Abstract
A 21-year-old male experienced frequent episodes of polymorphic ventricular tachycardia (PVT) initiated by a closely coupled premature ventricular complex (PVC) in the absence of QT prolongation and structural heart disease. Programmed stimulation at right ventricular apex (RVA), but not at the outflow tract (RVOT), provoked PVT degenerating into ventricular fibrillation (VF). Monophasic action potential duration (MAPD) was significantly shorter at RVA than RVOT. The maximum slope of MAPD restitution was much steeper at RVA than RVOT (1.91 versus 0.50). Such spatial heterogeneities of MAPD and its restitution may facilitate wavebreak and functional reentry predisposing to PVT and VF.
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