Computer based modeling of the congenital long-QT 2 syndrome in the Visible Man torso: From genes to ECG

The congenital long-QT syndrome is commonly associated with a high risk for polymorphic ventricular tachycardia and sudden cardiac death. This is probably due to an intensification of the intrinsic heterogeneities present in ventricular myocardium. Increasing the electrophysiological heterogeneities amplifies the dispersion of repolarization which directly affects the morphology of the T wave in the ECG. The aim of this work is to investigate the effects of LQT2, a specific subtype of the long-QT syndrome (LQTS), on the Body Surface Potential Maps (BSPM) and the ECG. In this context a three-dimensional, heterogeneous model of the human ventricles is used to simulate both physiological and pathological excitation propagation. The results are used as input for the forward calculation of the BSPM and ECG. Characteristic QT prolongation is simulated correctly. The main goal of this study is to prepare and evaluate a simulation environment that can be used prospectively to find features in the ECG or the BSPM that are characteristic for the LQTS. Such features might be used to facilitate the identification of LQTS patients.

[1]  Gergely Szabo,et al.  Apico-basal inhomogeneity in distribution of ion channels in canine and human ventricular myocardium. , 2005, Cardiovascular research.

[2]  K.H.W.J. ten Tusscher,et al.  Comments on 'A model for human ventricular tissue' : reply , 2005 .

[3]  Y. Rudy,et al.  Ionic Current Basis of Electrocardiographic Waveforms: A Model Study , 2002, Circulation research.

[4]  Dd. Streeter,et al.  Gross morphology and fiber geometry of the heart , 1979 .

[5]  David B. Geselowitz,et al.  On the theory of the electrocardiogram , 1989, Proc. IEEE.

[6]  P. Schwartz,et al.  Quantitative analysis of T wave abnormalities and their prognostic implications in the idiopathic long QT syndrome. , 1994, Journal of the American College of Cardiology.

[7]  C. Antzelevitch Heterogeneity of cellular repolarization in LQTS: the role of M cells , 2001 .

[8]  Olaf Dössel,et al.  Conditions for Equal Polarity of R and T Wave in Heterogeneous Human Ventricular Tissue , 2004 .

[9]  H. Wellens,et al.  Repolarizing K+ currents ITO1 and IKs are larger in right than left canine ventricular midmyocardium. , 1999, Circulation.

[10]  R. W. Lau,et al.  The dielectric properties of biological tissues: II. Measurements in the frequency range 10 Hz to 20 GHz. , 1996, Physics in medicine and biology.

[11]  Gan-XinYan,et al.  Cellular Basis for the Normal T Wave and the Electrocardiographic Manifestations of the Long-QT Syndrome , 1998 .

[12]  O. Dossel,et al.  Modeling human ventricular geometry and fiber orientation based on diffusion tensor MRI , 2006, 2006 Computers in Cardiology.

[13]  CharlesAntzelevitch,et al.  Sodium Channel Block With Mexiletine Is Effective in Reducing Dispersion of Repolarization and Preventing Torsade de Pointes in LQT2 and LQT3 Models of the Long-QT Syndrome , 1997 .

[14]  Y Rudy,et al.  Cellular arrhythmogenic effects of congenital and acquired long-QT syndrome in the heterogeneous myocardium. , 2000, Circulation.