Discriminating Long-QT Syndromes 1, 2 and 3 in Simulated Body Surface Potential Maps

Regional heterogeneity of electrophysiological properties within the human ventricular wall is based on changes in ion channel kinetics and densities. This leads to a dispersion of repolari- zation, which causes the positive T-wave in the ECG. Due to genetic defects, diseases, or drugs, which causes e.g. Long-QT syndrome, the physiological heterogeneous properties get out of tune.

The Long-QT Syndrome (LQTS) is characterized by changes in the morphology of the elec- trocardiogram (ECG). The QT-interval is always prolonged and the T-wave is broadened in some cases. The most common LQTS subtypes are LQT1, LQT2, and LQT3, where the slow- delayed rectifier potassium current IKs, the fast-delayed rectifier potassium current IKr, and the fast sodium current INa, were altered due to genetic defects.

The aim of this work is to investigate the effects of the LQTS on the body surface potentials in a realistic model of human anatomy and electrophysiology. An anisotropic, three- dimensional, heterogeneous model is used, which incorporates an electrophysiological model describing complex ionic processes and a monodomain excitation model. LQT1, LQT2, and LQT3 should be integrated in this model based on measurement data using an optimization framework in order to minimize the differences between measured and simulated ion channel data. Finally, the potentials on the body surface should be simulated in order to find specific electrodes in which the different LQT mutations show maximal differences and can thus be differentiated.