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(Circulation Research. 1999;84:153-156.)
© 1999 American Heart Association, Inc.

Original Contribution

A Novel Mechanism of Anode-Break Stimulation Predicted by Bidomain Modeling

Ravi Ranjan, Gordon F. Tomaselli, Eduardo Marbán

From the Department of Biomedical Engineering (R.R.) and the Section of Molecular and Cellular Cardiology (G.F.T., E.M.), Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Md. The current address for Dr Ranjan is Health Sciences and Technology, Harvard Medical School, Boston, MA 02115.

Correspondence to Eduardo Marbán, MD, PhD, Section of Molecular and Cellular Cardiology, 844 Ross Bldg, Johns Hopkins University School of Medicine, 720 Rutland Ave, Baltimore, MD 21205. E-mail marban{at}welchlink.welch.jhu.edu

Abstract—Anodal stimulation by external pacemakers has been explained on the basis of bidomain models of cardiac tissue. Bidomain models predict that anodal stimuli will hyperpolarize the underlying tissue while adjacent regions become depolarized (virtual cathodes), initiating excitation. We investigated the contribution of active cellular properties to anode-break stimulation. A bidomain model was implemented in which each cell contained realistic ionic currents, including those recruited by hyperpolarization. Simulations reveal that anode-break excitation can originate at the site of stimulation itself and not only from adjacent regions of induced depolarization. The threshold for initiating excitation at the site of stimulation is lower than that for stimulation initiating from adjacent depolarized regions. Thus, incorporation of active cellular properties into a bidomain model predicts a novel mechanism for anode-break stimulation of the heart. The results will improve our understanding of anodal pacing and its risks and benefits in patients.

Key Words: pacemaker • excitation • quantitative modeling • anisotropy

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