TY - GEN
T1 - Modeling transport of interstitial potassium in regional myocardial ischemia
T2 - 29th Annual International Conference of IEEE-EMBS, Engineering in Medicine and Biology Society, EMBC'07
AU - Potse, Mark
AU - Coronel, Ruben
AU - LeBlanc, A. Robert
AU - Vinet, Alain
PY - 2007
Y1 - 2007
N2 - Myocardial ischemia leads to an efflux of potassium ions from affected cells. The resulting depolarization of the resting membrane is one of the main features of ischemic myocardium. It has been shown experimentally that a part of the surplus interstitial potassium is transported out of the ischemic zone, even if no coronary blood flow is present in the affected area. We propose to model this transport mechanism mathematically with a diffusion equation. This model explains the measured spatial profiles of extracellular potential and potassium concentration. In addition, it allows a quantitative prediction of the transmembrane current that flows as a result of ischemia-induced depolarization. This current is thought to play a role in arrhythmogenicity, which is an important cause of mortality in acute myocardial infarction. Our model predicts that this current reaches its maximum exactly on the border of the hypoxic area. An important depolarizing current would be present just within the border, where hypoxia is accompanied by a resting membrane potential that is only slightly elevated, due to coupling with the adjacent normal tissue. Still, in the presence of potassium transport the predicted current density is not large enough to explain ectopic activation on the lateral border of the ischemia. This suggests that activation is more likely to occur at the endocardium, where the potassium gradient is steeper.
AB - Myocardial ischemia leads to an efflux of potassium ions from affected cells. The resulting depolarization of the resting membrane is one of the main features of ischemic myocardium. It has been shown experimentally that a part of the surplus interstitial potassium is transported out of the ischemic zone, even if no coronary blood flow is present in the affected area. We propose to model this transport mechanism mathematically with a diffusion equation. This model explains the measured spatial profiles of extracellular potential and potassium concentration. In addition, it allows a quantitative prediction of the transmembrane current that flows as a result of ischemia-induced depolarization. This current is thought to play a role in arrhythmogenicity, which is an important cause of mortality in acute myocardial infarction. Our model predicts that this current reaches its maximum exactly on the border of the hypoxic area. An important depolarizing current would be present just within the border, where hypoxia is accompanied by a resting membrane potential that is only slightly elevated, due to coupling with the adjacent normal tissue. Still, in the presence of potassium transport the predicted current density is not large enough to explain ectopic activation on the lateral border of the ischemia. This suggests that activation is more likely to occur at the endocardium, where the potassium gradient is steeper.
UR - http://www.scopus.com/inward/record.url?scp=57649193095&partnerID=8YFLogxK
U2 - https://doi.org/10.1109/IEMBS.2007.4353803
DO - https://doi.org/10.1109/IEMBS.2007.4353803
M3 - Conference contribution
C2 - 18003469
SN - 1424407885
SN - 9781424407880
VL - 2007
T3 - Annual International Conference of the IEEE Engineering in Medicine and Biology - Proceedings
SP - 6331
EP - 6334
BT - 29th Annual International Conference of IEEE-EMBS, Engineering in Medicine and Biology Society, EMBC'07
Y2 - 23 August 2007 through 26 August 2007
ER -