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Sustained polymorphic VT can be seen with any form of structural heart disease. However, unlike sustained monomorphic VT, polymorphic VT does not always indicate a structural abnormality or focus of automaticity. Reentry with continually changing reentrant paths, spiral wave reentry and multiple automatic foci are potential mechanisms (Chap. A9). 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 (see Table 249-1).

Polymorphic VT Associated with Acute Myocardial Infarction/Ischemia

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. Following defibrillation as per the Advanced Cardiac Life Support (ACLS) guidelines, management is as for acute MI (Chap. 269). Beta-adrenergic blockers, correction of electrolyte abnormalities, and prompt myocardial reperfusion are required. Repeated episodes of polymorphic VT 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 those that survive past hospital discharge are not at increased risk for arrhythmic sudden death. Long-term therapy for post-infarct ventricular arrhythmia is determined by residual left ventricular (LV) function with an implantable cardioverter defibrillator (ICD) being indicated for persistent severe left ventricular (LV) dysfunction (LV ejection fraction <0.35).

Repolarization Abnormalities and Genetic Arrhythmia Syndromes


Abnormal prolongation of the QT interval is associated with the polymorphic VT torsades des pointes (Fig. 250-1). 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. This characteristic initiation is termed “pause-dependent” (Fig. 250-1). 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 non-cardiac diseases, including erythromycin, pentamidine, haloperidol, phenothiazines, and methadone (Table 250-1). Individual susceptibility may be related to genetic polymorphisms or mutations that influence repolarization.

FIGURE 250-1

Torsades des pointes VT in patient with bradycardia and marked QT prolongation. A.12-lead ECG showing 2:1 AV block (P waves marked by blue arrows) with heart rate of 40 bpm and QT interval of 680 ms and corrected QT of 550 ms. ...

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