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Biomechanics of Cardiac Electromechanical Coupling and Mechanoelectric Feedback
Open accessAbstract
Cardiac mechanical contraction is triggered by electrical activation via an intracellular calcium-dependent process known as excitation–contraction coupling. Dysregulation of cardiac myocyte intracellular calcium handling is a common feature of heart failure. At the organ scale, electrical dyssynchrony leads to mechanical alterations and exacerbates pump dysfunction in heart failure. A reverse coupling between cardiac mechanics and electrophysiology is also well established. It is commonly referred as cardiac mechanoelectric feedback and thought to be an important contributor to the increased risk of arrhythmia during pathological conditions that alter regional cardiac wall mechanics, including heart failure. At the cellular scale, most investigations of myocyte mechanoelectric feedback have focused on the roles of stretch-activated ion channels, though mechanisms that are independent of ionic currents have also been described. Here we review excitation–contraction coupling and mechanoelectric feedback at the cellular and organ scales, and we identify the need for new multicellular tissue-scale model systems and experiments that can help us to obtain a better understanding of how interactions between electrophysiological and mechanical processes at the cell scale affect ventricular electromechanical interactions at the organ scale in the normal and diseased heart.
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“This process resembles the electromechanical coupling in the mammalian myocardium: cardiac mechanical contraction is triggered by electrical activation via increased cytoplasmic Ca 2+ concentration 54 .”
From Leaf-venation-directed cellular alignment for macroscale cardiac constructs with tissue-like functionalities (2023) · cites this paper as [54]
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“In plants, the leaf veins, consisting of densely packed cells and aligned fibers, allow the transmission of action potentials, which progression was characterized by the rapid propagation of local intracellular Ca 2+ concentration 53,54 .”
From Leaf-venation-directed cellular alignment for macroscale cardiac constructs with tissue-like functionalities (2023) · cites this paper as [54]
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Metadata
- Authors
- Pfeiffer, E. R., Tangney, J. R., Omens, J. H., & McCulloch, A. D.
- Affiliations
- University of California San Diego (US)
- Corresponding author
- McCulloch, Andrew D.
- Venue
- Journal of Biomechanical Engineering
- Publisher
- ASME International
- Published
- 2014-02-01
- Volume
- 136
- Issue
- 2
- Pages
- 021007-021007
- ISSN
- 0148-0731 (ISSN-L)
- 1528-8951
- PMC
- PMC4023651
- OpenAlex
- W2028446666
- Cited by
- 131
- References
- 152
- Citations by year
- 2026: 7 · 2025: 11 · 2024: 10 · 2023: 15 · 2022: 11 · 2021: 13 · 2020: 13 · 2019: 12 · 2018: 7 · 2017: 8 · 2016: 8 · 2015: 11 · 2014: 4
- FWCI
- 1.31
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Biomechanical Engineering (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01HL105242)
- National Institute of General Medical Sciences
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac pacing and defibrillation studies
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
- Keywords
- mechano-electric feedback, excitation-contraction coupling, intracellular calcium homeostasis, heart failure, electrical dyssynchrony, ventricular arrhythmias, stretch-activated channels, cardiomyocytes, ventricular mechanics
- MeSH terms
- Animals, Heart Conduction System, Humans, Models, Cardiovascular, Myocardial Contraction, Ventricular Function, Feedback, Physiological, Myocytes, Cardiac, Excitation Contraction Coupling
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