A single intravenous infusion of 750 mg of procainamide facilitated the induction of ventricular tachycardia in 66% of patients and abolished or modified it in 33%.
Does a single intravenous infusion of procainamide reduce the induction of ventricular tachycardia in patients with symptomatic chronic recurrent ventricular tachycardia?
Intravenous procainamide frequently facilitates rather than abolishes the induction of ventricular tachycardia in patients with chronic recurrent VT, highlighting the need for acute electrophysiologic drug trials to determine optimal therapy.
Absolute Event Rate: 83.3% vs 100%
The effects of a single intravenous infusion of 750 mg of procainamide was studied in 12 patients with symptomatic chronic recurrent ventricular tachycardia in whom arrhythmias could reproducibly be initiated and terminated by programmed electrical stimulation of the heart. Sustained ventricular tachycardia was induced in 6 patients and non-sustained tachycardia was induced in the remaining 6 patients during control studies. Following procainamide (plasma level 10.3 +/- 3.7 mcg/ml), ventricular tachycardia could be induced in 10/12 patients, sustained in 4 patients and non-sustained in the remaining 6 patients. In 8/12 patients (66%), induction of ventricular tachycardia was facilitated as demonstrated by: (1) tachycardia zone was widened in 4 patients and was unchanged in another 3 patients; (2) non-sustained ventricular tachycardia was sustained ventricular tachycardia in one patient. the ventricular tachycardia had a faster rate and a different QRS morphology; (3) in 4 patients tachycardia was inducible with a lesser number of extrastimuli and/or by spontaneously occurring ventricular premature depolarization and; (4) increase of the number of induced ventricular responses of non-sustained ventricular tachycardia. In 4/12 patients (33%), procainamide abolished or modified the induction of ventricular tachycardia as demonstrated by: (1) inability to induce ventricular tachycardia in 2 patients; (2) narrowing of the tachycardia zone and conversion from sustained into non-sustained ventricular tachycardia (one patient) and; (3) decrease in the number of induced ventricular responses in one patient. The response to procainamide could not be predicted from rates of spontaneous ventricular tachycardia, induced ventricular tachycardia during control studies, degree of slowing of ventricular tachycardia or from prolongation of the coupling interval after procainamide. These results suggest that instead of abolishing the arrhythmia, procainamide in frequently employed doses in patients with chronic recurrent ventricular tachycardia can facilitate its initiation sometimes at even faster rates. Patients not responsive to the usual doses of procainamide should undergo acute drug trials to determine the optimal dose/drug levels.
Kang et al. (Sat,) conducted a other in Symptomatic chronic recurrent ventricular tachycardia (n=12). Procainamide vs. Baseline (control studies) was evaluated on Induction of ventricular tachycardia. A single intravenous infusion of 750 mg of procainamide facilitated the induction of ventricular tachycardia in 66% of patients and abolished or modified it in 33%.