EFFECTS OF INTRAVENOUS ADENOSINE ON VERAPAMIL-SENSITIVE IDIOPATHIC VENTRICULAR-TACHYCARDIA

The mechanism of ventricular tachycardia (VT) that occurs in the absen ce of structural heart disease (''idiopathic'' VT) is unknown, but may involve triggered activity or reentry through calcium channel-mediate d conduction pathways. It has been suggested that termination of VT by adenosine is specific to ventricular arrhythmias caused by cyclic ade nosine monophosphate-mediated triggered activity. The effects of vagot onic maneuvers, and intravenous adenosine (up to 0.25 mg/kg in increme ntal doses) and verapamil (0.145 mg/kg) administered to 9 patients wit h ''idiopathic'' VT were studied during electrophysiologic study. Seve n patients had inducible fascicular VT and 2 had incessant right ventr icular outflow tract tachycardia. Vagal maneuvers did not have any eff ect on any VT. Adenosine interrupted both right ventricular outflow tr act 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 fas cicular VT. Verapamil produced stuttering termination of right ventric ular outflow tract tachycardia with no preceding change in RR interval in patients with this arrhythmia. Administration of verapamil to pati ents with fascicular VT was followed by gradual slowing of the arrhyth mia (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 d ifferential 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 trig gered activity. These findings also have implications for the use of a denosine as a diagnostic agent in broad-complex VT.