Effects of intravenous adenosine on verapamil-sensitive “idiopathic” ventricular tachycardia

Abstract

The mechanism of ventricular tachycardia (VT) that occurs in the absence of structural heart disease (“idiopathic” VT) is unknown, but may involve triggered activity or reentry through calcium channel-mediated conduction pathways. It has been suggested that termination of VT by adenosine is specific to ventricular arrhythmias caused by cyclic adenosine monophosphate-mediated triggered activity. The effects of vagotonic maneuvers, and intravenous adenosine (up to 0.25 mg/kg in incremental doses) and verapamil (0.145 mg/kg) administered to 9 patients with “idiopathic” VT were studied during electrophysiologic study. Seven patients had inducible fascicular VT and 2 had incessant right ventricular outflow tract tachycardia. Vagal maneuvers did not have any effect on any VT. Adenosine interrupted both right ventricular outflow tract tachycardias for a period (2 to 15 seconds) that was dependent on the dose of adenosine, but had no effect on VT in any patient with fascicular VT. Verapamil produced stuttering termination of right ventricular outflow tract tachycardia with no preceding change in RR interval in patients with this arrhythmia. Administration of verapamil to patients with fascicular VT was followed by gradual slowing of the arrhythmia (cycle length increased from 397 ± 45 to 506 ± 86 ms; p < 0.01) in all 7 patients and by termination of VT in 6. In conclusion, the differential response of fascicular and right ventricular outflow tract tachycardias to both adenosine and verapamil suggests that: (1) These 2 forms of idiopathic VT have different mechanisms. (2) Fascicular VT is unlikely to be due to cyclic adenosine monophosphate-mediated triggered activity. These findings also have implications for the use of adenosine as a diagnostic agent in broad-complex VT.