Effects of high-frequency biphasic shocks on ventricular vulnerability and defibrillation outcomes through synchronized virtual electrode responses

Figures

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  Fig 1. Optical mapping setting and typical waveform illustrations. (A) High-speed optical mapping setup for fluorescence imaging of isolated hearts. The inset figure displays the shock electrode placement on the lateral sides of the ventricles. (B) Four shock waveforms with different frequencies that were used as the S2s in the S1-S2 stimulation protocol.

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  Fig 2. Different frequencies of defibrillation observed using optical mapping. (A–D) Whole-heart optical potential response to shocks of 125–1000 Hz observed from the difference in fluorescence intensity between successive frames, displaying wavefront polarization. Red arrows indicate depolarizing virtual cathodes; white arrows indicate repolarizing virtual anodes. These virtual electrode responses were observed in only four of the six rat hearts. (E) Comparison of shock waveforms and shock responses of the virtual electrodes on the left and right ventricles of the four shock frequencies.

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  Fig 3. Different frequency responses at the midpoint of the heart and comparison of postshock action potential. (A) Three recording sites between the cathode and the midpoint on the heart. (B–E) The 125–1000-Hz shock-induced optical potentials. Vertical lines indicate instances of the shock waveform switching from positive to negative potential. The x-axis is the time scale (ms), and the y-axis is relative brightness with arbitrary units. (F) Postshock optical potential level at point (a) for the four shock frequencies (* represents p < 0.05).

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  Fig 4. Comparison of action potential rise time and shock isochronal maps among the four shock frequencies. (A) Responses to the four shock frequencies at point c in Fig 3B–3E were combined for comparison. The x-axis is the time scale (ms), and the y-axis is the relative brightness with arbitrary units. (B) Comparison of the optical potential rise time resulting from the four shock frequencies. (C) Isochronal maps of the shock-induced tissue response in the entire heart.

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  Fig 5. S1-S2 protocol-induced ventricular tachyarrhythmia (VTA) observed using electrocardiography and VTA observed using optical mapping. (A) Example of optical potential from S1-S2 pacing protocol without VTA induction. After applying eight S1 pacing pulses, S2 appeared as a premature stimulation (S1-S2 interval: 50 ms). (B) Successful VTA induction by a 1000-Hz shock (S1-S2 intervals: 100 ms). (C) Successful defibrillation by a 1000-Hz shock followed by the restored rhythm. (D) VTA wavefront observed using optical mapping. The yellow dotted lines and arrows indicate the direction of VTA wavefront propagation.

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  Fig 6. Ventricular tachyarrhythmia vulnerability bubble plot of S1-S2 coupling intervals and shock frequencies.