Why the study?
What is the role of early afterdepolarizations in familial long QTU syndrome and Torsade de Pointes, and how do antiarrhythmic drugs affect them?
What is the role of early afterdepolarizations in familial long QTU syndrome and Torsade de Pointes, and how do antiarrhythmic drugs affect them?
In a patient with familial long QTU syndrome, early afterdepolarizations were shown to drive Torsade de Pointes and could be inhibited by verapamil and propranolol.
Supports EAD-driven TdP in long QTU; case report leaves open clinical translation of verapamil or propranolol.
Torsade de pointes (TdP) syncopal episodes were almost invariably precipitated by emotional stress or menstruation in a 17-year-old girl. U wave accentuation occurred during sinus rhythm without pauses in periods of heightened sympathetic tone. To examine the role of early afterdepolarization (EAD), monophasic action potentials were recorded during ventricular extrasystoles and TdP occurring spontaneously and induced by ventricular pacing. The effects of lidocaine, verapamil, propranolol, and epinephrine were assessed. Our data show that: (1) EAD plays a significant role in the genesis of familial long QTU syndrome and TdP; (2) rapid ventricular pacing causes postpause-dependent EADs, U waves, and TdP; and (3) EAD is enhanced by epinephrine infusion in the absence of pause, whereas EAD-triggered firing is inhibited by verapamil and propranolol but not by lidocaine.
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ZHOU et al. (1992) studied this question.
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