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[Mechanism of action and the effectiveness of ethacizin in patients with paroxysmal atrioventricular nodal reciprocal tachycardia].

Abstract
An electrophysiologic study of ethacizin's mechanisms of action was carried out in patients with paroxysmal atrioventricular nodal tachycardia. Tachycardia was controlled by 0.5 mg/kg ethacizin in all patients. No patients demonstrated induced tachycardia in the presence of the drug, and 55% developed a complete retrograde atrioventricular block. The assessment of the preventive effect of oral ethacizin administration showed that paroxysms of tachycardia could not be provoked by esophageal electrostimulation of the heart in 87% of the patients. In the same patients, stable antiarrhythmic effect was maintained by long-term treatment with this drug. The suppression of retrograde stimulus conduction along the quick path of the atrioventricular node is assumed to be the principal electrophysiological mechanism of ethacizin action. Ethacizin can be used to control or prevent paroxysms of atrioventricular nodal tachycardia.
AuthorsV I Malakhov, Kh Kh Shugushev
JournalKardiologiia (Kardiologiia) Vol. 26 Issue 4 Pg. 48-54 (Apr 1986) ISSN: 0022-9040 [Print] Russia (Federation)
Vernacular TitleMekhanizm deĭstviia i effektivnost' etatsizina u bol'nykh s paroksizmal'noĭ atrioventrikuliarnoĭ uzlovoĭ retsiproknoĭ takhikardieĭ.
PMID3520090 (Publication Type: Clinical Trial, Comparative Study, English Abstract, Journal Article)
Chemical References
  • Anti-Arrhythmia Agents
  • Phenothiazines
  • diethylamino-ethmozine
  • Moricizine
Topics
  • Administration, Oral
  • Adult
  • Anti-Arrhythmia Agents (therapeutic use)
  • Atrioventricular Node (drug effects, physiopathology)
  • Clinical Trials as Topic
  • Electrocardiography
  • Female
  • Follow-Up Studies
  • Heart Conduction System (drug effects)
  • Humans
  • Injections, Intravenous
  • Male
  • Middle Aged
  • Moricizine (analogs & derivatives)
  • Phenothiazines (administration & dosage, therapeutic use)
  • Tachycardia, Paroxysmal (drug therapy, physiopathology)

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