Abstract
resonance imaging data suggesting right ventricular outflow tract dilatation in patients with Brugada syndrome as the resolution of imaging modalities has improved. 5 This fibrotic process would promote conduction delay in the right ventricle and may explain the presence of a coved ST-segment elevation pattern independent of specific ion channel mutations promoting transmural repolarization gradients. Invasive mapping studies of the right ventricle in patients with Brugada syndrome have confirmed the presence of significant conduction delay, and computer simulations incorporating these delays can reproduce the characteristic surface ECG features. 3,6 These conduction abnormalities could also increase arrhythmogenicity of the substrate through promoting conduction block and re-entry or causing destabilization of VT into VFn. This may help to explain significant variations in presentations and risk of sudden death in this condition. Letsas et al. 7 presented data addressing the problem of refining non-invasive risk stratification in patients with Brugada syndrome. They demonstrated that an increased Tpeak–Tend interval in leads V2 and V6 and Tpeak–Tend/QT ratio in lead V2 were associated with VT/VF inducibility in patients with Brugada syndrome with spontaneous or ajmaline-induced type 1 ECG patterns. The Tpeak–Tend interval-related repolarization parameters were measured in all precordial leads. The Tpeak–Tend/QT ratio now arrives in the context of the recent description of the fragmented QRS and late potentials as other high-risk markers in Brugada syndrome. 8 These surface ECG parameters may reflect common features of the arrhythmogenic substrate and may have the advantage of being non-invasive and capable of tracking progressive changes in the Brugada heart over time. However, there is some controversy as to what the Tpeak–Tend measurements actually represent. Although experiments using left ventricular wedge preparations have shown that the Tpeak–Tend interval was associated with transmural dispersion of repolarization, a study using an in vivo model questioned this. Opthof et al. 9 have demonstrated that the Tpeak–Tend interval represented
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