| Zugriffsnummer | 25142 |
| Dokumenttyp | Konferenzartikel |
| Sprache | Englisch |
| Titel | Electrical excitation of the human heart and the effect of contraction |
| Autor(in); Institution |
Fruhner, Stefan; 8.4, Mathematische Modellierung und Datenanalyse, PTB-Berlin
Engel, Harald; TU, Institut für Theoretische Physik, Berlin, GERMANY
Bär, Markus; 8.4, Mathematische Modellierung und Datenanalyse, PTB-Berlin
|
| Quelle/Jahr | Proceedings of the 6th ESGCO 2010:(2010), 4 S. |
| Availability | [CD-ROM] |
| Verlag | Berlin: |
| Konferenzangaben | ESGCO 2010: 6th Conference of the European Study Group on Cardiovascular Oscillations, Berlin, 12-14, April, 2010, Germany |
| Freie Schlagworte | Finite element simulation ; electrocardiogram ; ECG ; contrtaction ; excitation ; ionic models |
| Zusammenfassung | In simulations realistic heart models often include detailed physiological knowledge about ionic dynamics of cardiac cells and accurately account for anatomical details like fibre orientation or heterogeneity of heart tissue. Additionally describing the feedback between propagating waves of electric activity and cardiac contraction might be essential for a deeper understanding of the mechanism of cardiac arrhythmias like tachycardia and fibrillation. Using magnetic resonance images two-dimensional finiteelement meshes have been generated in order to perform simulations of waves of electrical activity propagating in a beating human heart. Different cellular models have been applied to analyze the differences in the effect of motion, e.g. the excitation speed or the time that it takes until a certain region in the heart de- or repolarizes after an excitation was initiated. We compare static with dynamic simulations to access the impact of the heart’s motion on electrical propagation. Important features of the ECG change substantially if dynamic geometries are used. The approach also offers the opportunity to calculate the mechanical stresses during cardiac contraction from experimental data without using detailed models on calcium dynamics and stress-activated channels in cardiac myocytes. |