The early repolarization variant--normal or a marker of heart disease in certain subjects
1Division of Cardiology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA. schuesslerd@wustl.edu
Insights
Early repolarization variant may be a substrate for dangerous heart conditions like sudden death and arrhythmias, not always benign. This cardiovascular anomaly may share genetic origins with Brugada syndrome.
Area of Science:
- Cardiology
- Electrophysiology
- Genetics
Background:
- Early repolarization variant (ERV) is often considered a benign finding on electrocardiograms.
- However, recent observations suggest a potential association with adverse cardiac events.
Purpose of the Study:
- To investigate the potential arrhythmogenic substrate of the early repolarization variant.
- To explore its relationship with other nonischemic ST-elevation syndromes and its possible genetic basis.
Main Methods:
- Theoretical advancement and synthesis of existing clinical and genetic data.
- Comparative analysis with Brugada syndrome and other cardiovascular anomalies.
Main Results:
- The early repolarization variant may not always be benign.
- It can serve as a substrate for ventricular arrhythmias, sudden death, and hypercontractility cardiomyopathy, particularly in athletes.
- ERV may represent part of a spectrum of cardiovascular anomalies linked to nonischemic ST elevation.
Conclusions:
- The early repolarization variant warrants further investigation as a potential risk factor for sudden cardiac death.
- A molecular genetic origin with variable penetrance is suggested for ERV.
- ERV may be related to Brugada syndrome and other nonischemic ST-elevation conditions.
Abstract:
The theory is advanced that the early repolarization variant may not always be benign and that it can become a substrate for ventricular arrhythmias, sudden death, and hypercontractility cardiomyopathy in some subjects, including certain high-performance athletes. In addition, it is suggested that it likely represents part of a spectrum of cardiovascular anomalies related to nonischemic ST elevation including Brugada syndrome, and that it may also have a molecular genetic origin of variable penetrance.
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