Electrophysiological Effects of a New Antiarrhythmic Drug Aksaritmin

Abstract

The purpose of this report was to study the pharmacodynamics of aksaritmin and its effect on cardiac electrophysiological parameters in patients with various heart arrhythmias. Materials and Methods: Fifty-one patients with various heart arrhythmias aged between 18 and 60 years (mean age of 38.4±11.6 years) were examined. The effect of aksaritmin on cardiac electrophysiological parameters was studied using 12 lead ECG, transesophageal electrophysiological study (TES) and intracardiac electrophysiological study (EPS). Effects of aksaritmin (25-50 mg per os) using 12 lead ECG were studied in an acute drug test (ADT) (3 hours after the start of testing) and during the course of treatment (on the fifth day). TES was performed on patients with paroxysmal tachycardias. Aksaritmin was used once at a dose of 50 mg per os, and all indicators were measured 3 hours after patients took the drug. In TES, we studied the sinus-node recovery time (SRT), the Wenckebach point, ERP of the atrioventricular node (ERP-AVN) and accessory atrioventricular connection (ERP-AAVC). The effect of the drug in intracardiac EPS was studied 3 hours after patients were given a single dose of aksaritmin (50 mg) per os. All parameters were measured according to the standard EP protocol. Results: The action of aksaritmin begins 45-60 minutes after the drug is taken and reaches a maximum after 3-4 hours; effects last an average of 8 hours, which allows one to prescribe aksaritmin 3 times a day. The drug in ADT and during the course of treatment increases HR by 8.1% and 4.9%, respectively. Aksaritmin slows down the conduction of impulses via the atria, AV node and His-Purkinje system, and does not affect ventricular ERP. Accordingly, on ECG, the duration of PQ interval and QRS complex is significantly longer, while the duration of the QTc interval does not change. Aksaritmin prolongs ERP-AVN in the retrograde direction by 8.1% and completely blocks anterograde conduction via the AAV pathway in WPW patients.

Keywords

• aksaritmin
• pharmacodynamics
• electrophysiological parameters
• effective refractory period