Quantifying the spatiotemporal influence of acute myocardial ischemia on volumetric conduction velocity.

INTRODUCTION: Acute myocardial ischemia occurs when coronary perfusion to the heart is inadequate, which can perturb the highly organized electrical activation of the heart and can result in adverse cardiac events including sudden cardiac death. Ischemia is known to influence the ST and repolarization phases of the ECG, but it also has a marked effect on propagation (QRS); however, studies investigating propagation during ischemia have been limited. METHODS: We estimated conduction velocity (CV) and ischemic stress prior to and throughout 20 episodes of experimentally induced ischemia in order to quantify the progression and correlation of volumetric conduction changes during ischemia. To estimate volumetric CV, we 1) reconstructed the activation wavefront; 2) calculated the elementwise gradient to approximate propagation direction; and 3) estimated conduction speed (CS) with an inverse-gradient technique. RESULTS: We found that acute ischemia induces significant conduction slowing, reducing the global median speed by 20 cm/s. We observed a biphasic response in CS (acceleration then deceleration) early in some ischemic episodes. Furthermore, we noted a high temporal correlation between ST-segment changes and CS slowing; however, when comparing these changes over space, we found only moderate correlation (corr. = 0.60). DISCUSSION: This study is the first to report volumetric CS changes (acceleration and slowing) during episodes of acute ischemia in the whole heart. We showed that while CS changes progress in a similar time course to ischemic stress (measured by ST-segment shifts), the spatial overlap is complex and variable, showing extreme conduction slowing both in and around regions experiencing severe ischemia.

Estimation and Validation of Cardiac Conduction Velocity and Wavefront Reconstruction Using Epicardial and Volumetric Data.

OBJECTIVE: In this study, we have used whole heart simulations parameterized with large animal experiments to validate three techniques (two from the literature and one novel) for estimating epicardial and volumetric conduction velocity (CV). METHODS: We used an eikonal-based simulation model to generate ground truth activation sequences with prescribed CVs. Using the sampling density achieved experimentally we examined the accuracy with which we could reconstruct the wavefront, and then examined the robustness of three CV estimation techniques to reconstruction related error. We examined a triangulation-based, inverse-gradient-based, and streamline-based techniques for estimating CV cross the surface and within the volume of the heart. RESULTS: The reconstructed activation times agreed closely with simulated values, with 50-70% of the volumetric nodes and 97-99% of the epicardial nodes were within 1 ms of the ground truth. We found close agreement between the CVs calculated using reconstructed versus ground truth activation times, with differences in the median estimated CV on the order of 3-5% volumetrically and 1-2% superficially, regardless of what technique was used. CONCLUSION: Our results indicate that the wavefront reconstruction and CV estimation techniques are accurate, allowing us to examine changes in propagation induced by experimental interventions such as acute ischemia, ectopic pacing, or drugs. SIGNIFICANCE: We implemented, validated, and compared the performance of a number of CV estimation techniques. The CV estimation techniques implemented in this study produce accurate, high-resolution CV fields that can be used to study propagation in the heart experimentally and clinically.

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

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: From the intermittently sampled electrograms we both reconstruct the activation profile and compute the reciprocal of the gradient of activation times and a series of streamlines that allows for the CV estimation. RESULTS: The reconstructed activation times agreed closely with simulated values, with 50% to 70% of the nodes ≤ 1ms of absolute error. We found close agreement between the CVs calculated using reconstructed versus simulated activation times. Across the reconstructed stimulation sites we saw that the reconstructed CV was on average 3.8% different than the ground truth CV. 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.