Quantifying the Spatiotemporal Influence of Acute Myocardial Ischemia on Volumetric Conduction Velocity

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.

Which bidomain conductivity is the most important for modelling heart and torso surface potentials during ischaemia?

“…In this work, we use a model of partial thickness ischaemia, rather than subendocardial ischaemia; that is, we consider ischaemia that begins partway through the ventricular wall. This is in accord with recent experimental work [25,26] that found that, in the acute early phase, ischaemia develops within the wall and does not often begin at the endocardium. The bi-ventricular heart is then placed within a torso so that potentials can be calculated on both the epicardial and torso surfaces.…”

Electrophysiological Changes of Human-Induced Pluripotent Stem Cell-Derived Cardiomyocytes during Acute Hypoxia and Reoxygenation

“…FPP time was observed to decrease significantly during hypoxia, whereas reoxygenation improved the propagation although it did not recover to the baseline level. Decrease in electrical conduction and formation of conduction blocks in cardiac tissue is a well-known effect of ischemia and responsible for its part in generating arrhythmias, as orderly propagation of the depolarization wavefront is important in healthy cardiac contraction [37][38][39]. Slowing of cardiac conduction velocity is thought to be due to, e.g., changes in cellto-cell coupling via connexin 43, but not all mechanisms are fully understood [38].…”

Non-invasive estimation of QLV from the standard 12-lead ECG in patients with left bundle branch block

“…The total activation duration for each constructed sequence is matched to the QRS duration by adapting the overall used propagation velocity. The used propagation velocity is maintained within the physiological range of the myocardial velocity, i.e., between 0.6 and 0.85 m/s ( Roberts et al, 1979 ; Spach and Kootsey, 1983 ; Kléber and Rudy, 2004 ; Cantwell et al, 2015 ; Good et al, 2020 ).…”