Circulation, Vol 87, 382-390, Copyright © 1993 by American Heart Association
BB Lerman
BACKGROUND. Reentrant ventricular tachycardia (VT) is known to be
insensitive to the nucleoside adenosine. However, we have previously
identified a form of nonreentrant, catecholamine-mediated VT that can be
initiated with rapid pacing, demonstrates cycle length dependence, and is
sensitive to exogenous adenosine as well as to the Valsalva maneuver. The
mechanism of this tachycardia is thought to be due to a
catecholamine-induced, cAMP-mediated increase in intracellular calcium,
resulting in delayed afterdepolarizations and triggered activity. The
antiarrhythmic effects of exogenous adenosine and Valsalva on this form of
VT may be due to receptor-mediated inhibition of adenylate cyclase or to
noncardiac receptor-mediated effects, i.e., exogenous adenosine may
modulate VT through alterations in autonomic tone by activation of arterial
chemoreceptors, and Valsalva has been shown to decrease venous return,
resulting in a reduction in cardiac dimensions and myocardial stretch. To
clarify this issue and circumvent both autonomic and noncardiac receptor
effects, the response of nonreentrant catecholamine- mediated VT to
endogenous adenosine and acetylcholine was evaluated. METHODS AND RESULTS.
Group 1 (n = 8): Dipyridamole (0.56 mg/kg i.v.), a nucleoside transport
blocker that potentiates the effects of endogenous adenosine, reproducibly
abolished sustained nonreentrant, nonautomatic, catecholamine-mediated VT
in the five patients in whom it was evaluated. VT recurred with the
addition of aminophylline, a competitive adenosine A1-receptor antagonist.
Edrophonium (10 mg i.v.), a cholinesterase inhibitor that potentiates the
effects of acetylcholine at the muscarinic cholinergic receptor, terminated
VT in four of four patients, an effect that was reversed by atropine. Group
2 (n = 6): In patients with reentrant VT, dipyridamole and edrophonium had
no effect on VT cycle length or duration. Group 3 (n = 4): Adenosine and
vagal maneuvers had no effect on catecholamine-mediated VT caused by
automaticity in three of four patients tested. In one patient, adenosine
transiently suppressed VT (< 5 seconds), after which it spontaneously
resumed. CONCLUSIONS. The results of this study further delineate the
mechanism of a newly recognized form of clinical VT. It can be identified
by termination of the tachycardia in response to activation of the
adenosine A1 or muscarinic cholinergic receptor, which results in
inhibition of adenylate cyclase. These receptor- mediated effects appear to
be specific for identifying nonreentrant, nonautomatic,
catecholamine-mediated VT.
ARTICLES
Response of nonreentrant catecholamine-mediated ventricular tachycardia to endogenous adenosine and acetylcholine. Evidence for myocardial receptor-mediated effects
Department of Medicine, New York Hospital-Cornell University Medical College, NY 10021.
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