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Sustained polymorphic ventricular tachycardia (VT) has a continuously changing QRS configuration from beat to beat, indicating a continually changing ventricular activation sequence. However, unlike sustained monomorphic VT, polymorphic VT does not necessarily indicate a fixed structural abnormality or focus of automaticity. Reentry can occur with continually changing reentrant paths, spiral wave reentry, and multiple automatic foci as potential mechanisms. This type of reentry can occur near fibrotic areas of myocardium, potentiated by proximity to damaged Purkinje cells or ventricular hypertrophy. Abnormal transmural dispersion of repolarization can occur in the setting of channelopathies or antiarrhythmic drugs in the absence of structural heart disease. Sustained polymorphic VT usually degenerates into ventricular fibrillation (VF). Polymorphic VT is typically seen in association with acute myocardial infarction or ischemia (MI), ventricular hypertrophy, and a number of genetic mutations that affect cardiac ion channels.


Acute MI or ischemia is a common cause of polymorphic VT and should be the initial consideration in management. Approximately 10% of patients with acute MI develop VT that degenerates to VF, likely related to reentry through the infarct border zone. The risk is greatest in the first hour of acute MI. More rarely, surviving Purkinje cells with automaticity can initiate polymorphic VT. Following defibrillation as per the Advanced Cardiac Life Support (ACLS) guidelines, management is as for acute MI. β-Adrenergic blockers, correction of electrolyte abnormalities, and prompt myocardial reperfusion are required. Repeated episodes of polymorphic VT may suggest ongoing MI and warrant assessment of adequacy of myocardial reperfusion. Polymorphic VT and VF that occur within the first 48 h of acute MI are associated with greater in-hospital mortality, but patients who survive past hospital discharge are not at increased risk for arrhythmic sudden death. Long-term therapy for postinfarct ventricular arrhythmia is determined by residual left ventricular (LV) function, with an implantable cardioverter defibrillator (ICD) indicated for persistent severe LV dysfunction (LV ejection fraction <35%).



Abnormal prolongation of the QT interval is associated with the polymorphic VT torsades des pointes. The VT often has a characteristic initiation sequence of a premature ventricular beat that induces a pause, followed by a sinus beat that has a longer QT interval and interruption of the T wave by the premature ventricular contraction (PVC) that is the first beat of the polymorphic VT (Fig. 255-1). This characteristic initiation is termed pause-dependent. Causes of QT prolongation include electrolyte abnormalities, bradycardia, and a number of medications that block repolarizing potassium currents, notably the antiarrhythmic drugs sotalol, dofetilide, and ibutilide, but also a number of other medications used for noncardiac diseases, including erythromycin, pentamidine, haloperidol, phenothiazines, and methadone. Individual susceptibility may be related to genetic polymorphisms or mutations that influence repolarization. The website is an excellent resource ...

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