Electropharmacological test with pentisomide (CM 7857) in patients with sustained ventricular tachycardia
Vergara, G.; Inama, G.; Guarnerio, M.; Rando, F.; Oldani, V.; Furlanello, F.
Giornale Italiano di Cardiologia 20(6): 543-548
1990
ISSN/ISBN: 0046-5968 PMID: 2227224 Document Number: 358048
Pentisomide (CM 7857) is a new class I antiarrhythmic drug whose effect on sustained ventricular tachycardia has only been slightly investigated to date. The aim of this paper is to examine the pentisomide action on selected patients with ventricular tachycardia inducible during intracavitary electrophysiological study. Thus, 12 patients (9 M, 3 F, mean age: 45.2 years, range: 24-78), all but two with detectable heart disease, underwent electropharmacological tests with pentisomide after they had resulted "non responders" (8 patients) or had had a proarrhythmic worsening effect (3 patients) to electropharmacological tests with amiodarone or flecainide or propafenone or mexiletine. After the inducibility and the reproducibility of ventricular tachycardia had been assessed in the basal state, all patients underwent several attempts to reinduce ventricular tachycardia, during the i.v. infusion of pentisomide 1.5 mg/kg/5 min followed by continuous infusion of 1 mg/kg/h, at the same time drug plasma level was assessed. Ventricular tachycardia inducibility was suppressed in 2/21 patients; in 10/12 patients the ventricular tachycardia was still inducible after pentisomide, but with a longer cycle length (446 .+-. 88 versus 337 .+-. 82 msec) than in the basal state (p < 0.0025). No patients had proarrhythmic worsening effects. The pentisomide plasma level (available in 5 patients) ranged from 3.4 to 22.3 (mean 8.9 .mu.g/ml). Four patients underwent chronic oral treatment (in 1 pt in association with amiodarone) with a good clinical outcome (mean follow-up 6.25 months, range 1-12). We stress the absence of proarrhythmic worsening effects and the powerful effect of the drug on ventricular tachycardia cycle length. The latter effect, together with persistent ventricular inducibility after pentisomide, suggests that the action of the drug on ventricular conduction velocity and refractoriness is not uniform and unsuitable at least at presently employed drug doses.