Polymorphic ventricular tachycardia induced by programmed stimulation

Response to procainamide

Alfred E. Buxton, Mark E. Josephson, Francis E. Marchlinski, John Miller

Research output: Contribution to journalArticle

33 Citations (Scopus)

Abstract

Objectives. This study was designed to evaluate the effects of procainamide on polymorphic ventricular tachycardia induced by programmed stimulation and to correlate the responses with heart disease, left ventricular endocardial activation abnormalities and the signal-averaged electrocardiogram (ECG). Background. Polymorphic ventricular tachycardia is induced frequently during electrophysiologic studies. In many patients this response is an artifact of programmed stimulation; in others, it appears to be clinically relevant. Previous observations have suggested that in some patients type IA antiarrhythmic agents can change the response to programmed stimulation from polymorphic to uniform ventricular tachycardia. Methods. Programmed right ventricular stimulation was performed in the absence of antiarrhythmic drugs and after procainamide. Signal-averaged ECGs and left ventricular maps were performed during sinus rhythm in the absence of antiarrhythmic drugs. Results. We evaluated 79 consecutive patients undergoing clinical electrophysiologic studies, in whom polymorphic ventricular tachycardia was the only arrhythmia induced in the absence of antiarrhythmic drugs. After procainamide administration, uniform monomorphic ventricular tachycardia was induced in 24 patients (Group 1), inducible polymorphic ventricular tachycardia persisted in 30 patients (Group 2) and no ventricular tachycardia could be induced in the remaining 25 patients (Group 3). Twenty-three (96%) of 24 patients developing uniform ventricular tachycardia after procainamide administration had coronary artery disease compared with 63% of Group 2 and 48% of Group 3 patients (p = 0.003). Left ventricular aneurysms were also found more frequently (46%) in the patients developing uniform ventricular tachycardia after procainamide than in either Group 2 or Group 3 (13% and 0%, respectively, p <0.008). Abnormalities of the signal-averaged ECG typically seen in patients with spontaneous reentrant sustained ventricular tachycardia were significantly more frequent in patients who developed inducible uniform ventricular tachycardia after procainamide than in those who did not. Similarly, patients developing uniform ventricular tachycardia after procainamide had more extensive abnormalities of left ventricular endocardial activation revealed by catheter maps during sinus rhythm. Conclusions. The conversion of inducible polymorphic ventricular tachycardia to uniform ventricular tachycardia after procainamide administration occurs almost exclusively in patients with coronary disease, previous myocardial infarction and abnormal left ventricular function. This response may permit activation mapping of tachycardias, allowing the appllcation of surgical or catheter ablation techniques that would otherwise not be possible in such patients.

Original languageEnglish (US)
Pages (from-to)90-98
Number of pages9
JournalJournal of the American College of Cardiology
Volume21
Issue number1
DOIs
StatePublished - 1993
Externally publishedYes

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Procainamide
Ventricular Tachycardia
Anti-Arrhythmia Agents
Electrocardiography
Ablation Techniques
Catheter Ablation
Left Ventricular Function
Tachycardia
Artifacts

ASJC Scopus subject areas

  • Nursing(all)

Cite this

Polymorphic ventricular tachycardia induced by programmed stimulation : Response to procainamide. / Buxton, Alfred E.; Josephson, Mark E.; Marchlinski, Francis E.; Miller, John.

In: Journal of the American College of Cardiology, Vol. 21, No. 1, 1993, p. 90-98.

Research output: Contribution to journalArticle

Buxton, Alfred E. ; Josephson, Mark E. ; Marchlinski, Francis E. ; Miller, John. / Polymorphic ventricular tachycardia induced by programmed stimulation : Response to procainamide. In: Journal of the American College of Cardiology. 1993 ; Vol. 21, No. 1. pp. 90-98.
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abstract = "Objectives. This study was designed to evaluate the effects of procainamide on polymorphic ventricular tachycardia induced by programmed stimulation and to correlate the responses with heart disease, left ventricular endocardial activation abnormalities and the signal-averaged electrocardiogram (ECG). Background. Polymorphic ventricular tachycardia is induced frequently during electrophysiologic studies. In many patients this response is an artifact of programmed stimulation; in others, it appears to be clinically relevant. Previous observations have suggested that in some patients type IA antiarrhythmic agents can change the response to programmed stimulation from polymorphic to uniform ventricular tachycardia. Methods. Programmed right ventricular stimulation was performed in the absence of antiarrhythmic drugs and after procainamide. Signal-averaged ECGs and left ventricular maps were performed during sinus rhythm in the absence of antiarrhythmic drugs. Results. We evaluated 79 consecutive patients undergoing clinical electrophysiologic studies, in whom polymorphic ventricular tachycardia was the only arrhythmia induced in the absence of antiarrhythmic drugs. After procainamide administration, uniform monomorphic ventricular tachycardia was induced in 24 patients (Group 1), inducible polymorphic ventricular tachycardia persisted in 30 patients (Group 2) and no ventricular tachycardia could be induced in the remaining 25 patients (Group 3). Twenty-three (96{\%}) of 24 patients developing uniform ventricular tachycardia after procainamide administration had coronary artery disease compared with 63{\%} of Group 2 and 48{\%} of Group 3 patients (p = 0.003). Left ventricular aneurysms were also found more frequently (46{\%}) in the patients developing uniform ventricular tachycardia after procainamide than in either Group 2 or Group 3 (13{\%} and 0{\%}, respectively, p <0.008). Abnormalities of the signal-averaged ECG typically seen in patients with spontaneous reentrant sustained ventricular tachycardia were significantly more frequent in patients who developed inducible uniform ventricular tachycardia after procainamide than in those who did not. Similarly, patients developing uniform ventricular tachycardia after procainamide had more extensive abnormalities of left ventricular endocardial activation revealed by catheter maps during sinus rhythm. Conclusions. The conversion of inducible polymorphic ventricular tachycardia to uniform ventricular tachycardia after procainamide administration occurs almost exclusively in patients with coronary disease, previous myocardial infarction and abnormal left ventricular function. This response may permit activation mapping of tachycardias, allowing the appllcation of surgical or catheter ablation techniques that would otherwise not be possible in such patients.",
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N2 - Objectives. This study was designed to evaluate the effects of procainamide on polymorphic ventricular tachycardia induced by programmed stimulation and to correlate the responses with heart disease, left ventricular endocardial activation abnormalities and the signal-averaged electrocardiogram (ECG). Background. Polymorphic ventricular tachycardia is induced frequently during electrophysiologic studies. In many patients this response is an artifact of programmed stimulation; in others, it appears to be clinically relevant. Previous observations have suggested that in some patients type IA antiarrhythmic agents can change the response to programmed stimulation from polymorphic to uniform ventricular tachycardia. Methods. Programmed right ventricular stimulation was performed in the absence of antiarrhythmic drugs and after procainamide. Signal-averaged ECGs and left ventricular maps were performed during sinus rhythm in the absence of antiarrhythmic drugs. Results. We evaluated 79 consecutive patients undergoing clinical electrophysiologic studies, in whom polymorphic ventricular tachycardia was the only arrhythmia induced in the absence of antiarrhythmic drugs. After procainamide administration, uniform monomorphic ventricular tachycardia was induced in 24 patients (Group 1), inducible polymorphic ventricular tachycardia persisted in 30 patients (Group 2) and no ventricular tachycardia could be induced in the remaining 25 patients (Group 3). Twenty-three (96%) of 24 patients developing uniform ventricular tachycardia after procainamide administration had coronary artery disease compared with 63% of Group 2 and 48% of Group 3 patients (p = 0.003). Left ventricular aneurysms were also found more frequently (46%) in the patients developing uniform ventricular tachycardia after procainamide than in either Group 2 or Group 3 (13% and 0%, respectively, p <0.008). Abnormalities of the signal-averaged ECG typically seen in patients with spontaneous reentrant sustained ventricular tachycardia were significantly more frequent in patients who developed inducible uniform ventricular tachycardia after procainamide than in those who did not. Similarly, patients developing uniform ventricular tachycardia after procainamide had more extensive abnormalities of left ventricular endocardial activation revealed by catheter maps during sinus rhythm. Conclusions. The conversion of inducible polymorphic ventricular tachycardia to uniform ventricular tachycardia after procainamide administration occurs almost exclusively in patients with coronary disease, previous myocardial infarction and abnormal left ventricular function. This response may permit activation mapping of tachycardias, allowing the appllcation of surgical or catheter ablation techniques that would otherwise not be possible in such patients.

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