A Simulation Study on Electrical Activity of Ventricular Endocardial Tissue due to SCN5A L812Q Mutation.

Brugada Syndrome is a rare arrhythmia, hereditary in nature. It is caused due to mutation in genes that encodes sodium ion channels and it results sudden cardiac death in young adults. This paper aims to model a two dimensional SCN5A L812Q mutated endocardial tissue by modifying the model equations for sodium ion channel in the Ten Tusscher model for human ventricular tissue. Results show that the propagation of electrical activity in the mutated cells is slower when compared to the normal cells of the endocardial tissue. From this it is concluded that there is a large reduction of sodium current in the mutated region of the endocardial tissue. This leads to reduction in the total ionic current as well and further reduces the membrane potential. It also leads to the slower propagation of action potential in the mutated region when compared to the normal endocardial tissue.Clinical Relevance- This establishes the propagation of electrical activity in endocardial tissue for SCN5A L812Q gene mutation that results in arrhythmia called Brugada Syndrome.