Key result
In a computer simulation of Long QT Syndrome, pause-induced early afterdepolarizations started reentry near the boundary between the endocardial and M cell domains.
Computer simulations suggest that in Long-QT Syndrome, reentry initiated by pause-induced early afterdepolarizations begins near the boundary of endocardial and M cell domains.
Hypothesis-generating for LQTS reentry mechanisms; leaves open translation to experimental models or clinical practice.
Reentry is the main form of arrhythmia. To know when and where the reentry starts in Long QT Syndromes (LQTS) and its relation with M cells distribution, the Luo-Rudy dynamic ionic model (LRdOO) of the mammalian ventricular action potential (AP) was used in a two dimensional transmural tissue sheets simulation. LQTS was 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 was paced 10 times at a constant basic cycle length (BCL) of 500 ms (S1), and following a 2000 ms pause, a S2 stimulus was applied, or also a S3 stimulus was applied. The simulation was processed by changing shape, size and position of M cell domain, and S2S3 interval. We found that pause induced early after depolarization (EAD) started reentry near the boundary between endocardial domain and M cells domain. Only S3 stimulus that located in vulnerable windows could form reentry. The started position of the reentry depended upon the distribution of island of M cells and the position of extrasystole.
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Jin et al. (2009) studied Long QT Syndromes (LQTS). Computer simulation of LQTS was evaluated on Start position and timing of reentry. In a computer simulation of Long QT Syndrome, pause-induced early afterdepolarizations started reentry near the boundary between the endocardial and M cell domains.
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