Modelling Cardiac Stretch-Induced Arrhythmogenesis
Catherine
Lloyd
Bioengineering Institute, University of Auckland
Model Status
This is the original unchecked version of the model imported from the previous
CellML model repository, 24-Jan-2006.
Model Structure
Cardiac mechanoelectric coupling (that is, the influence of mechanical activity on the electrical state of the heart) has been well documented. It has been suggested that hearts that have been mechanically compromised by congestive heart failure display an increased prevalence of arrhythmia. In addition, in vitro studies have shown that sudden cardiac tissue stretch can stimulate arrhythmias. One hypothesised mechanism for the stretch sensitivity of cardiac muscle is the presence of stretch-activated channels (SACs).
In their 1998 study, Riemer et al. investigate the potential role of SACs in excitability and arrhythmogenesis. To do this they added a linear, time-independent, stretch-sensitive current to the Luo-Rudy membrane model for guinea pig ventricular myocytes (see Luo-Rudy I model and Zeng et al. 1995 model for more details, and also see the figure below). Model simulations showed that increased stretch conductance led to resting potential depolarisation, a decreased excitation threshold, altered action potential duration, and, under certain conditions, early afterdepolarisations. From these results Riemer et al. concluded that stretch increases cellular excitability, making the heart prone to ectopic activity. Regional effects of stretch on action potential are influenced by factors such as the SAC reversal potential, ionic conditions and baseline refractoriness throughout the heart and therefore an increased risk of arrhythmia.
The complete original paper reference is cited below:
Stretch-induced changes in arrhythmogenesis and excitability in experimentally based heart cell models, Tara L. Riemer, Eric A. Sobie, and Leslie Tung, 1998,
American Journal of Physiology
, 275, H431-H442. (Full text and PDF versions of the article are available for journal members on the American Journal of Physiology website.) PubMed ID: 9683430
cell diagram
A schematic diagram describing the ionic components of the Riemer et al. 1998 mathematical model of a guinea pig ventricular myocyte. The model is based on the Luo-Rudy dynamic model, with an added stretch-activated channel (SAC).
excitation-contraction coupling
ventricular myocyte
arrhythmia
mechanoelectric coupling
calcium dynamics
Ventricular Myocyte
electrophysiology
myofilament mechanics
cardiac
9683430
Eric
Sobie
A
2003-04-05
keyword
c.lloyd@auckland.ac.nz
2003-01-02
The University of Auckland
The Bioengineering Institute
1998-08
Stretch-induced changes in arrhythmogenesis and excitability in
experimentally based heart cell models
275
H431
H442
Catherine
Lloyd
May
Riemer et al's 1998 mathematical model of stretch-induced changes in
arrhythmogenesis and excitability in guinea pig ventricular myocytes.
This model is based on the the Luo-Rudy I model, 1991.
Ventricular Myocyte
Mammalia
Autumn
Cuellar
A
This is the CellML description of Riemer et al's 1998 mathematical
model of stretch-induced changes in arrhythmogenesis and excitability
in guinea pig ventricular myocytes. This model is based on the the
Luo-Rudy I model, 1991.
Tara
Riemer
L
Catherine Lloyd
Catherine
Lloyd
May
Leslie
Tung
Corrected equations: alpha_h in fast_sodium_current_h_gate. Added non-specific currents.
2003-07-30
The University of Auckland, The Bioengineering Institute
Changed the model name so the model loads in the database easier.
American Journal of Physiology