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European Heart Journal 1987 8(2):154-163;
Copyright © 1987 by the European Society of Cardiology.
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© 1987 The European Society of Cardiology

Effects of intravenous disopyramide and quinidine on normal myocardium and on the characteristics of arrhythmias: intraindividual comparison in patients with sustained ventricular tachycardia

I RIZOS{dagger}, J. BRACHMANN*, W. LENGFELDER{dagger}, C. SCHMITT*, K. VON OLSHAUSEN*, W. KÜBLER* and J. SENGES{dagger},

{dagger}Medizinische Klinik B (Kardiologie), Klinikum der Stadt Ludwigshafen am Rhein Ludwigshafen, F.R.G.
*Abteilung Innere Medizin III (Kardiologie), Medizinische Universitätsklinik Heidelberg

Received 14 March 1986; revised 16 July 1986; .

Address for correspondence: Jochen Senges, Medizinische Klinik B, Klinikum Ludwigshafen, Bremserstr 79, D-6700 Ludwigshafen, F.R.G.

Abstract

Intraindividual comparison of the acute response to intravenous quinidine and to intravenous disopyramide was performed in 27 patients with sustained ventricular tachycardia ( VT) who underwent serial electrophysiological studies. In each patient, sustained VT could be reproducibly initiated by programmed ventricular stimulation during control studies. Quinidine and disopyramide prevented inducibility of sustained VT in 7 and 8 of the 27 patients, respectively. Six patients were concordant responders to both drugs and 18 patients were concordant non-responders resulting in a total of 24 patients (89%) who had a concordant result (P<0.01). In the 18 non-responders with inducible sustained VT after both drugs, quinidine and disopyramide caused qualitatively and quantitatively similar changes in the characteristics of the VT: prolongation of the interval between the initiating extrastimulus and the first beat of VT by 36 and 39%, and an increase in VT cycle length by 21 and 29%, respectively. The QRS morphology of VT was concordantly altered in 13 of these 18 patients (72%). In all 27 patients, quinidine and disopyramide caused a quantitatively similar prolongation of ventricular refractoriness by 12 and 14%, of the QRS duration by 14 and 13% and of the QTc interval by 13 and 13%, respectively. The clinical data obtained at comparable plasma concentrations confirm the experimental presumption that quinidine and disopyramide have qualitatively and quantitatively similar electrophysiological effects not only on normal myocardium but also on the characteristics of VT, resulting in a significant concordance of antiarrhythmic responses.

Key Words: Antiarrhythmic drugs • ventricular tachycardia • electrophysiological studies • programmed stimulation • sudden death.


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