Procainamide in Patients with Uniform VT. Introduction: Although intravenously administered procainamide has been used extensively during electropharmacologic testing for more than II) years, there is little information available on the effects of incremental dosing of procainamide in patients with inducible, monomorphic ventricular tachycardia (VT).
Methods and Results: Twenty-nine patients with coronary artery disease had sustained monomorphic VT reproducibly induced in the baseline, drug-free state. Programmed stimulation was repeated 5 minutes after loading infusion (50 mg/min) of 7.5 and 15 mg/kg (all patients) and 22.5 mg/kg of procainamide (15 patients), while maintaining continuous infusion of 0.055, 0.11, and 0.165 mg/kg per minute after each increment in dose, respectively. Corresponding procainamide plasma concentrations were 5.6 ± 2, 10.5 ± 3, and 14.5 ± 3 mg/L before, and 4.7 ± 2, 9.6 ± 3, and 14.6 ± 4 4 mg/L after electrophysiologic study at each increment in dose of procainamide, respectively. Each incremental dose of procainamide resulted in significant prolongation of tachycardia cycle length and QRS duration during sinus rhythm and right ventricular pacing. Five (17%), 7 (24%), and 1 (7%) patients, respectively, had no inducible sustained VT following the incremental dosing of procainamide. Three of five patients who had no inducible VT at 7.5 mg/kg had VT induced again at a higher dose of procainamide. Four of 24 patients whose VT remained inducible at 7.5 mg/kg of procainamide had no VT induced at 15 mg/kg of procainamide. Twelve (41%), 15 (52%), and 6 (40%) patients, respectively, no longer had VT with baseline morphology induced following the incremental dosing of procainamide. VT with new morphology compared to baseline was induced in more than 40% of patients at one or more of the three different procainamide dosing regimens. The mean cycle length of VTs with new morphology was significantly shorter than the cycle length of tachycardias with baseline morphology at each particular dose of procainamide.
Conclusion: Similar serum procainamide concentrations before and after programmed stimulation can be achieved at the described dosing regimen. Although 7.5 and 15 mg/kg of procainamide are both effective in suppressing induction of all VT in 20% to 25% of patients, non-inducibility at a particular dose of procainamide does not predict noninducibility at a respectively higher or lower dose. New morphologies of VT that are frequently faster than VTs with baseline morphology at a particular dose of procainamide can be induced in approximately half of the patients, and the clinical significance of these arrhythmias remains to be determined.