Introduction: Adenosine has no direct electrophysiologic function in ventri
cular tissue, but in the presence of cyclic adenosine monophosphate (cAMP),
stimulation exerts a potent antiadrenergic effect. This effect has been ex
ploited in the recognition and treatment of ventricular tachycardia (VT) du
e to cAMP-mediated triggered activity and automaticity, which are respectiv
ely terminated and suppressed by adenosine. However, the effects of adenosi
ne on catecholamine-facilitated reentrant VT are unknown. A pivotal issue i
s whether termination of VT with adenosine is mechanism specific, or whethe
r it represents a nonspecific antiadrenergic effect. The purpose of this st
uds, therefore, was to define the effects of adenosine in a well-characteri
zed group of patients with catecholamine-facilitated reentrant VT.
Methods and Results: Fourteen patients with catecholamine-facilitated reent
ry were studied. In the 12 patients with structural heart disease (includin
g two with arrhythmogenic right ventricular dysplasia), adenosine (260 to 5
50 mu g/kg) failed to slow or terminate VT. Two patients without structural
heart disease had intrafascicular tachycardia confined to the left posteri
or fascicle, a calcium-dependent, verapamil-sensitive arrhythmia. In the ab
sence of isoproterenol, verapamil terminated VT but adenosine did not. Howe
ver, when isoproterenol was subsequently required for facilitation of tachy
cardia, adenosine terminated VT in both patients.
Conclusion: Adenosine has no antiadrenergic (antiarrhythmic) effect in pati
ents with catecholamine-facilitated VT due to structural heart disease. Pat
ients with verapamil-sensitive, left posterior intrafascicular reentry have
an unusual dual response to adenosine. In the unstimulated state, adenosin
e has no effect on basal inward calcium current and, therefore, no effect o
n VT. However, when induction of VT requires amplification of the inward ca
lcium current through stimulation of cAMP, adenosine sensitivity of VT beco
mes manifest. These results indicate that with few exceptions, termination
of VT with adenosine is strongly suggestive of a cAMP-mediated triggered me
chanism rather than reentry.