Development of 3‐D Intramural and Surface Potentials in the LV: Microstructural Basis of Preferential Transmural Conduction

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Excerpt

The extracellular potentials (ECPs) on epicardial and endocardial surfaces of the cardiac chambers provide information on local activation timing and can also be used to detect changes in regional electrical behavior due, for instance, to ischemia and infarction.1 In the clinical setting, intracardiac electrode arrays are widely used to map reentrant electrical circuits in the heart.3 However, ECPs are affected by cardiac anatomy and tissue structure, and are integrated across relatively large volumes. As a result, the extent to which unique information about electrical events that originate deep within the LV wall can be extracted from surface recordings remains contentious.
These issues have been addressed extensively by electrophysiologists, bioengineers and biophysicists. LV epicardial potentials have been mapped with dense electrode plaques during intramural stimulation.5 Corresponding potentials throughout the LV wall have been predicted using computer activation models that incorporate detailed information on LV surface geometry and transmural myofiber orientation, assuming that myocardial electrical properties are axially anisotropic (isotropic transverse to the myofiber direction).7 While these models capture some features of epicardial activation, they have not been validated by comparing predicted and observed intramural potential distributions. Studies in which intramural potentials generated by passive current injection12 and the 3‐D spread of electrical activation13 have been mapped at high density within the LV wall demonstrate that the electrical properties of LV myocardium are fully orthotropic rather than axially anisotropic reflecting the laminar architecture of LV myocardium.
Laminar ventricular structure has been confirmed using various 3‐D imaging modalities.14 We have argued that ventricular laminar structure has limited impact on the spread of electrical activity in normal sinus rhythm and acts to increase the safety of electrical propagation in the normal heart. On the other hand, we have proposed that slow propagation normal to layers following ectopic intramural activation may give rise to QRS broadening and also contribute to a substrate for reentry, particularly in the presence of structural heart disease.15 We hypothesize that these material properties will (i) give rise to preferred transmural directions of potential spread during activation and (ii) impact the associated potentials measured on epicardial and endocardial surfaces.
In this study, we have recorded ECPs generated by intramural point stimulation in the LV with a high density 3‐D electrode array. MRI and extended volume imaging have been used to measure the spatial locations of electrodes and characterize tissue architecture (myofiber and myolaminar orientations) throughout the recording volume. This has enabled us for the first time to reconstruct intramural potentials throughout activation accurately in 3‐D and relate them directly to tissue structure. Passive and actively generated intramural potentials both spread in preferred transmural directions, confirming that ventricular myocardium has different conductivities associated with three microstructurally defined axes. Moreover, while epicardial surface potentials reflect initial electrical events at the stimulus location, endocardial potentials do not, particularly adjacent to papillary muscles. Structurally detailed computer models were used to interpret our experimental data. Intramural potentials are better captured by models that incorporate fully orthotropic rather than axially anisotropic electrical properties, but these models failed to reproduce key features of the spatiotemporal development of intramural potentials during activation.
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