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1 Nora Eccles Harrison CVRTI, University of Utah, Salt Lake City, Utah, United States
2 Nora Eccles Harrison CVRTI, University of Utah, Salt Lake City, Utah, United States; Bioengineering, University of Utah, Salt Lake City, Utah, United States
3 Dipartimento di Biologia Evolutiva e Funzionale, Universita di Parma, Parma, Italy
4 Bioengineering, University of Utah, Salt Lake City, Utah, United States; Nora Eccles Harrison CVRTI, University of Utah, Salt Lake City, Utah, United States; SCI, University of Utah, Salt Lake City, Utah, United States
5 Nora Eccles Harrison CVRTI, University of Utah, Salt Lake City , Utah, United States
* To whom correspondence should be addressed. E-mail: punske{at}cvrti.utah.edu.
Published studies show that ventricular pacing in canine hearts produces three distinct patterns of epicardial excitation: elliptical isochrones near an epicardial pacing site, with asymmetrical bulges; areas with high propagation velocity, up to 2 or 3 m/s and numerous breakthrough sites; lower velocity areas (< 1 m/s) where excitation moves across the epicardial projection of the septum. With increasing pacing depth the magnitude of epicardial potential maxima becomes asymmetrical. The electrophysiological mechanisms that generate the distinct patterns have not been fully elucidated. In this study we investigated those mechanisms experimentally. Under pentobarbital anesthesia epicardial and intramural excitation isochrone and potential maps have been recorded from 22 exposed or isolated dog hearts, by means of epicardial electrode arrays and transmural plunge electrodes. In 5 experiments, a ventricular cavity was perfused with diluted Lugol solution. Results: The epicardial bulges result from electrotonic attraction from the helically shaped subepicardial portions of the wave front. The high velocity patterns and the associated multiple breakthroughs are due to involvement of the Purkinje network. The low velocity at the septum crossing is due to the missing Purkinje involvement in that area. The asymmetric magnitude of the epicardial potential maxima and the shift of the breakthrough sites provoked by deep stimulation are a consequence of the epi-endocardial obliqueness of the intramural fibers. These results improve our understanding of intramural and epicardial propagation during PVCs and paced beats. This can be useful for interpreting epicardial maps recorded at surgery or inversely computed from body surface ECGs.
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