THERAPY AND PREVENTION VENTRICULAR TACHYCARDIA Polymorphous ventricular tachycardia: clinical characterization, therapy, and the QT interval

Forty-five consecutive patients with polymorphous ventricular tachycardia (PVT) were studied. The arrhythmia proved to be of a drug-related cause in 27 and due to an electrolyte disorder in four patients. Coexistent cardiac diseases without metabolic or drug-related abnormalities included ischemic heart disease in three, cardiomyopathy in three, and mitral valve prolapse in two. PVT was exercise-induced in four and associated with bradyarrhythmias in two. A prolonged QT or corrected QT interval was inconsistently related to the occurrence of PVT. In patients in whom PVT was induced by certain type I drugs, other type I antiarrhythmic drugs were usually either ineffective or resulted in aggravation of arrhythmia. For the group as a whole, treatment with lidocaine resulted in inconsistent beneficial effects, while cardiac pacing was almost universally effective for those with drug-induced PVT, regardless of the length of the QT interval. Long-term amiodarone therapy proved safe and effective for 12 of the 24 patients with drug-induced PVT who required long-term therapy for their original arrhythmia. We conclude that identification of PVT is the key clinical issue and that the QT interval is not necessarily the prime abnormality nor the variable to be considered in predicting success of therapy. Temporary cardiac pacing appears to be very effective in the short-term management of these patients. Use of type I antiarrhythmic agents in patients with drug-induced PVT generally resulted in aggravation of arrhythmia. In contrast, long-term amiodarone therapy for control of the original arrhythmia appears to be a promising approach for those with PVT associated with type I agents. Circulation 74, No. 2, 340-349, 1986. THE CLINICAL characterization of polymorphous ventricular tachycardia (PVT) has been incomplete. The definition of PVT we have used is similar to that proposed by the North American Society of Pacing and Electrophysiology, namely ventricular tachycardia with an unstable (continuously varying) QRS complex morphology in any recorded electrocardiographic lead.' In addition, we require a ventricular rate greater than 200/min for at least 10 complexes. This definition includes but is not limited to the classic torsade de pointes pattern.2 Diagnostic criteria for torsade de pointes includes the presence of a prolonged QT interval, and others have emphasized the clinical importance of this arrhythmia. ` Since the clinical implication of PVT is not clear, the purpose of the present study is threefold: (1) to define the clinical characteristics of PVT, (2) to assess the efficacy of available emergent and long-term therapy for this arrhythmia, and (3) to examine the imporFrom the Department of Medicine and the Cardiovascular Research Institute, University of California, San Francisco. Address for correspondence: Melvin M. Scheinman, M.D., Room 312 Moffitt Hospital, University of California, San Francisco, CA 94143-0214. Received Oct. 29, 1985; revision accepted April 24, 1986. tance of the QT interval in patients with this arrhythmia. Materials and methods Data for this study were collected retrospectively for 1 year and prospectively over 1.8 years for all patients admitted to the University of California Medical Center, San Francisco, with the diagnosis of PVT. PVT was defined as a rapid (> 200/min) irregular ventricular tachycardia with continuous variation in QRS complexes of greater than 10 beat duration. This definition included but was not limited to the classic torsade de pointes pattern. All rhythm strips were reviewed to ascertain that the tachycardia fulfilled the above requirements. All patients had symptomatic arrhythmias and were continuously monitored in a coronary care unit. PVT was defined as drug induced if it developed as a new rhythm disturbance after initiation of drug therapy and it disappeared after cessation of administration of that drug. A total of 45 patients met these criteria and were included in the study. We excluded all patients who developed PVT as part of a preterminal cardiac state (i.e., those with severe end-stage heart failure or cardiogenic shock). In addition, patients with familial or idiopathic long QT syndrome were excluded, since these patients are described in detail in a separate report.8 Patients were included only if 12-lead sinus rhythm electrocardiograms had been recorded in them either just before or during interludes between bouts of PVT. Posttreatment QT intervals were not measured in seven patients who received permanent pacemakers. The following data were extracted from the medical records: age, sex, cardiac diagnosis, concurrent drug therapy, and drug CIRCULATION 340 by gest on A ril 4, 2017 http://ciajournals.org/ D ow nladed from THERAPY AND PREVENTION-VENTRICULAR TACHYCARDIA and electrolyte levels. The QT interval and the corrected QT to be absent at follow-up after hospital discharge. A treatment (QTc) were determined from a 12-lead sinus rhythm electrocarregiinen was deemed unsuccessful if PVT frequency remained diogram that was obtained on hospital admission, during interthe same or increased or if PVT recurred more than four drug ludes between episodes of active arrhythmia, and just before half-lives after discontinuing an offending drug. The total numdischarge. Retrospective data were obtained by examination of ber of episodes of PVT during short-term therapy was recorded all medical records, including daily electrocardiographic (see table 2). rhythm strips. There was no significant difference in the incidence of PVT in retrospective vs prospectively entered patients. Results The QT interval was measured according to the method suggested by Lepeshkin9 and the QT was corrected for heart rate: QTc The clinical data on the 45 patients are recorded in = QT/VRR. Shortand long-term therapy was noted and foltables 1 to 3. There were 22 female and 23 male palow-up information was obtained either during visits to our tients ranging in age from 15 to 82 years. The majority arrhythmia clinic or from private physicians. A treatment regimen for PVT was judged successful if there had organic cardiac disease, most frequently coronary was complete cessation of the arrhythmia and was considered artery disease and/or hypertension. Coexistent cardiac possibly successful if the arrhythmia decreased in frequency diseases without metabolic or drug-related abnormalconsistent with the drug half-life. In addition, for treatment to be considered successful PVT or symptomatic arrhythmias had ity included ischemic heart disease in three, cardioTABLE 1 Drug-induced PVT