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Circulation: Arrhythmia and Electrophysiology
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Circulation: Arrhythmia and Electrophysiology. 2009;2:433-440
Published online before print June 18, 2009, doi: 10.1161/CIRCEP.108.830133
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Original Articles

Three Distinct Directions of Intramural Activation Reveal Nonuniform Side-to-Side Electrical Coupling of Ventricular Myocytes

Bryan J. Caldwell, PhD; Mark L. Trew, PhD; Gregory B. Sands, PhD; Darren A. Hooks, MBChB, PhD; Ian J. LeGrice, MBChB, PhD and Bruce H. Smaill, PhD

From the Auckland Bioengineering Institute (B.J.C., M.L.T., G.B.S., D.A.H., I.J.L., B.H.S.) and the Department of Physiology (I.J.L., B.H.S.), Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand.

Correspondence to Bruce H. Smaill, PhD, Auckland Bioengineering Institute, University of Auckland, Private Bag 92019, Auckland 1001, New Zealand. E-mail b.smaill{at}auckland.ac.nz

Received October 19, 2008; accepted June 8, 2009.

Background— The anisotropy of cardiac tissue is a key determinant of 3D electric propagation and the stability of activation wave fronts in the heart. The electric properties of ventricular myocardium are widely assumed to be axially anisotropic, with activation propagating most rapidly in the myofiber direction and at uniform velocity transverse to this. We present new experimental evidence that contradicts this view.

Methods and Results— For the first time, high-density intramural electric mapping (325 electrodes at {approx}4x4x1-mm spacing) from pig left ventricular tissue was used to reconstruct 3D paced activation surfaces projected directly onto 3D tissue structure imaged throughout the same left ventricular volume. These data from 5 hearts demonstrate that ventricular tissue is electrically orthotropic with 3 distinct propagation directions that coincide with local microstructural axes defined by the laminar arrangement of ventricular myocytes. The maximum conduction velocity of 0.67±0.019 ms–1 was aligned with the myofiber axis. However, transverse to this, the maximum conduction velocity was 0.30±0.010 ms–1, parallel to the myocyte layers and 0.17±0.004 ms–1 normal to them. These orthotropic conduction velocities give rise to preferential activation pathways across the left ventricular free wall that are not captured by structurally detailed computer models, which incorporate axially anisotropic electric properties.

Conclusions— Our findings suggest that current views on uniform side-to-side electric coupling in the heart need to be revised. In particular, nonuniform laminar myocardial architecture and associated electric orthotropy should be included in future models of initiation and maintenance of ventricular arrhythmia.

Key Words: anisotropy • mapping • structure • computer modeling • intramural pacing


 

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