Key result
Monophasic action potential duration at 90% repolarization showed a strong linear correlation with plasma drug levels for both procainamide and quinidine (p<0.0001).
Why the study?
Quantitative and immediate assessment of antiarrhythmic drug effects using monophasic action potential recordings in coronary artery disease patients was needed.
Does monophasic action potential recording accurately quantify the electrophysiologic effect of intravenous procainamide and quinidine in patients with coronary artery disease?
Does monophasic action potential recording accurately quantify the electrophysiologic effect of intravenous procainamide and quinidine in patients with coronary artery disease?
Monophasic action potential duration closely correlates with plasma drug levels and can serve as an immediate, quantitative indicator of myocardial drug effect for antiarrhythmic agents.
Answers are grounded in this paper and cite their sources.
MAP recordings enable in vivo quantification of antiarrhythmic effects on repolarization; hypothesis-generating for guiding therapy or future trials.
A contact electrode catheter, which permits clinical recording of cardiac monophasic action potentials (MAPs), was used as a means of quantifying the electrophysiologic effect of 2 antiarrhythmic drugs, procainamide and quinidine. MAP recordings were made in continuous fashion from the right ventricle in 16 patients, before and after the intravenous administration of procainamide (11 patients) or quinidine (5). Increases in the MAP duration at 90% repolarization (MAPD90) were used as indexes of drug effect and related to plasma drug level. Surface electrocardiographic (QRS duration, corrected QT interval [QTC]) and electrophysiologic (ventricular effective refractory period) measurements, in addition to MAPD90, were made at the same time as blood sampling for plasma drug level determination. Dose response curves, plotting change in MAPD90 versus plasma drug level, showed strong linear correlation for both procainamide (p less than 0.0001) and quinidine (p less than 0.0001). The variance (error of estimation) of the predictive relation, change in MAPD90 versus plasma drug level, was significantly lower than that of change in QTC (p less than 0.001), QRS duration (p less than 0.0001) or ventricular effective refractory period (p less than 0.0001) versus plasma drug level for both procainamide and quinidine. Changes in MAP duration closely correlate with plasma drug level, and as such, may serve as an immediate, quantitative indicator of myocardial drug effect during the administration of antiarrhythmic agents.
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Platia et al. (1988) studied Coronary artery disease (n=16). Intravenous procainamide or quinidine vs. Baseline (before administration) was evaluated on Correlation between change in MAPD90 and plasma drug level (p=<0.0001). Monophasic action potential duration at 90% repolarization showed a strong linear correlation with plasma drug levels for both procainamide and quinidine (p<0.0001).
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