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Stretch-induced changes in arrhythmogenesis and excitability in experimentally based heart cell models
T L Riemer1, E A Sobie, L Tung
1Department of Biomedical Engineering, Johns Hopkins University, Baltimore, Maryland 21205, USA.
The American Journal of Physiology
|July 31, 1998
Summary
Cardiac stretch-activated channels (SACs) increase cellular excitability, raising arrhythmia risk. Modeling shows SACs alter resting potential and action potentials, potentially causing ectopic beats and increased refractoriness dispersion.
Area of Science:
- Cardiovascular Physiology
- Computational Biology
- Cardiac Electrophysiology
Background:
- Mechanoelectric coupling in the heart is linked to arrhythmia.
- Stretch-activated channels (SACs) are hypothesized to mediate cardiac stretch sensitivity.
Purpose of the Study:
- To model the influence of SACs on cardiac electrophysiology.
- To investigate the role of SACs in arrhythmia mechanisms.
Main Methods:
- Incorporated a putative SAC model into guinea pig and frog ventricular membrane models.
- Simulated SACs as linear, time-independent conductances with specific reversal potentials (-20 or -50 mV).
Main Results:
- Increased SAC conductance caused resting potential depolarization and decreased excitation threshold.
- Altered action potential duration and induced early afterdepolarizations under certain conditions.
- Demonstrated that SACs increase cellular excitability and can lead to ectopic activity.
Conclusions:
- Cardiac stretch increases excitability via SACs, promoting arrhythmia.
- SACs contribute to increased dispersion of refractoriness, elevating arrhythmia risk.
- Regional variations in SAC effects depend on reversal potential, ionic conditions, and baseline currents.