Key result
Accentuation of transmural dispersion of repolarization underlies both Brugada and long-QT syndromes, driven by right ventricular epicardial abbreviation and M cell prolongation, respectively.
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This review highlights how amplification of electrical heterogeneities, specifically transmural dispersion of repolarization, contributes to arrhythmogenesis in Brugada and long-QT syndromes.
Regional differences in repolarization characteristics of distinct cell types are responsible for the inscription of the J wave and T wave of the electrocardiogram (ECG). Amplification of these electrical heterogeneities contributes to the development of a variety of cardiac arrhythmias. This brief review examines the ionic and cellular basis for these heterogeneities and their role in the Brugada and long-QT syndromes. Both cases involve an accentuation of transmural dispersion of repolarization (TDR). In the case of the Brugada syndrome. TDR is accentuated as a result of a preferential abbreviation of the right ventricular epicardial action potential, whereas in the long-QT syndrome, accentuation of TDR is secondary to a preferential prolongation of the action potential of the M cell.
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Charles Antzelevitch (2004) conducted a review in Brugada and long-QT syndromes. Accentuation of transmural dispersion of repolarization underlies both Brugada and long-QT syndromes, driven by right ventricular epicardial abbreviation and M cell prolongation, respectively.
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