Abstract
Changes in action potentials of atrial myocytes and various ionic channels induced by chronic atrial fibrillation (AF) have been described in the human. The mechanisms underlying the AF-induced action potential duration (APD) shortening have not been clearly identified. In this study we modify two different computational models of electrical activity of human atrial myocytes by incorporating chronic AF induced changes in several of the ionic channels systems found in myocytes. We examine the ionic mechanisms underlying the AF induced APD reduction and the relative roles of different remodeled ionic channels in producing the APD reduction. In both models we have found that AF induced changes in the ionic channel conductances and kinetics are able to reproduce the APD reduction seen experimentally. AF-induced down regulation of L-type Ca current is insufficient to account for the observed APD reduction, but up regulation of IKl has a much greater influence.
| Original language | English |
|---|---|
| Title of host publication | Computers in Cardiology, 2003 |
| Editors | Alan Murray |
| Place of Publication | Piscataway, NJ |
| Publisher | IEEE |
| Pages | 777-780 |
| Number of pages | 4 |
| Volume | 30 |
| ISBN (Print) | 078038170X |
| DOIs | |
| Publication status | Published - Sep 2003 |
| Event | Computers in Cardiology - Thessaloniki, Greece Duration: 21 Sep 2003 → 24 Sep 2003 Conference number: 30 |
Conference
| Conference | Computers in Cardiology |
|---|---|
| Abbreviated title | CinC |
| Country/Territory | Greece |
| City | Thessaloniki |
| Period | 21/09/03 → 24/09/03 |
Keywords
- Bioelectric potentials
- Biomembrane transport
- Calcium
- Cardiology
- Cellular biophysics
- Physiological models