RESEARCH ARTICLE
QT Interval Prolongation and Atypical Proarrhythmia: Monomorphic Ventricular Tachycardia with Trimebutine
Michele Schiariti1, Angela Saladini2, Attilio Placanica1, Marta Saolini1, Paolo E. Puddu*, 3
Article Information
Identifiers and Pagination:
Year: 2009Volume: 3
First Page: 32
Last Page: 36
Publisher Id: TOPHARMJ-3-32
DOI: 10.2174/1874143600903010032
Article History:
Received Date: 13/5/2009Revision Received Date: 27/5/2009
Acceptance Date: 29/5/2009
Electronic publication date: 8/7/2009
Collection year: 2009
open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
A 59-year old woman was admitted at emergency for palpitation and dizziness. Medication history showed trimebutine 450 mg daily, because of meteorism, increased to 450 mg TID a week earlier. At admittance, sustained monomorphic ventricular tachycardia was interrupted by 100 mg intravenous lidocaine and a largely prolonged QTc (523 ± 12 ms) was seen. Discontinuation of trimebutine achieved normalisation of QTc (420 ± 10 ms, p<0.001).
This is the first report in man to illustrate a probable proarrhythmic action of trimebutine. A weak inhibitory effect on both rapid and slow components of the delayed rectifier in guinea-pig ventricular myocytes calls for further investigations in human myocardial tissues. Trimebutine inhibition of Na and Ca++ channels in cardiac tissues of rabbits and guinea-pigs also call for further studies in human myocardial tissues.