Figure 5.

Rate and pause-dependence of the J wave in an experimental model and two clinical cases of BrS. A: Transmural ECG and transmembrane action potentials (APs) simultaneously recorded from a canine right ventricular wedge preparation: Prominent J waves and associated AP notches were observed during basic stimulation (S1-S1=4000ms). Premature stimulation (S1-S2=300ms) reduced the epicardial AP notch and J wave amplitude. B: Plot of epicardial AP notch (□) and J wave (○) amplitude over a range of S1-S2 intervals. Restitution of action potential notch amplitude parallels that of the J wave. Reproduced from ¹⁶⁹ with permission. C: ECG lead V4-V5 recorded from a 34 year-old Chinese man with idiopathic ventricular fibrillation, showing prominent J waves that are more accentuated after a pause (thick arrows) compared to those (thin arrows) recorded at shorter R-R intervals. Note that the amplified J wave after the pause was accompanied by T wave inversion (V5), an ECG marker associated with a high risk of ventricular fibrillation. D: A J-wave-like deflection at the terminal portion of the QRS in a patient with intra-ventricular conduction delay. In contrast to the J wave behavior observed in Figure 5C, the end of QRS notch observed in this case is tachycardia-dependent. The terminal deflection is attenuated at longer the R-R interval (thin arrows) and amplified at the shorter R-R interval (thick arrows). Reproduced from ⁸⁶, with permission.