Abstract
Right ventricular outflow tract (RVOT) arrhythmias show left bundle branch block and inferior axis (LBBB-IA) aspect and include three main clinical forms: (1) repetitive monomorphic (LBBB-IA) nonsustained ventricular tachycardia (VT); (2) paroxysmal stress- and catecholamine-mediated sustained VT; (3) fre- quent and/or repetitive monomorphic ventricular premature beats [1–7]. Some patients can have both forms of RVOT-VT, and during exercise stress testing they may show initial suppression of nonsustained VT, final induction of sustained VT or relapse of the arrhythmia immediately after the peak exercise. The mechanism of RVOT-VT is due to catecholamine-mediated delayed after-depolarizations [8]. This model of triggered activity depends on the stimulation of cAMP, which caus- es an increase in intracellular calcium. The mechanism of triggered activity is supported by the difficult induction of RVOT-VT with programmed ventricular stimulation, by the facilitating effect of isoproterenol infusion on VT induction by ventricular pacing and by the cycle-length dependence of VT appearance [3, 8].
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Proclemer, A., Fresco, C., Muner, G., De Cristofaro, M., Bertaglia, E. (2000). Is Right Ventricular Outflow Tract Tachycardia a Minor Form of Arrhythmogenic Right Ventricular Cardiomyopathy?. In: Raviele, A. (eds) Cardiac Arrhythmias 1999. Springer, Milano. https://doi.org/10.1007/978-88-470-2139-6_35
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DOI: https://doi.org/10.1007/978-88-470-2139-6_35
Publisher Name: Springer, Milano
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