Polymorphic ventricular tachycardia in
association with a normal QT interval
Polymorphic (or polymorphous) ventricular tachycardia (VT) is defined as an
unstable rhythm with a continuously varying QRS complex morphology in any
recorded electrocardiographic (ECG) lead (
show
ECG 1) [
1].
The simultaneous recording of more than one ECG lead is often necessary to
detect these changes. A rate of at least 200 beats/min is the commonly
accepted minimum for polymorphic VT, but an absolute number has not been
established and VT at a slower rate may manifest changing QRS morphology [
2,3].
Some episodes of polymorphic VT cause hemodynamic collapse and have the
potential to degenerate into ventricular fibrillation (VF); however, many
episodes terminate spontaneously (
show
ECG 2).
Polymorphic VT is often associated with underlying myocardial ischemia and has
a more ominous prognosis than monomorphic VT (
show
ECG 3). (
See
"Sustained monomorphic ventricular tachycardia in coronary heart
disease"). Polymorphic VT is also frequently induced during
electrophysiologic studies, even in patients without a history of ventricular
arrhythmia. Families with polymorphic ventricular tachycardia in whom there is
no recognized underlying condition have been identified [
4,5].
Polymorphic ventricular tachycardias are classified based upon their
association with either normal or prolonged QT segments. This card will review
the mechanisms and clinical features seen in polymorphic VT associated with a
normal QT interval. Polymorphic ventricular tachycardias associated with
prolonged QT intervals are discussed separately. (
See
"Risk factors for and diagnosis of the long QT syndrome and torsade de
pointes"). In this setting, the arrhythmia typically has a torsade de
pointes ("twisting of points") pattern.
MECHANISM ！ Spontaneous polymorphic VT or
polymorphic VT induced by programmed stimulation in the presence of a normal
QT interval usually occurs in the setting of coronary heart disease. However,
this arrhythmia is also infrequently seen in a structurally normal heart.
Programmed stimulation in dogs 24 hours after myocardial infarction (MI)
induces fast polymorphic VT that sometimes degenerates into VF. Mapping of
ventricular activation during this polymorphic VT suggests that the arrhythmia
is due to a reentrant mechanism (
show
figure 1) [
6].
The varying QRS configuration is explained by the changing activation pattern
of the ventricles, because of the constant change in the site and
configuration of the reentrant circuits. These circuits result from the
effects of ischemia on repolarization.
Electrophysiologic similarities may exist between rapid polymorphic VT in the
normal heart and idiopathic VF [
7,8,9,10].
As an example, idiopathic VF is often initiated by a ventricular premature
beat with a very short coupling interval; VT may also be preceded by a
short-long-short cardiac cycle. The induction of polymorphic VT during
electrophysiologic testing in patients without structural heart disease may be
a nonspecific response that is of variable use in guiding therapy (see
Polymorphic VT induced by electrophysiologic testing below) [
9].
Familial polymorphic ventricular tachycardia ！
Studies of familial polymorphic ventricular tachycardia, which occurs in the
absence of structural heart disease or known associated syndromes, have shown
many variations, which suggests multiple mechanisms. Some studies have shown a
tendency toward sinus bradycardia, U-waves, a short PR interval, or arrhythmia
induced by sinus tachycardia occurring with exercise or exercise testing,
emotion, or catecholamine infusion [
5].
These various etiologies suggest that the mechanism may be reentry and delayed
afterpotentials or changes in autonomic tone.
Although the genetic basis for familial polymorphic VT is uncertain, it was
examined in a report of two unrelated families with 24 members who had
experienced exercise-induced VT or syncope or had an episode of sudden death [
11].
The disorder was found to be inherited in an autosomal dominant pattern and
was linked to chromosome 1q42-q43. Some of the family members had delayed
clinical manifestations, which necessited continued observation and repeated
evaluation.
TREATMENT ！ The therapeutic approach to
polymorphic VT varies with the clinical setting: myocardial ischemia; with a
structurally normal heart; and during electrophysiologic studies.
Polymorphic VT in myocardial ischemia ！
Polymorphic VT associated with a normal QT interval is an uncommon arrhythmia
following an acute MI or ischemic episode (
show
ECG 3). When it occurs, it is often associated with signs or symptoms of
recurrent myocardial ischemia. It is not consistently related to electrolyte
abnormalities, sinus bradycardia, preceding sinus pauses, or an abnormally
long QT interval [
12].
The appropriate management of polymorphic VT in patients with myocardial
ischemia is not well defined. The best therapy is prevention or correction of
ischemia by coronary revascularization (via surgery or angioplasty), reversal
of acute ischemia with intravenous
nitroglycerin,
or, in the presence of coronary vasospasm, the administration of a calcium
channel blocker [
12,13].
The arrhythmia is suppressed in some patients by intravenous
amiodarone,
but has a variable and usually poor response to class I antiarrhythmic agents
[
12,14].
One study, for example, found the following responses in 10 patients with
polymorphic VT after an acute MI [
12]:
• Intravenous
lidocaine
was effective in one of 10 patients.
• Intravenous
procainamide
was beneficial in one of six patients; the other five had recurrent episodes.
•
Bretylium
was effective in none of five patients.
• Overdrive pacing failed to suppress recurrent
arrhythmias in all four patients in whom it was used.
Polymorphic VT and idiopathic VF in a
structurally normal heart ！ There are a few reports of polymorphic VT in
patients with no significant structural heart disease. One report evaluated 15
such patients who presented with syncope, presyncope, or aborted sudden death
[
13].
The arrhythmia was induced by exercise in four and by coronary vasospasm in
two. In addition, approximately five percent of survivors of sudden cardiac
death (often the result of polymorphic VT and VF) have no structural heart
disease.
There are presently no consensus treatment guidelines in the management of
polymorphic VT in patients with a normal heart. Therapy may be directed by the
following observations:
• Chronic beta blocker administration may be
effective in some patients whose polymorphic VT is reproducibly initiated by
an infusion of
isoproterenol
or by exercise [
13].
• The use of pacing, beta blockade, and calcium
channel blockers alone or in combination may be effective if the arrhythmia is
pause-dependent.
However, an implantable cardioverter-defibrillator is often the treatment of
choice, because patients with polymorphic VT and minimal or no structural
heart disease are at risk for sudden death and respond erratically to
antiarrhythmic drugs [
9,13].
There is also no clear recommended strategy for the management of idiopathic
VF. Pharmacologic therapy, for example, is of unproven benefit in the
management of this disorder. However, a recent report followed 28 survivors of
VF with minimal or no structural heart abnormalities who were treated with an
implantable cardioverter-defibrillator. No cardiac deaths were noted after an
average follow-up period of 30 months [
9].
Sixteen of these patients experienced 36 shock episodes, suggesting they were
at continued risk for recurrent VF.
Thus, in patients with idiopathic VF, an implantable cardioverter-defibrillator
is the preferred therapy since the effect of antiarrhythmic drugs is
unpredictable with long-term use and there is a risk of recurrent VF.
Polymorphic VT induced during electrophysiologic
testing ！ Polymorphic ventricular tachycardia is frequently induced by
programmed ventricular stimulation. Although the prognostic significance of
this finding is controversial, it may help guide patient management if
considered in combination with the patient's presenting arrhythmia (
show
figure 1) [
15].
As an example, induced polymorphic VT is probably a valid end-point in
patients with documented ventricular fibrillation or with a high likelihood of
having had such an arrhythmia [
16].
These patients are therefore candidates for an implantable cardioverter-defibrillator
rather than serial antiarrhythmic drug trials.
In patients without such a history, the induction of a polymorphic VT is
considered a nonspecific response to programmed stimulation that lacks
prognostic significance. This is particularly true when the test is performed
a few weeks after an MI or when a vigorous protocol is used [
17,18,19].
However, the electrophysiologic rationale for this point of view is not clear:
induced polymorphic VT in the presence of ischemic heart disease is most
likely due to reentry, the same mechanism that may underlie the spontaneous
arrhythmia.
In addition, a recent study demonstrated that, in patients with a prior MI,
left ventricular dysfunction, and a history of a sustained ventricular
tachyarrhythmia, the conversion of inducible polymorphic VT into inducible
monomorphic VT after
procainamide
occurred in approximately 30 percent of patients [
2].
This conversion may be helpful, since it permits electrophysiologic mapping of
the ventricular tachycardia and successful application of surgical or catheter
ablative therapeutic techniques.
Familial polymorphic ventricular tachycardia ！
Most patients with potentially fatal arrhythmias are treated with an
implantable cardioverter-defibrillator. However, one study of a family with
catecholamine-sensitive polymorphic VT, followed for 25 years, reported that
beta blocker therapy, guided by serial exercise testing, was effective for
preventing recurrent arrhythmia [
5].
SUMMARY ！ The following summarizes the
major issues concerning polymorphic VT in the setting of a normal QT interval:
• Polymorphic VT in the course of acute MI is
uncommon and usually reflects recurrent ischemia. Appropriate management of
the arrhythmia in this setting is not well defined but prevention of ischemia
should be the primary goal.
• Polymorphic VT with a normal QT interval in
patients without significant structural heart disease may be
electrophysiologically similar to idiopathic VF. Management strategy in these
patients usually involves placement of an implantable cardioverter-defibrillator.
• Polymorphic VT is not infrequently induced by
programmed ventricular stimulation in the electrophysiology laboratory.
Induced polymorphic VT is considered a valid end-point only in patients with
documented VF or with a high likelihood of having had such an arrhythmia.
