Comparison of the Effect of Class IA Antiarrhythmic Drugs on Transmembrane Potassium Currents in Rabbit Ventricular Myocytes

Abstract

Although quinidine, disopyramide, and procainamide are all classified as Class IA antiarrhythmics, these drugs had different effects on various potassium currents, which may partially explain their distinct effect on repolarization in various cardiac tissues and on cardiac arrhythmias in clinical settings.

Pathophysiological mechanisms of Brugada syndrome: Depolarization disorder, repolarization disorder, or more?

“…Accordingly, 4-aminopyridine, which blocks I to , restored the AP dome and electrical homogeneity in the canine wedge preparation [84,100], consistent with the clinical efficacy of quinidine, an antiarrhythmic drug with I to blocking properties, in normalizing the ECG pattern [28,116] and preventing spontaneous or induced arrhythmias [80,117]. However, this effects may be due to quinidine's anticholinergic action [118,119], while prolongation of AP duration by blockade of the delayed rectifier potassium channel [120,121] may also act to suppress reentrant arrhythmias.…”

Multifocal Ectopic Purkinje-Related Premature Contractions

“…Clinically relevant effects of this drug are thought to be due to alteration of the Na ϩ current, the transient outward current I to (27,28), and the repolarizing delayed rectifier current I Kr (29,30). In addition, quinidine also inhibits Ca 2ϩ and other K ϩ currents, although in a lower extent (31,32). Therefore, inhibition of these latter currents was not considered.…”

Role of late sodium current in modulating the proarrhythmic and antiarrhythmic effects of quinidine

“…By virtue of its electrophysiologic actions of inhibiting I K and increasing the ventricular effective refractory period, quinidine can also reduce arrhythmic activity in patients with short QT syndrome caused by gain of function of potassium channels3,4 and in patients with Brugada syndrome caused by loss-of-function sodium channelopathies 3–6. However, it has been recognized for decades that clinical use of quinidine is associated with recurrent syncope (i.e., quinidine syncope) and sudden death due to QT prolongation and polymorphic ventricular tachycardia (torsade de pointes [TdP]) 1,2. The incidence of TdP caused by quinidine is 1.5% to 8.8% or higher per patient-year of treatment 1,7.…”