Related Experiment Video
Updated: Nov 7, 2025
Real-time Pressure-volume Analysis of Acute Myocardial Infarction in Mice
Published on: July 2, 2018
Quantifying the Spatiotemporal Influence of Acute Myocardial Ischemia on Volumetric Conduction Speeds
Wilson W Good1,2,3, Brian Zenger1,2,3,4, Jake A Bergquist1,2,3
1Scientific Computing and Imaging Institute, University of Utah, SLC, UT, USA.
Insights
Acute myocardial ischemia significantly slows heart electrical conduction speed. This study reveals a strong temporal link between ischemia severity and conduction slowing, with complex spatial patterns observed.
Area of Science:
- Cardiology
- Electrophysiology
- Medical Imaging
Background:
- Acute myocardial ischemia disrupts normal cardiac electrical activation.
- Previous studies lacked volumetric data on activation changes due to sampling limitations.
Purpose of the Study:
- To investigate the volumetric changes in myocardial conduction speed (CS) during acute myocardial ischemia.
- To analyze the spatial and temporal correlations between ischemic severity and CS.
- To explore the relationship between ST-segment changes and CS slowing.
Main Methods:
- Utilized a large-animal experimental model.
- Employed high-resolution volumetric mapping to measure CS.
- Assessed CS and electrocardiographic ST-segment changes across 11 controlled ischemic episodes.
Main Results:
- Ischemia induced significant conduction slowing, with a global median speed reduction of 25 cm/s.
- A high temporal correlation (r=0.93) was observed between ischemic severity and CS.
- Spatial correlations revealed complex patterns, with significant CS slowing at the periphery of ST-segment changes.
Conclusions:
- This is the first study to document volumetric CS changes during acute myocardial ischemia in an experimental model.
- Conduction speed changes are spatiotemporally correlated with ischemic severity.
- Findings illustrate a biphasic response in CS, consistent with cellular studies.
Abstract:
Acute myocardial ischemia compromises the ordered electrical activation of the heart, however, because of sampling limitations, volumetric changes in activation have not been measured. We used a large-animal experimental model and high-resolution volumetric mapping to study the effects of ischemia on conduction speeds (CS) throughout the myocardium. We estimated CS and electrocardiographic changes (ST segments) and evaluated the spatial and temporal correlations between them across 11 controlled episodes. We found that ischemia induces significant conduction slowing, reducing the global median speed by 25 cm/s. Furthermore, there was a high temporal correlation between the development of ischemic severity and CS (corr. = 0.93) through each episode. The spatial correlations between ST-segment changes and CS slowing were more spatially complex than expected with substantial slowing at the periphery of the zones that showed ST-segment changes. This is the first study that has documented in an experimental model volumetric changes of CS during acute myocardial ischemia and explored the relationships between ischemia development in space and time. We showed that conduction speed changes are spatiotemporally correlated to ischemic severity and illustrated the biphasic response long proposed from cellular studies.
