The effect of oral quinidine on intraventricular conduction in man: Correlation of plasma quinidine with changes in QRS duration

Indoramin‐prolongation of repolarization time, a mechanism of bradycardia in man?

“…It is not possible to interpret changes in QT or QTc intervals as necessarily reflecting changes in monophasic action potential duration which are observed at a cellular level in micro-electrode studies. Nevertheless, (Harron et al, 1984b) but others such as quinidine also prolong QTc (Heissenbuttel & Bigger, 1970). Although indoramin has local anaesthetic and membrane stabilizing activity similar to Class I antiarrhythmic drugs (Alps et al, 1971), QRS duration was not prolonged in the present study.…”

Heterogeneous Effect of Quinidine on the Ventricular Depolarization Process Assessed by the Spatial Velocity Electrocardiogram of the QRS Complex

“…However, the ventricular rcpolarization modifications are mainly found with a low er concentration of quinidine and arc frequently regarded as the therapeutic effect. Moreover, the prolongation of the Q-T interval is more often used alone in humans to assess its electropharmacodynamic effects [30][31][32][33], Only the re sults reported by Heissenbuttel and Bigger [3] who used different methods in a population that was different from ours suggested that the increased width of the QRS com plex was an indicator of quinidine activity at concentra tions within the therapeutic range.…”

“…Quinidine, a class 1A antiarrhythmic agent, exerts a depressing effect on the maximum upstroke velocity of phase 0 (Vmax) of the transmembrane action potential of the myocardial fibers, which is responsible for an intra ventricular delay [1], This is reflected in the surface elec trocardiogram by a prolonged QRS duration, which has been described in many experimental [2,[19][20][21] and clin ical studies [3,[22][23][24][25], Two studies showed [2,3] a more pronounced negative conduction effect at the onset (sep tal activation) and the end (posterobasal activation) of the QRS complex, unrelated to bundle branch block, suggest ing a heterogeneous conduction effect of quinidine. The reason could be the polymorphic anatomical substratum of septal and posterobasal zones compared with the more homogeneous and concentric architecture of the ventricu lar free wall leading to a regular endoepicardial activation [26].…”

“…The results of two studies suggested that quini dine has a heterogeneous ventricular conduction effect, i.e. a more pronounced negative conduction effect at the onset and the end of the QRS complex, unrelated to the bundle branch block [2,3], In order to verify this hypothe sis, we performed a randomized placebo-controlled trial using the spatial velocity electrocardiogram of the QRS complex (SVECG-QRS) which allows a good representa tion of the successive ventricular depolarization phases [4,5], Before its introduction and application by Hellerstein and Hamlin [4], this method had only been used in healthy subjects and as a diagnostic tool in various cardiac diseases [6][7][8][9][10][11][12][13][14][15], This study involves the first application of SVECG-QRS for assessing the electropharmacodynamic effect of antiarrhythmic drugs.…”

Antimalarial agents: specific treatment regimens

“…The electrocardiographic effects of quinidine have been noted frequently (prolongation of the Q-Tc interval, widening of the QRS complex, and T-wave flattening) and are associated with high plasma quinidine levels (13,17). However, dysrhythmias have not been seen in patients receiving rate-controlled infusions.…”