Validation of Intramural Wavefront Reconstruction and Estimation of 3D Conduction Velocity

Wilson Good1, Karli Gillette2, Jake Bergquist3, Brian Zenger3, Jess Tate3, Gernot Plank2, Rob MacLeod3
1The SCI Institute, 2Institute of Biophysics - Medical University of Graz, 3University of Utah


Introduction: Changes in conduction velocity are indicative of a wide variety of cardiac abnormalities yet measuring conduction velocity is challenging, especially within the myocardial volume. In this study we investigated a novel technique to reconstruct activation fronts and estimate three-dimensional (3D) conduction velocity (CV) from experimental intramural recordings.

Methods: Our method is based on irregularly sampled electrograms from within the myocardium, which we capture in experiments using intramural needle electrodes. From the electrograms we reconstruct the activation pro- file, which we use to compute the gradient of the activation times and a series of streamlines. Onto these stream- lines we then map the activation times to estimate 3D conduction velocity along the streamline. To assess the ac- curacy of our reconstruction techniques, we utilized the CARPentry simulation platform, which calculated the activation times throughout the region sampled by the intra- mural needles. We then compared our simulated activation times to those we reconstructed. We also used CARPentry’s simulations to validate our estimation of 3D CV.

Results: The reconstructed activation times agreed closely with simulated values, with an average RMSE of 0.65ms and 89% percent of the volume with errors < 1ms. We found close agreement between the CVs calculated using reconstructed versus simulated activation times. Across the reconstructed stimulations sites we saw an average CV of 459cm/s with a standard deviation of 131cm/s versus 435cm/s with a standard deviation of 132cm/s with simulated data.

Discussion: This study used simulated datasets to validate our methods for reconstructing 3D activation fronts and estimating conduction velocities. Our results indicate that our method allows accurate reconstructions from sparse measurements, thus allowing us to examine changes in activation induced by experimental interventions such as acute ischemia, ectopic pacing, or drugs.