Computational analysis of the electromechanical consequences of short QT syndrome.

Christopher L.-H Huang

doi:10.3389/fphys.2015.00044

Abstract

Computational analysis of the electromechanical consequences of short QT syndrome.

Highlights

Exceptional scientific work inquires into new areas or utilizes techniques circumventing existing limitations to study
Adeniran et al (2011, 2012) had introduced a first paradigm shift complementing relatively sparse available experimental data through computational explorations of the electrophysiological basis for arrhythmia in short QT syndrome (SQTS). They used Markov and/or Hodgkin-Huxley formulations developed from experimental data obtained from expression systems modeling N588KhERG and D172N-Kir2.1 mutations to replicate SQT1 and SQT3
Previous studies modeling arrhythmogenesis in SQTS had not extended to considering mechanical properties

Summary

Introduction

Exceptional scientific work inquires into new areas or utilizes techniques circumventing existing limitations to study. Classical physiological analysis demonstrated that K+ channel openers increase transmural repolarization dispersion and shorten ventricular effective refractory period potentially producing arrhythmogenic substrate in left ventricular wedge preparations (Patel and Antzelevitch, 2008). Adeniran et al (2011, 2012) had introduced a first paradigm shift complementing relatively sparse available experimental data through computational explorations of the electrophysiological basis for arrhythmia in SQTS.

Results

Conclusion