CORRESPONDENCE: LETTER TO THE EDITOR
Repolarization Measurement in Brugada Syndrome
Arthur M. Yue, MA, DM*
* Wessex Cardiac Center, Southampton University Hospital, Southampton SO16 6YD, United Kingdom (Email: arthur{at}yue.com).
The simultaneous publication of 2 articles in a recent issue of the Journal (1,2) exemplified the value of activation-recovery interval (ARI) determination in understanding the electrophysiological mechanisms of Brugada syndrome. These publications also highlighted the current controversies surrounding how ARI should be measured in vivo: Nagase et al. (1) determined ARIs at the maximum positive slope of the positive T-wave (conventional approach), whereas Hayashi et al. (2) determined ARIs at the negative slope of the positive T-wave (alternative approach).
Despite a statistically significant correlation between ARI determined by the conventional method and monophasic action potential recordings in experimental models, there is still no satisfactory explanation why clinical validation with monophasic action potentials using contact and noncontact unipolar mapping appears to show that the conventional approach underestimates repolarization timings (3–5). Hence, the timing relationship between epicardial and endocardial repolarization in the Brugada patients in the Nagase et al. study (1) might vary depending on the specific method chosen to measure ARI durations.
In the same study (1), body surface type 1 Brugada electrocardiogram changes corresponded to epicardial unipolar recordings showing coved type ST-segment elevation (Fig. 3 in [1]), but this was not consistently reflected by a concurrent negative deflection in the endocardial signal during phase 1 repolarization. Thus, in Figure 3C in this article, pilsicainide challenge induced prominent J-point positive deflection in the epicardial unipolar recording, whereas the endocardial signal remained isoelectric with no changes in ST/T-wave morphology. This would suggest that coved-type ST-segment elevation might not be fully explained by a unidirectional transmural ventricular gradient originating from the endocardium. Further clinical evaluation, such as noninvasive electrocardiographic imaging, might be valuable to clarify the role of trans-epicardial electrophysiological changes in patients with type 1 Brugada electrocardiogram pattern.
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1. Nagase S, Kusano KF, Morita H, et al. Longer repolarization in the epicardium at the right ventricular outflow tract causes type 1 electrocardiogram in patients with Brugada syndrome J Am Coll Cardiol 2008;51:1154-1161.[Abstract/Free Full Text]2. Hayashi M, Takatsuki S, Maison-Blanche P, et al. Ventricular repolarization restitution properties in patients exhibiting type 1 Brugada electrocardiogram with and without inducible ventricular fibrillation J Am Coll Cardiol 2008;51:1162-1168.[Abstract/Free Full Text] 3. Chen PS, Moser KM, Dembitsky WP, et al. Epicardial activation and repolarization patterns in patients with right ventricular hypertrophy Circulation 1991;83:104-118.[Abstract/Free Full Text] 4. Yue AM, Paisey JR, Robinson S, Betts TR, Roberts PR, Morgan JM. Determination of human ventricular repolarization by noncontact mapping: validation with monophasic action potential recordings Circulation 2004;110:1343-1350.[Abstract/Free Full Text] 5. Yue AM. Significant correlation between monophasic action potential (MAP) durations and activation-recovery intervals (ARIs) determined at the maximum positive slope of the positive T wave (conventional method) Heart Rhythm 2007;4:120-121.[Web of Science][Medline]
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