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ST segment elevation induced by class IC antiarrhythmic agents: underlying electrophysiologic mechanisms and insights
1Harvard-Thorndike Electrophysiology Institute, Beth Israel Deaconess Hospital, Boston, Massachusetts 02215, USA.
Journal of Cardiovascular Electrophysiology
|December 3, 1998
Insights
Class IC sodium channel blockers can cause ST segment elevation in specific ECG leads (V1-V3). This finding is linked to drug-induced proarrhythmia and Brugada syndrome, a cause of idiopathic ventricular fibrillation.
Area of Science:
- Cardiology
- Clinical Electrophysiology
- Pharmacology
Background:
- Class IC sodium channel blockers are used to treat cardiac arrhythmias.
- ST segment elevation on an electrocardiogram (ECG) can indicate myocardial infarction or other conditions.
- Brugada syndrome is an inherited disorder that increases the risk of sudden cardiac death.
Observation:
- Three patients experienced ST segment elevation in ECG leads V1 through V3.
- This ECG finding occurred after administration of Class IC sodium channel blockers.
- The observed ST segment elevation was transient and resolved after drug discontinuation.
Findings:
- Class IC sodium channel blockers can induce a specific ECG pattern characterized by ST segment elevation in leads V1-V3.
- This phenomenon is related to the electrophysiologic effects of these drugs on cardiac sodium channels.
- The induced ECG changes share similarities with the diagnostic criteria for Brugada syndrome.
Implications:
- The findings highlight a potential proarrhythmic effect of Class IC sodium channel blockers.
- This ECG manifestation may serve as an indicator of increased risk for ventricular arrhythmias in susceptible individuals.
- Understanding this drug-induced effect is crucial for differentiating it from acute coronary syndromes and for managing patients with Brugada syndrome or at risk for it.
Abstract:
Three patients in whom Class IC sodium channel blockers induced ST segment elevation in leads V1 through V3 are described. The underlying electrophysiologic mechanism, implications for drug-induced proarrhythmia, and the relationship of the finding to the Brugada syndrome type of idiopathic ventricular fibrillation are discussed.