OBJECTIVES: We sought to obtain new insights into the pathophysiologic basis of Brugada syndrome (BrS) by studying changes in various electrocardiographic depolarization and/or repolarization variables that occurred with the development of the signature type 1 BrS electrocardiogram (ECG) during ajmaline provocation testing. BACKGROUND: BrS is associated with sudden cardiac death. Its pathophysiologic basis, although unresolved, is believed to reside in abnormal cardiac depolarization or abnormal repolarization. METHODS: Ajmaline provocation was performed in 269 patients suspected of having BrS with simultaneous recording of ECGs, vectorcardiograms, and 62-lead body surface potential maps. RESULTS: A type 1 ECG was elicited in 91 patients (BrS patients), 162 patients had a negative test result (controls), and 16 patients had an abnormal test result. Depolarization abnormalities were more prominent in BrS patients and were mapped to the right ventricle (RV) by longer right precordial filtered QRS complex durations (142 +/- 23 ms vs. 125 +/- 14 ms, p < 0.01) and right terminal conduction delay (60 +/- 11 ms vs. 53 +/- 9 ms, p < 0.01). Repolarization abnormalities remained concordant with depolarization abnormalities as indicated by steady low nondipolar content (12 +/- 8% vs. 8 +/- 4%, p = NS), lower spatial QRS-T integrals (33 +/- 12 mV.ms vs. 40 +/- 16 mV.ms, p < 0.05), similar spatial QRS-T angles (92 +/- 39 degrees vs. 87 +/- 31 degrees , p = NS), similar T(peak)-T(end) interval (143 +/- 36 ms vs. 138 +/- 25 ms, p = NS), and similar T(peak)-T(end) dispersion (47 +/- 37 ms vs. 45 +/- 27 ms, p = NS). CONCLUSIONS: The type 1 BrS ECG is characterized predominantly by localized depolarization abnormalities, notably (terminal) conduction delay in the RV, as assessed with complementary noninvasive electrocardiographic techniques. We could not define a separate role for repolarization abnormalities but suggest that the typical signs of repolarization derangements seen on the ECG are secondary to these depolarization abnormalities. Copyright (c) 2010 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
OBJECTIVES: We sought to obtain new insights into the pathophysiologic basis of Brugada syndrome (BrS) by studying changes in various electrocardiographic depolarization and/or repolarization variables that occurred with the development of the signature type 1 BrS electrocardiogram (ECG) during ajmaline provocation testing. BACKGROUND: BrS is associated with sudden cardiac death. Its pathophysiologic basis, although unresolved, is believed to reside in abnormal cardiac depolarization or abnormal repolarization. METHODS:Ajmaline provocation was performed in 269 patients suspected of having BrS with simultaneous recording of ECGs, vectorcardiograms, and 62-lead body surface potential maps. RESULTS: A type 1 ECG was elicited in 91 patients (BrS patients), 162 patients had a negative test result (controls), and 16 patients had an abnormal test result. Depolarization abnormalities were more prominent in BrS patients and were mapped to the right ventricle (RV) by longer right precordial filtered QRS complex durations (142 +/- 23 ms vs. 125 +/- 14 ms, p < 0.01) and right terminal conduction delay (60 +/- 11 ms vs. 53 +/- 9 ms, p < 0.01). Repolarization abnormalities remained concordant with depolarization abnormalities as indicated by steady low nondipolar content (12 +/- 8% vs. 8 +/- 4%, p = NS), lower spatial QRS-T integrals (33 +/- 12 mV.ms vs. 40 +/- 16 mV.ms, p < 0.05), similar spatial QRS-T angles (92 +/- 39 degrees vs. 87 +/- 31 degrees , p = NS), similar T(peak)-T(end) interval (143 +/- 36 ms vs. 138 +/- 25 ms, p = NS), and similar T(peak)-T(end) dispersion (47 +/- 37 ms vs. 45 +/- 27 ms, p = NS). CONCLUSIONS: The type 1 BrS ECG is characterized predominantly by localized depolarization abnormalities, notably (terminal) conduction delay in the RV, as assessed with complementary noninvasive electrocardiographic techniques. We could not define a separate role for repolarization abnormalities but suggest that the typical signs of repolarization derangements seen on the ECG are secondary to these depolarization abnormalities. Copyright (c) 2010 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
Authors: Edmond M Cronin; Frank M Bogun; Philippe Maury; Petr Peichl; Minglong Chen; Narayanan Namboodiri; Luis Aguinaga; Luiz Roberto Leite; Sana M Al-Khatib; Elad Anter; Antonio Berruezo; David J Callans; Mina K Chung; Phillip Cuculich; Andre d'Avila; Barbara J Deal; Paolo Della Bella; Thomas Deneke; Timm-Michael Dickfeld; Claudio Hadid; Haris M Haqqani; G Neal Kay; Rakesh Latchamsetty; Francis Marchlinski; John M Miller; Akihiko Nogami; Akash R Patel; Rajeev Kumar Pathak; Luis C Saenz Morales; Pasquale Santangeli; John L Sapp; Andrea Sarkozy; Kyoko Soejima; William G Stevenson; Usha B Tedrow; Wendy S Tzou; Niraj Varma; Katja Zeppenfeld Journal: J Interv Card Electrophysiol Date: 2020-10 Impact factor: 1.900
Authors: Albert C Gaw; Byron Lee; Giselle Gervacio-Domingo; Charles Antzelevitch; Romeo Divinagracia; Felipe Jocano Journal: Philipp J Intern Med Date: 2011-07