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. Author manuscript; available in PMC: 2023 Aug 1.
Published in final edited form as: Trends Cardiovasc Med. 2021 Jul 10;32(6):350–363. doi: 10.1016/j.tcm.2021.07.001

Figure 5.

Figure 5.

Cellular basis for the ECG and arrhythmic manifestation of BrS. Each panel shows transmembrane action potentials recorded from one endocardial (top) and two epicardial sites together with a transmural ECG recorded from a canine coronary-perfused right ventricular wedge preparation. A: Control (Basic cycle length (BCL) 400 msec). B: Combined sodium and calcium channel block with terfenadine (5 μM) accentuates the epicardial AP notch creating a transmural voltage gradient that manifests as an ST segment elevation or exaggerated J wave in the ECG. C: Continued exposure to terfenadine results in all-or-none repolarization at the end of phase 1 at some epicardial sites but not others, creating a local epicardial dispersion of repolarization (EDR) as well as a transmural dispersion of repolarization (TDR). D: Phase 2 reentry occurs when the epicardial AP dome propagates from a site where it is maintained to regions where it has been lost giving rise to a closely coupled extrasystole. E: Extrastimulus (S1-S2 = 250 msec) applied to epicardium triggers a polymorphic VT. F: Phase 2 reentrant extrasystole triggers a brief episode of polymorphic VT. Modified from (135), with permission.