Multi-scale modeling of excitation-contraction coupling in the normal and failing heart
- PMID: 19963818
- PMCID: PMC2896048
- DOI: 10.1109/IEMBS.2009.5332708
Multi-scale modeling of excitation-contraction coupling in the normal and failing heart
Abstract
Here we describe new computational models of cardiac electromechanics starting from the cellular scale and building to the tissue, organ and system scales. We summarize application to human genetic diseases (LQT1 and LQT3) and to modeling of congestive heart failure.
Figures
References
-
- Flaim SN, Giles WR, McCulloch AD. Contributions of sustained INa and IKv4.3 to transmural heterogeneity of early repolarization and arrhythmogenesis in canine left ventricular myocytes. Am. J. Physiol. Heart Circ. Physiol. 2006;291(6):H2617–29. - PubMed
-
- Saucerman JJ, Healy SN, Belik ME, Puglisi JL, McCulloch AD. Proarrhythmic consequences of a KCNQ1 AKAP-binding domain mutation: computational models of whole cells and heterogeneous tissue. Circ. Res. 2004;95:1216–1224. - PubMed
-
- Flaim SN, Giles WR, McCulloch AD. Arrhythmogenic consequences of Na+ channel mutations in the transmurally heterogeneous mammalian left ventricle: analysis of the I1768V SCN5A mutation. Heart Rhythm. 2007;4(6):768–78. - PubMed
-
- Flaim SN, McCulloch AD. Acetylcholine-induced shortening of the epicardial action potential duration may increase repolarization gradients and LQT3 arrhythmic risk. J. Electrocardiol. 2007;40:S66–9. - PubMed
Publication types
MeSH terms
Grants and funding
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical