Abstract
Cardiac alternans are observed as action potential duration (APD) alternans and/or Ca2+ transient (CaT) alternans. This study aims to investigate the mechanism underlying the genesis of the two types of alternans, their difference and correlation. Two human ventricle models were used for generating cardiac alternans. APD restitution and CaT-SR content curves were constructed to investigate possible different mechanisms. Results showed that alternans produced by the ORd model sustained with significant CaT but no obvious APD alternans, whereas alternans generated by the TP model manifested as obvious APD but insignificant CaT alternans. CaT alternans in the ORd model was correlated with a much steeper CaT-SR content curve, while the APD alternans in the TP model was correlated with a steeper APD restitution curve. Furthermore, I CaL clamp simulations showed the magnitude of ICaL was crucial for generating the CaT alternans as a large ICaL could change its alternating status. Our results suggest that each of the APD or the CaT alternans has its own primary mechanism, and sustained CaT alternans is not necessarily related to APD alternans.
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