Quinidine in the Management of Recurrent Ventricular Arrhythmias: A Reappraisal.


Journal

JACC. Clinical electrophysiology
ISSN: 2405-5018
Titre abrégé: JACC Clin Electrophysiol
Pays: United States
ID NLM: 101656995

Informations de publication

Date de publication:
10 2021
Historique:
received: 19 01 2021
revised: 17 03 2021
accepted: 23 03 2021
pubmed: 5 7 2021
medline: 29 10 2021
entrez: 4 7 2021
Statut: ppublish

Résumé

This study aimed to review the utility of quinidine in patients presenting with recurrent sustained ventricular arrhythmia (VA) and limited antiarrhythmic drug (AAD) options. Therapeutic options are often limited in patients with structural heart disease and recurrent VAs. Quinidine has an established role in rare arrhythmic syndromes, but its potential use in other difficult VAs has not been assessed in the present era. We performed a retrospective analysis of 37 patients who had in-hospital quinidine initiation after multiple other therapies failed for VA suppression at our tertiary referral center. Clinical data and outcomes were obtained from the medical record. Of 30 patients with in-hospital quantifiable VA episodes, quinidine reduced acute VA from a median of 3 episodes (interquartile range [IQR]: 2 to 7.5) to 0 (IQR: 0 to 0.5) during medians of 3 days before and 4 days after quinidine initiation (p < 0.001). VA events decreased from a median of 10.5 episodes per day (IQR: 5 to 15) to 0.5 episodes (IQR: 0 to 4) after quinidine initiation in the 12 patients presenting with electrical storm (p = 0.004). Among the 24 patients discharged on quinidine, 13 (54.2%) had VA recurrence during a median of 138 days. Adverse effects in 9 of the 37 patients (24.3%) led to drug discontinuation, most commonly gastrointestinal intolerance. In patients with recurrent VAs and structural heart disease who have limited treatment options, quinidine can be useful, particularly as a short-term therapy.

Sections du résumé

OBJECTIVES
This study aimed to review the utility of quinidine in patients presenting with recurrent sustained ventricular arrhythmia (VA) and limited antiarrhythmic drug (AAD) options.
BACKGROUND
Therapeutic options are often limited in patients with structural heart disease and recurrent VAs. Quinidine has an established role in rare arrhythmic syndromes, but its potential use in other difficult VAs has not been assessed in the present era.
METHODS
We performed a retrospective analysis of 37 patients who had in-hospital quinidine initiation after multiple other therapies failed for VA suppression at our tertiary referral center. Clinical data and outcomes were obtained from the medical record.
RESULTS
Of 30 patients with in-hospital quantifiable VA episodes, quinidine reduced acute VA from a median of 3 episodes (interquartile range [IQR]: 2 to 7.5) to 0 (IQR: 0 to 0.5) during medians of 3 days before and 4 days after quinidine initiation (p < 0.001). VA events decreased from a median of 10.5 episodes per day (IQR: 5 to 15) to 0.5 episodes (IQR: 0 to 4) after quinidine initiation in the 12 patients presenting with electrical storm (p = 0.004). Among the 24 patients discharged on quinidine, 13 (54.2%) had VA recurrence during a median of 138 days. Adverse effects in 9 of the 37 patients (24.3%) led to drug discontinuation, most commonly gastrointestinal intolerance.
CONCLUSIONS
In patients with recurrent VAs and structural heart disease who have limited treatment options, quinidine can be useful, particularly as a short-term therapy.

Identifiants

pubmed: 34217656
pii: S2405-500X(21)00327-3
doi: 10.1016/j.jacep.2021.03.024
pii:
doi:

Substances chimiques

Anti-Arrhythmia Agents 0
Quinidine ITX08688JL

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

1254-1263

Informations de copyright

Copyright © 2021 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Funding Support and Author Disclosures The authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Auteurs

Dan L Li (DL)

Cardiovascular Division, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.

Zachary L Cox (ZL)

Department of Pharmaceutical Services, Vanderbilt University Medical Center, Nashville, Tennessee, USA; Lipscomb University College of Pharmacy, Nashville, Tennessee, USA.

Travis D Richardson (TD)

Cardiovascular Division, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.

Arvindh N Kanagasundram (AN)

Cardiovascular Division, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.

Pablo J Saavedra (PJ)

Cardiovascular Division, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.

Sharon T Shen (ST)

Cardiovascular Division, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.

Jay A Montgomery (JA)

Cardiovascular Division, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.

Katherine T Murray (KT)

Cardiovascular Division, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA; Division of Clinical Pharmacology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.

Dan M Roden (DM)

Cardiovascular Division, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA; Division of Clinical Pharmacology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.

William G Stevenson (WG)

Cardiovascular Division, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA. Electronic address: william.g.stevenson@vumc.org.

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Classifications MeSH