The mechanism of propafenone-induced slowing of ventricular tachycardia in man as defined by analysis of resetting response patterns

Abstract

The major finding in this study was that all VTs in patients treated with propafenone had a fully excitable gap. As only well tolerated, uniform VT in patients with chronic coronary artery disease was included for study, this result may not apply for ventricular arrhythmias in other patient populations. This is incompatible with the hypothesis that propafenone slows VT by increasing refractoriness within the VT circuit. Instead, the drug-mediated prolongation in VT cycle length is caused by effects on conduction velocity in fully recovered tissue and/or a change in the barriers of the circuit.