The DOI matches its Crossref record; 45 of the 45 references it cites were found in a registry or an index.
Microfibrosis Produces Electrical Load Variations Due to Loss of Side‐to‐Side Cell Connections; A Major Mechanism of Structural Heart Disease Arrhythmias
Abstract
The purpose of this article is to demonstrate how adaptive changes in myocardial microstructure provide mechanisms for emergent new conduction disturbances that initiate reentrant arrhythmias. The mechanisms are based on discontinuous conduction phenomena produced by increases in cellular hading; these increases result from changes in the normal distribution of the gap junctions. Recent studies indicate that at a microscopic level propagation in normal mature cardiac muscle is stochastic. For example, the nonuniform and irregular distribution of the gap junctions in such normal muscle produces load variations that are associated with changes in V max inside individual cells during both longitudinal and transverse propagation. The stochastic nature of normal propagation at a microscopic level offers considerable protection against arrhythmias by reestablishing the general trend of wavefront movement after small variations in excitation events occur. If such microscopic diversity is decreased, large fluctuations in load develop that are distributed over more cells than usual. The decrease in diversity may be caused by loss of side‐to‐side coupling between fibers, which produces relatively isolated groups of cells with microfibrosis. With loss of side‐to‐side fiber coupling, the myocardial architecture may fail to reestablish a smoothed wavefront at the macroscopic level. Spatial nonuniformities of electrical loading then give rise to conduction block and reentry.
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Citations
Cites
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Self-citationSlow conduction in the infarcted human heart. 'Zigzag' course of activation.
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Self-citationCollagen Network of the Myocardium: Function, Structural Remodeling and Regulatory Mechanisms
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Electrical constants of trabecular muscle from mammalian heart
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Cited by
Calkins, H., Hindricks, G., Cappato, R., Kim, Y.-H., Saad, E. B., Aguinaga, L., Akar, J. G., Badhwar, V., Brugada, J., Camm, J., et al. (2017) · Heart Rhythm · doi:10.1016/j.hrthm.2017.05.012 · Cited by 2,755
Cardiac Fibrosis: The Fibroblast Awakens
Travers, J. G., Kamal, F. A., Robbins, J., Yutzey, K. E., & Blaxall, B. C. (2016) · Circulation Research · doi:10.1161/circresaha.115.306565 · Cited by 1,596
Fibrosis–a common pathway to organ injury and failure
Rockey, D. C., Bell, P. D., & Hill, J. A. (2015) · New England Journal of Medicine · doi:10.1056/nejmra1300575 · Cited by 1,428
Pathophysiological mechanisms of atrial fibrillation: a translational appraisal
Schotten, U., Verheule, S., Kirchhof, P., & Goette, A. (2011) · Physiological Reviews · doi:10.1152/physrev.00031.2009 · Cited by 1,273
Oakes, R. S., Badger, T. J., Kholmovski, E. G., Akoum, N., Burgon, N. S., Fish, E. N., Blauer, J. J. E., Rao, S. N., DiBella, E. V. R., Segerson, N. M., et al. (2009) · Circulation · doi:10.1161/circulationaha.108.811877 · Cited by 1,123
Metadata
- Authors
- SPACH, M. S., & BOINEAU, J. P.
- Venue
- Pacing and Clinical Electrophysiology
- Publisher
- Wiley
- Published
- 1997-02
- Volume
- 20
- Issue
- 2
- Pages
- 397-413
- ISSN
- 0147-8389 (ISSN-L)
- 1540-8159
- OpenAlex
- W2074992357
- Cited by
- 329
- References
- 45
- FWCI
- 2.79
- Type
- journal article
- Language
- en
- Open access
- closed
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- CoChat. (2026). Citation check: Microfibrosis Produces Electrical Load Variations Due to Loss of Side‐to‐Side Cell Connections; A Major Mechanism of Structural Heart Disease Arrhythmias. https://app.cochat.ai/papers/10.1111/j.1540-8159.1997.tb06199.x
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- SPACH, M. S., & BOINEAU, J. P. (1997). Microfibrosis Produces Electrical Load Variations Due to Loss of Side‐to‐Side Cell Connections; A Major Mechanism of Structural Heart Disease Arrhythmias. Pacing and Clinical Electrophysiology. https://doi.org/10.1111/j.1540-8159.1997.tb06199.x
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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