Catecholamine facilitated reentrant ventricular tachycardia: Uncoupling ofadenosine's antiadrenergic effects

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.