Circulation, Vol 74, 270-280, Copyright © 1986 by American Heart Association
BB Lerman, L Belardinelli, GA West, RM Berne and JP DiMarco
Catecholamine-induced triggered activity is thought to be caused by
intracellular calcium overload mediated by elevation of intracellular
cyclic AMP (cAMP). Although shown to occur in isolated preparations,
evidence supporting its clinical existence has been lacking.
Electrophysiologic studies were performed in four patients with
structurally normal hearts who had exertionally related sustained
ventricular tachycardia (VT). Programmed stimulation reproducibly initiated
and terminated VT in all patients. Induction of tachycardia was also
facilitated by infusion of isoproterenol. Adenosine, an endogenous
nucleoside, whose only known electrophysiologic effect on ventricular
myocardium and Purkinje fibers is antagonism of catecholamine-induced
stimulation of intracellular cAMP production, reproducibly terminated all
episodes of VT. The tachycardia was also terminated by intravenous
verapamil and by the Valsalva maneuver and/or carotid sinus massage.
Beta-Adrenergic receptor blockade with propranolol either terminated or
prevented induction of VT during programmed stimulation or catecholamine
challenge. Adenosine was also administered during VT to 14 patients whose
arrhythmias fulfilled standard criteria for reentry, two of whom also had
exercise-induced VT. Adenosine, at a dose (112.5 to 225 micrograms/kg iv)
sufficient to cause either sinus slowing/arrest or ventriculoatrial block
during ventricular pacing, failed to slow or terminate any episode of VT in
these patients. Verapamil and autonomic modulation were also ineffective in
this group of patients. Adenosine, verapamil, vagal maneuvers
(acetylcholine), and beta-adrenergic receptor blockade are all known to
decrease the slow-inward calcium current either directly by modulating
calcium channels or indirectly by inhibiting production of cellular cAMP.
Therefore the observation in this study that interventions that lower
intracellular cAMP either terminate or prevent induction of VT in patients
with structurally normal hearts and exercise-induced VT suggests that the
mechanism of tachycardia may be cAMP-mediated triggered activity.
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Adenosine-sensitive ventricular tachycardia: evidence suggesting cyclic AMP-mediated triggered activity
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