Download Verapamil-induced polymorphous ventricular tachycardia

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
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VI
V4
II
oV L
V2
V5
ill
oVF
V3
Vs
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Figure 1. Electrocardiogram recorded on presentation to the emergency room, revealing a supraventricular tachycardia at a rate of 150 beats/min.
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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.
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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
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verapamil on cardiac arrhythmias. Br Med J 1972; 1:660-2.
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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.