 16) when they had exacerbation of inducible arrhythmias. The drug test-positive group's clinical characteristics differed markedly from those of the drug test-negative group. Compared with the drug test-negative group, the drug test-positive group had reduced (less than 40%) left ventricular ejection fractions (80% vs 39%, p = 0.005) and higher prevalences of myocardial infarctions (81% vs 35%, p = 0.027), left ventricular aneurysms (27% vs 5%, p = 0.026), and bundle branch blocks (53% vs 16%, p = 0.005). Thus exacerbation of ventricular tachycardia induction after antiarrhythmic agent administration was most common in patients with significant organic heart disease. The drug test-positive group was more frequently treated with antiarrhythmic therapy than was the drug test-negative group.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Internal Medicine, Yale University School of Medicine, New Haven, Conn.
authors.forename: P T
authors.initials: PT
authors.lastname: Sager
authors.forename: R A
authors.initials: RA
authors.lastname: Perlmutter
authors.forename: L E
authors.initials: LE
authors.lastname: Rosenfeld
authors.forename: W P
authors.initials: WP
authors.lastname: Batsford
mesh_terms: D000889:Anti-Arrhythmia Agents / Q000009:adverse effects; D002304:Cardiac Pacing, Artificial / Q000379:methods; D016757:Death, Sudden, Cardiac / Q000453:epidemiology; D004594:Electrophysiology; D005500:Follow-Up Studies; D015637:Gated Blood-Pool Imaging; D006352:Heart Ventricles / Q000187:drug effects / Q000503:physiopathology; D006801:Humans; D013318:Stroke Volume / Q000187:drug effects / Q000502:physiology; D013610:Tachycardia / Q000209:etiology* / Q000401:mortality / Q000503:physiopathology
chemical_list: D000889:Anti-Arrhythmia Agents