CORRESPONDENCE: LETTER TO THE EDITOR
Reply
Satoshi Nagase, MD*,
Kengo Fukushima Kusano, MD,
Hiroshi Morita, MD and
Tohru Ohe, MD
* Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Department of Cardiovascular Medicine, 2-5-1 Shikata-cho, Okayama, Okayama 700-8558, Japan (Email: snagase{at}cc.okayama-u.ac.jp).
We thank Dr. Yue for his interest in our article (1). In general, direct measurement of action potential duration (APD) in humans is very difficult and complicated. Consequently, activation recovery interval (ARI) has been used in several studies for the evaluation of APD in humans. It is still unclear, and further examination is needed to evaluate APD by the ARI method, especially in cases of a positive T-wave. Haws and Lux (2) have reported that ARI was a good measurement of APD irrespective of T-wave polarity. Recently, Coronel et al. (3) also reported that maximum derivative of the T-wave always coincided with final repolarization in any T-wave polarity. However, Yue et al. (4)and Chen et al. (5) have reported that minimum derivative of the T-wave corresponded to final repolarization with positive T-wave.
Because the methods used in their study to validate the use of ARI were inhomogeneous and because the assessment of polarity is difficult in a complicated T-wave, it is still not clear which method is more accurate and appropriate. The limitation of the ARI method is that ARI represents spatial average and contains a far field effect. We should carefully apply and assess the ARI method for evaluation of APD in consideration of this limitation.
Yan and Antzelevitch (6) found in their experimental study that a prominent transient outward current-mediated action potential notch in epicardial cells, but not that in endocardial cells, creates a transmural voltage gradient and thus causes ST-segment elevation. Further accentuation of the notch leads to preferential prolongation of the epicardial action potential, resulting in the development of coved-type ST-segment elevation and terminal inverted T-wave (type 1 electrocardiogram [ECG]) in right precordial leads in Brugada syndrome. In our study, we also found that type 1 ECG is closely related to the prolongation of repolarization in the epicardium compared with that in the endocardium in Brugada syndrome (1). The administration of pilsicainide predominantly affected the epicardial repolarization, and the effect of pilsicainide administration was small in the endocardial site. We cannot completely rule out the possibility that epicardial heterogeneity of the action potential causes type 1 ECG. However, these results suggest that the pathological and critical change mainly observed in epicardial cells caused typical Brugada-type ECG.
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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. Haws CW, Lux RL. Correlation between in vivo transmembrane action potential durations and activation-recovery intervals from electrograms: effects of interventions that alter repolarization time Circulation 1990;81:281-288.[Abstract/Free Full Text] 3. Coronel R, de Bakker JMT, Wilms-Schopman FJG, et al. Monophasic action potentials and activation recovery intervals as measures of ventricular action potential duration: Experimental evidence to resolve some controversies Heart Rhythm 2006;3:1043-1050.[CrossRef][Web of Science][Medline] 4. Yue AM, Paisey JR, Robinson S, et al. Determination of human ventricular repolarization by noncontact mapping: validation with monophasic action potential recordings Circulation 2004;110:1343-1350.[Abstract/Free Full Text] 5. 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] 6. Yan GX, Antzelevitch C. Cellular basis for the Brugada syndrome and other mechanisms of arrhythmogenesis associated with ST-segment elevation Circulation 1999;100:1660-1666.[Abstract/Free Full Text]
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