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Conduction Block in the Human Ischemic Myocardium: Insights from a 1D Electromechanical Model
Alexander Kursanov1,2, Nathalie A Balakina-Vikulova1, Olga Solovyova1,2
1Laboratory of Mathematical Physiology, Institute of Immunology and Physiology, Ural Branch of the Russian Academy of Sciences, 620049 Ekaterinburg, Russia.
International Journal of Molecular Sciences
|July 28, 2026
Summary
Acute myocardial ischemia impairs heart function by reducing sodium current, leading to conduction block. Reduced gap junction function may prevent or transiently block electrical signal propagation.
Area of Science:
- Cardiovascular Physiology
- Computational Biology
- Electrophysiology
Background:
- Acute myocardial ischemia disrupts coronary blood flow, causing significant electrophysiological and mechanical dysfunction in cardiomyocytes.
- Electrophysiological alterations include changes in action potential morphology and impaired electrotonic coupling.
- Mechanical dysfunction manifests as reduced contractile force and discoordination.
Purpose of the Study:
- To investigate the effects of acute ischemia on the electromechanical activity of human cardiomyocytes and myocardial tissue using multi-scale mathematical modeling.
- To identify conditions for conduction block initiation and restoration in ischemic myocardial tissue.
- To analyze the underlying mechanisms of these phenomena.
Main Methods:
- Multi-scale mathematical modeling of a single human cardiomyocyte and a one-dimensional myocardial tissue.
- Simulation of acute ischemia conditions.
- Analysis of electrophysiological parameters, including fast sodium current (iNa) and gap junction conductance.
Main Results:
- Conduction slowing and block in ischemic tissue are primarily caused by hyperkalemia-induced reduction in the fast sodium current (iNa).
- This iNa reduction is amplified by direct electromechanical coupling and mechano-electric/mechano-calcium feedback.
- Under simulated 15 min ischemia, iNa reduction leads to conduction block, amplified by mechano-calcium feedback.
Conclusions:
- Reduced fast sodium current (iNa) is a key mechanism for conduction block during acute myocardial ischemia.
- Mechano-calcium feedback exacerbates iNa reduction and conduction block.
- Moderate reduction in gap junction conductance may act as a compensatory mechanism, converting persistent conduction block to transient block or preventing it.
