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

This simulation study is carried out in two-dimensional tissue of Luo-Rudy model of mammalian ventricular myocytes. Mechanism of reentry triggered by early afterdepolarizations (EADs) in long-QT syndrome (LQTS) has been study in this paper. LQTS is simulated by reducing the membrane conductance of I
_Ks
for LQT1 and I
_Kr
for LQT2, and by altering the steady-state inactivation of the fast sodium current I
_Na
for LQT3. The endocardium is paced 10 times at a constant basic cycle length (BCL) of 500 ms, and following a 2000 ms 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 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