Effects of β-blockers on ventricular repolarization documented by 24-hour electrocardiography in long QT syndrome type 2.


Journal

Heart rhythm
ISSN: 1556-3871
Titre abrégé: Heart Rhythm
Pays: United States
ID NLM: 101200317

Informations de publication

Date de publication:
09 2022
Historique:
received: 07 01 2022
revised: 11 04 2022
accepted: 27 04 2022
pubmed: 8 5 2022
medline: 9 9 2022
entrez: 7 5 2022
Statut: ppublish

Résumé

Long QT syndrome (LQTS) is an inherited arrhythmia disorder characterized by ventricular repolarization abnormalities and a risk of sudden cardiac death. The electrophysiological components generating the high risk of arrhythmias in LQTS are prolonged repolarization, increased dispersion of repolarization, and early afterdepolarizations, which are clinically estimated as QT interval, T-wave peak to T-wave end (TPE) interval, and T2/T1-wave amplitude ratio, respectively. In experimental LQTS type 2 (LQT2) models, β-blockers decrease dispersion of repolarization and prevent early afterdepolarizations. In clinical studies in patients with LQT2 , β-blockers are more effective against exercise-induced than arousal-induced cardiac events. The aim of the study was to investigate the effects of β-blocker therapy on repolarization properties in LQT2. QT and TPE intervals and maximal T2/T1-wave amplitude ratios recorded by 24-hour electrocardiograms before and during β-blocker therapy were evaluated in 25 patients with LQT2. β-Blocker therapy decreased the maximal T2/T1-wave amplitude ratio from 2.9 ± 1.1 to 1.8 ± 0.7 (P < .001), but did not change the pause-induced T2/T1-wave amplitude ratio. Under medication, abrupt maximal TPE intervals were shorter at heart rates of ≥75 beats/min and maximal QT intervals were shorter at a heart rate of 100 beats/min. β-Blockers stabilize ventricular repolarization in LQT2 by reducing electrocardiographic early afterdepolarizations and by reducing abrupt prolongation of electrocardiographic dispersion of repolarization and ventricular repolarization duration at elevated heart rates. The effect of β-blockers on pause-induced electrocardiographic early afterdepolarizations is weak. The findings provide electrocardiographic explanation for the protective effects of β-blockers against exercise-induced cardiac events in LQT2.

Sections du résumé

BACKGROUND
Long QT syndrome (LQTS) is an inherited arrhythmia disorder characterized by ventricular repolarization abnormalities and a risk of sudden cardiac death. The electrophysiological components generating the high risk of arrhythmias in LQTS are prolonged repolarization, increased dispersion of repolarization, and early afterdepolarizations, which are clinically estimated as QT interval, T-wave peak to T-wave end (TPE) interval, and T2/T1-wave amplitude ratio, respectively. In experimental LQTS type 2 (LQT2) models, β-blockers decrease dispersion of repolarization and prevent early afterdepolarizations. In clinical studies in patients with LQT2 , β-blockers are more effective against exercise-induced than arousal-induced cardiac events.
OBJECTIVES
The aim of the study was to investigate the effects of β-blocker therapy on repolarization properties in LQT2.
METHODS
QT and TPE intervals and maximal T2/T1-wave amplitude ratios recorded by 24-hour electrocardiograms before and during β-blocker therapy were evaluated in 25 patients with LQT2.
RESULTS
β-Blocker therapy decreased the maximal T2/T1-wave amplitude ratio from 2.9 ± 1.1 to 1.8 ± 0.7 (P < .001), but did not change the pause-induced T2/T1-wave amplitude ratio. Under medication, abrupt maximal TPE intervals were shorter at heart rates of ≥75 beats/min and maximal QT intervals were shorter at a heart rate of 100 beats/min.
CONCLUSION
β-Blockers stabilize ventricular repolarization in LQT2 by reducing electrocardiographic early afterdepolarizations and by reducing abrupt prolongation of electrocardiographic dispersion of repolarization and ventricular repolarization duration at elevated heart rates. The effect of β-blockers on pause-induced electrocardiographic early afterdepolarizations is weak. The findings provide electrocardiographic explanation for the protective effects of β-blockers against exercise-induced cardiac events in LQT2.

Identifiants

pubmed: 35525424
pii: S1547-5271(22)01952-X
doi: 10.1016/j.hrthm.2022.04.028
pii:
doi:

Substances chimiques

Adrenergic beta-Antagonists 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1491-1498

Informations de copyright

Copyright © 2022 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.

Auteurs

Mikael Koponen (M)

Heart and Lung Center, Helsinki University Hospital, Helsinki, Finland. Electronic address: mikael.koponen@helsinki.fi.

Annukka Marjamaa (A)

Heart and Lung Center, Helsinki University Hospital, Helsinki, Finland.

Heikki Väänänen (H)

Department of Neuroscience and Biomedical Engineering, Aalto University, Espoo, Finland.

Annukka M Tuiskula (AM)

Department of Medicine, Helsinki University Hospital and University of Helsinki, Helsinki, Finland; HUS Diagnostic Center, Laboratory of Genetics, Helsinki University Hospital and University of Helsinki, Helsinki, Finland.

Kimmo Kontula (K)

Department of Medicine, Helsinki University Hospital and University of Helsinki, Helsinki, Finland.

Heikki Swan (H)

Heart and Lung Center, Helsinki University Hospital, Helsinki, Finland.

Matti Viitasalo (M)

Heart and Lung Center, Helsinki University Hospital, Helsinki, Finland.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH