Electrical Remolding and Mechanical Changes in Heart Failure: A Model Study
We have developed a canine cardiac cellular electromechanics model to simulate electrophysiological remodeling of heart failure (HF) and predicted cardiomyocyte contractility after HF. INa.L is integrated into this model to study its role to the prolongation of action potential (AP) in control and HF conditions, which was not established well in the past. It may have a great contribution to prolongation of AP in control and even greater contribution to that of HF. Ionic remolding after HF is modeled by downregulation of Itol, Ik1,, IKs, SR pump function and upregulation of Na+-Ca2+ exchange (NCX) and Ina.L. The HF model could successfully simulate the prolonged AP, reduced ICaL, enhanced INaCa and blunted Ca2+ transient. With computed Ca2+ being the input to myofilament model, myofilament forces are determined. Compared with control, reduced amplitude, increased latency to onset of contraction, increased time to peak (TTP) and attenuated cell shortening are found in HF model. The model could also be embedded into tissue electromechanics model to simulate the altered activation sequence and mechanical function.
Yunliang Zang Ling Xia
Department of Biomedical Engineering, Zhejiang University, Hangzhou 310027, China
国际会议
无锡
英文
421-429
2010-09-17（万方平台首次上网日期，不代表论文的发表时间）