PulseExploreJournal ClubResearchersJournals
Instagram
HomeJournal ClubExplore
Synapse
⌘+K
Synapse
June 26, 2003Journal of Cardiovascular Pharmacology

Delayed Sodium Channel Inactivation Mimics Long QT Syndrome 3

View Full Paper
Ask AI
Bookmark
Share

Why the study?

Does acute administration of DPI 201-106 provoke long QT syndrome and ventricular tachyarrhythmias?

Population

Patients receiving acute administration of DPI 201-106

Design

Case_series

Follow-up

Acute

Key result

Acute administration of DPI 201-106 prolonged the QT interval and provoked ventricular tachyarrhythmias in 3 patients, mimicking long QT syndrome type 3.

Authors

VKVolker KühlkampCMChristian MewisRBRalph Bosch

Discussion

Loading...

Member takes

Overview

Alerts clinicians to proarrhythmic risk with DPI 201-106; leaves open generalizability and need for controlled evaluation.

Study Design

Type

Case Report (n=3)

Structured PICO

Does acute administration of DPI 201-106 provoke long QT syndrome and ventricular tachyarrhythmias?

P
Population
Patients receiving acute administration of DPI 201-106
I
Intervention
Acute administration of DPI 201-106
O
Outcome
QT interval prolongation and occurrence of ventricular tachyarrhythmiassafety

Delaying sodium channel inactivation with DPI 201-106 causes an acquired form of long QT syndrome mimicking LQT3, leading to dangerous ventricular arrhythmias.

Cite This Study

Kühlkamp et al. (2003) conducted a case report in Acquired long QT syndrome (n=3). DPI 201-106 was evaluated on QT interval prolongation and ventricular tachyarrhythmias. Acute administration of DPI 201-106 prolonged the QT interval and provoked ventricular tachyarrhythmias in 3 patients, mimicking long QT syndrome type 3.

synapsesocial.com/papers/6a12311b92637892a9a60a6bhttps://doi.org/10.1097/00005344-200307000-00017
View Full Paper
Ask AI
Bookmark
Share