Polymorphic ventricular tachycardia (PVT) can be seen in LQTS (congenital and acquired), acute myocardial ischemia/infarction, and as a primary electrical disturbance in patients with structurally normal hearts (57-64). A particular morphology of PVT associated with QT prolongation has been referred to as torsades de pointes, a term coined by Dessertenne in 1955 (65). The underlying mechanism of PVT is unclear, although the mechanisms for the initiation and propagation of torsades de pointes are believed to differ. Early after-depolarization-induced triggered activity in a milieu of heterogeneous recovery of excitability initiates the tachycardia. This produces a nonstationary excitatory wavefront whose propagation depends upon shifting sites of reentry along the epicardial surface. The dynamic and migratory nature of the reentrant circuit results in the polymorphic morphology of the tachycardia.
Management of patients who present with PVT requires a careful inspection of the patient's history, including a search for culprit drugs, electrolyte abnormalities, and ischemia/infarction (Fig. 10). Electrocardiographic documentation of the initiation of the arrhythmia is invaluable. First, temporary pacing may prevent recurrent episodes of pause-dependent PVT (Fig. 11). Secondly, in patients with prior myocardial infarction, documentation of the initiation allows differentiation of rapid monomorphic ventricular
tachycardia and subsequent degeneration to PVT from primary PVT. The former suggest the presence of prior MI and a fixed reentrant circuit, in which revascularization alone is insufficient for patient management. ICD therapy should be considered. Patients who develop primary PVT in the setting of acute MI may be treated conservatively with revascularization alone, provided that revascularization is successful and complete (66).
Acute management of patients who present with ischemic PVT is revascularization, reducing the ischemic burden and preventing recurrences with drug therapy. Long-term arrhythmia management depends upon 1) the rhythm at initiation; 2) left ventricular function; and 3) the success of revascularization. Patients with acute ischemia whose PVT results from degeneration of monomorphic VT are unlikely to benefit from revascularization alone, and ICD implantation should be considered. Patients with acute ischemia whose PVT is the initial rhythm may be treated with revascularization alone, if revascularization is complete and LV function preserved. Patients with acute ischemia and PVT whose initial rhythm is not documented should be considered for ICD implantation, especially in the setting of reduced left ventricular function, for which monomorphic VT may have been the precipitating event. After revascularization, electrophysiology testing may be helpful in determining if patients with borderline left ventricular dysfunction are susceptible to SMVT.
Nonischemic PVT is most often seen in the setting of LQTS. Both congenital and acquired causes of QT prolongation have been described (57). PVT in congenital LQTS is often "adrenergically dependent." Treatment of PVT in congenital LQTS should always include beta-blocker therapy. Other adjunctive treatments include pacemaker implantation, left stellate ganglionectomy, and ICD therapy. The major goal for patients with acquired LQTS is to treat any condition causing QT prolongation (e.g., drugs or electrolyte abnormalities). Because PVT in acquired LQTS is often "pause-dependent," acute management to prevent recurrent episodes include temporary pacing or isoproter-enol administration to increase heart rate and intravenous (iv) magnesium infusion.
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