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Catecholaminergic polymorphic ventricular tachycardia and other polymorphic ventricular tachycardias with a normal QT interval

Alfred Buxton, MD
Section Editor
Peter J Zimetbaum, MD
Deputy Editor
Brian C Downey, MD, FACC


Polymorphic (or polymorphous) ventricular tachycardia (VT) is defined as a ventricular rhythm at a rate greater than 100 beats per minute with a continuously varying QRS complex morphology in any recorded electrocardiographic (ECG) lead (waveform 1). The simultaneous recording of more than one ECG lead is often necessary to detect these changes. Most polymorphic VTs are rapid (often >200 bpm), but an absolute rate has not been established, and VT at a slower rate can manifest changing QRS morphology [1]. Some episodes of polymorphic VT cause hemodynamic collapse, and some degenerate into ventricular fibrillation (VF); however, many episodes terminate spontaneously (waveform 1).

Polymorphic VTs are classified based upon their association with a normal or prolonged QT interval. Spontaneous polymorphic VT in the presence of a normal QT interval usually occurs in the setting of coronary heart disease or non-ischemic cardiomyopathy. However, some patients have no structural heart disease and may have a familial syndrome.

Polymorphic VT associated with a normal QT interval will be reviewed here. Polymorphic ventricular tachycardia associated with a prolonged QT interval, which has a different etiology and mechanism, is known as torsades de pointes ("twisting of points") and is discussed separately. (See "Acquired long QT syndrome", section on 'Torsades de pointes' and "Clinical features of congenital long QT syndrome", section on 'Polymorphic VT/torsades de pointes'.)


Polymorphic ventricular tachycardia (VT) is seen most often during episodes of acute myocardial ischemia. It occurs in 2 to 4 percent of acute myocardial infarctions (waveform 1 and waveform 2), usually within the first 12 hours after the onset of symptoms. Polymorphic VT frequently accompanies episodes of coronary vasospasm (Prinzmetal's angina). In some patients, the arrhythmia may be the only manifestation of ischemia (without angina or other more typical symptoms) [2]. The arrhythmia is not consistently related to electrolyte abnormalities, sinus bradycardia, preceding sinus pauses, or an abnormally long QT interval [2]. Polymorphic VT/ventricular fibrillation (VF) may also occur as a secondary phenomenon in patients with severe heart failure or cardiogenic shock complicating acute MI. Such patients have extremely high mortality, and there is no evidence that specific antiarrhythmic therapy improves mortality. (See "Clinical features and treatment of ventricular arrhythmias during acute myocardial infarction".)

Although polymorphic VT after an acute MI is usually associated with a normal QT interval, some patients (8 of 434 consecutive patients in one series) develop typical pause-dependent torsades de pointes in association with progressive QT interval prolongation [3]. These events typically occur at days 3 to 11 during the healing phase of the infarct in the absence of recurrent ischemia. (See "Acquired long QT syndrome".)

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Literature review current through: Sep 2017. | This topic last updated: Jun 22, 2017.
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