Mechanism of Reentry Trigged by EADs in Long-QT Syndrome: A Simulation Study.

This simulation study is carried out in two-dimensional two-dimensional two-dimensional tissue of Luo-Rudy model of mammalian ventri-cular ventri-cular ventri-cular myocytes. Mechanism of reentry trigged by early after-depolarizations after-depolarizations after-depolarizations (EADs) in long-QT syndrome (LQTS) has been study in this paper. LQTS is simulated by reducing the membrane conductance of IKsfor LQT1 and IKrfor LQT2, and by altering the steady-state inactivation of the fast sodium current INafor LQT3. The endocardium is paced 10 times at a constant basic cycle length (BCL) of 500ms, and following a 2000ms pause, a S2 stimulus is applied. If shape, size and position of M cell domain is suitable, EADs with higher amplitude formation near the boundary between endocardial domain and M cell domain provide the trigger for reentrant excitation. Reentry once initiated is more likely to self-terminate self-terminate self-terminate in LQT1 tissue. In LQT2 tissue, functional reentry is maintained by the continuously generating of EADs in the mid of M cell domain. In LQT3 tissue, functional reentry is maintained for the reason that the conduction velocity of EAD induced reentrant wave is very slowly, and the tip of it is anchored at the mid of M cell domain.