Disease relevance of Ethacizine

• Injection of 25 and 50 micrograms/ml of ethacizin into the atrioventricular (AV) node artery significantly (p less than 0.001) prolonged AV conduction time with occasional second degree heart block [1].
• Injections of ethacizin, 5, 10 and 25 micrograms/ml, into the sinus node artery caused an immediate and significant (p less than 0.001) sinus bradycardia of 2, 6 and 11%, respectively [1].
• Ethacizin reduced the total number of ventricular premature beats (VPBs) from 17,263/24 hours (on placebo) to 3458/24 hours (p less than 0.001) and suppressed couplets and ventricular tachycardia (VT) runs by 90% in 94% and 96% of patients, respectively [2].
• Antiarrhythmic efficacy of ethacizine assessed by programmed electrical stimulation in patients with ventricular tachycardia [3].

High impact information on Ethacizine

• With this combination, conduction delay after pause was shorter than with ethacizin alone, which is consistent with the competition of the drugs for the same binding site inside the sodium channel [4].
• In contrast, reflex changes in sympathetic activity elicited by baroreceptor challenges were not affected by ethacizin [5].
• Maximum blood plasma concentration of ethacizin was observed in 110 to 120 minutes and accounted for 300 to 447 ng/ml (mean 354 +/- 77 ng/ml), with a minimum therapeutic drug plasma concentration ranging from 29 to 101 ng/ml (mean 73 +/- 27 ng/ml) [2].
• Computer simulation using the "guarded-receptor" model predicted that the combination of ethacizin and ethmozin should exert a greater decrease in excitability and conduction at short coupling intervals, but little effect at normal heart rates (HR) [6].
• 2. The pathways of metabolism of ethacizin include N-de-ethylation, sulphoxidation, N-10 amide hydrolysis, aromatic hydroxylation and conjugation [7].

Biological context of Ethacizine

• The negligible shift in channel inactivation and the reduction of apparent binding and unbinding rates with more polarized membrane potentials imply the active moiety of ethacizin blocks open channels and is trapped within the channel at resting membrane potentials [8].

Anatomical context of Ethacizine

• In this study we examined the defibrillating potency of two antiarrhythmic phenothiazines, ethmozine (ETM) and ethacizine (ETA), as well as their effects on catecholamine uptake and on the electrophysiological properties of the myocardial cell membrane [9].

References