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257 JACC Vol. 6, No. I July 1985:257-9 Verapamil-Induced Polymorphous Ventricular Tachycardia STEPHEN L. WINTERS, MD, PAUL SCHWEITZER, MD, FACC, JOEL KUPERSMITH, MD, FACC, JOSEPH A. GOMES, MD, FACC New York. New York A 31 year old woman who developed an atypical ven· tricular tachycardia after administration of intravenous verapamil for control of a recurrent supraventricular tachycardia is presented. Possible explanations for the observed arrhythmia, polymorphous ventricular tachy· Intravenous verapamil administration is a well recognized means of terminating paroxysmal supraventricular tachyarrhythmias (1). However, deleterious effects can occur in patients with poor left ventricular function secondary to the drug's negative inotropic and hypotensive effects. This report describes another potential complication of intravenous verapamil administration, polymorphous ventricular tachycardia, during the conversion of paroxysmal supraventricular tachycardia to sinus rhythm. Case Report The patient was a 31 year old woman with a history of supraventricular arrhythmias since childhood. Prophylaxis with digitalis, beta-adrenergic blocking agents and various type I antiarrhythmic agents had been unsuccessful in controlling recurrent episodes. One year before hospital admission, the patient presented to this medical center with paroxysmal supraventricular tachycardia. No pre-excitation pattern was seen on electrocardiograms at rest or 24 hour continuous ambulatory monitoring. She had no structural heart disease and electrophysiologic testing revealed an atrioventricular (A V) nodal reentrant tachycardia, the induction of which was prevented by intravenous verapamil. The patient was maintained on a regimen of 120 mg verapamil (lsoptin) orally, three times daily. Three days before admission, her prescription was refilled with the CaJan From the Division of Cardiology, Department of Medicine, The Mount Sinai Medical Center, New York, New York. Manuscript received December 20, 1984; revised manuscript received February 12, 1985, accepted February 22, 1985. Address for reprints: Stephen L. Winters. MD. Division of Cardiology. The Mount Sinai Medical Center, One Gustave Levy Place, New York, New York 10029. © 1985 by the American College of Cardiology cardia, are discussed. Verapamil must be considered one of the pharmacologic agents that can cause this arrhythmia. () Am Coli Cardiol 1985;6:257-9) brand of verapamil. Concerned that she might have received the wrong medicine, she did not take any verapamil over the following 3 days. She subsequently had an onset of rapid heartbeats and presented to the emergency room with profound light-headedness and diaphoresis. The electrocardiogram (Fig. 1) revealed a regular, narrow complex tachycardia, at a rate of 150 beats/min, without discernible P waves. The systolic blood pressure was 70 mm Hg with the cuff method, and no diastolic pressure could be measured. Five milligrams of intravenous verapamil were administered slowly, and while she noted an irregularity to her palpitation, the rhythm in Figure 2 was recorded and lasted for approximately 30 seconds. The tracing revealed an atypical ventricular tachycardia, with varying QRS configuration rotating around a stable baseline, interspersed with sinus rhythm. The rhythm then converted to sinus tachycardia at a rate of 110 beats/min (Fig. 3). The patient was observed overnight and discharged taking her previous medication. Discussion Mechanism. In this young woman, AV nodal reentrant tachycardia transiently progressed to an irregular, wide complex tachycardia with varying QRS configuration in response to intravenous verapamil. The two possible causes of this tachyarrhythmia include atrial fibrillation with aberrancy and polymorphous ventricular tachycardia. The former is unlikely because 1) a premature ventricular complex initiated the arrhythmia; 2) the baseline was isoelectric; 3) the wide QRS complexes show marked variation and did not reveal classic aberrant right or left bundle branch block patterns; and 4) intermittent sinus beats with fusion complexes were present (Fig. 2). Furthermore, termination of supraventricular tachycardia has been associated with wide 0735-1097/85/$3.30 258 JACC Vol. 6, No. I WINTERS ET AL. VERAPAMIL-INDUCED ARRHYTHMIA July 1985:257-9 oVR VI V4 II oV L V2 V5 ill oVF V3 Vs I Figure 1. Electrocardiogram recorded on presentation to the emergency room, revealing a supraventricular tachycardia at a rate of 150 beats/min. ~~-- J .j,,).)J...!JJ QRS rhythms that are ventricular in origin. Conversion arrhythmias, including premature ventricular complexes and short runs of nonsustained ventricular tachycardia, have been associated with the use of intravenous verapamil for therapy of supraventricular tachycardia (2,3). The transition rhythm in our case represents polymorphous ventricular tachycardia. As is characteristic, the rhythm is an atypical form of ventricular tachycardia with QRS complexes of varying amplitudes that rotate around the baseline (4-6). Etiology. Polymorphous ventricular tachycardia of this duration has not previously been reported to occur as a conversion rhythm in patients with supraventricular tachycardias acutely treated with verapamil. Such rhythms are associated with long-term antiarrhythmic therapy with quinidine, procainamide and disopyramide (4-6). Bradycardia, autonomic dysfunction, electrolyte imbalances, phenothiazine use and myocardial ischemia can also result in episodes of polymorphous ventricular tachycardia (4-6). Usually, such rhythm disturbances are associated with prolonged VI (Continuous tracing) ·'1 [ .. y'-...J.-4--1--t-~ ---Y---;-\.-~'1- ~-.--"-J-~'t--+- -+-....,.--"\---t '. \ \ I l.NLfv\.lv\it--10d-.y'V\.I'A·lL1-~U l.t I.. J. ~vl+-lflJJ4ll Figure 2. Electrocardiographic rhythm strips recorded at time of administration of intravenous verapamil, revealing periods of atypical ventricular tachycardia with QRS complexes rotating around the baseline. Figure 3. Electrocardiogram recorded after conversion to sinus rhythm. JACC Vol. 6. No. I July 1985:257-9 repolarization, detected as a lengthened corrected QT (QTJ interval on surface electrocardiogram (4-6). However, in our patient the serum electrolytes were normal, none of the other preceding conditions was suspected and there was no observed QTc prolongation before the onset of the conversion arrhythmia. The cause of verapamil-induced ventricular arrhythmias is unclear. Interference with the inward calcium current disturbs A V nodal conduction, permitting reentrant rhythms to cease (l). Simultaneously, verapamil induces a catecholamine surge, in part because of its hypotensive effects. Thus, a high state of adrenergic tone could have resulted in triggered forms of automaticity and caused the particular arrhythmia. Myocardial ischemia due to profound hypotension may cause the arrhythmia; however, the absence of chest pain or ischemic changes on the electrocardiogram makes this possibility unlikely. In conclusion, we report a case of polymorphous ventricular tachycardia, requiring no intervention, during conversion from an A V nodal reentrant tachycardia to sinus rhythm with intravenous verapamil administration. The rhythm observed was well tolerated and terminated spontaneousl y. However, in patients with compromised left ventricular WINTERS ET AL. VERAPAMIL-INDUCED ARRHYTHMIA 259 function, such an arrhythmia could prove deleterious and require further intervention. Cautious monitoring is essential when administering verapamil to treat supraventricular arrhythmias. We gratefully thank Valentin Fuster. MD for his encouragement and support and Millie Tolson for secretarial assistance. References I. Schamroth I. Krikler DM. Garrett C. Immediate effects of intravenous verapamil on cardiac arrhythmias. Br Med J 1972; 1:660-2. 2. Vohra J. Peter T. Hunt D. Sloman G. Verapamil induced premature beats before reversion of supraventricular tachycardia. Br Heart J 1974;36:1186-93. 3. Feigl D, Ravid M. Electrocardiographic observations on the termination of supraventricular tachycardia by verapamil. J Electrocardiol 1979;1 2: 129-36. 4. Schweitzer P. Mark H. Delayed repolarization syndrome. Am J Med 1983;75:393-400. 5. Krikler DM. Curry PVL. Torsades de pointes: an atypical ventricular tachycardia. Br Heart J 1976;38: 117-20. 6. Fontaine G. Frank R. Grosgogeat Y. Torsades de pointes: definition and management. Mod Concepts Cardiovasc Dis 1982;51:1 03-8.