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Front Physiol. 2017 Mar 30;8:195. doi: 10.3389/fphys.2017.00195. eCollection 2017.

Mechanisms Underlying the Emergence of Post-acidosis Arrhythmia at the Tissue Level: A Theoretical Study.

Author information

1
School of Computer Science and Technology, Harbin Institute of TechnologyHarbin, China.
2
State Key Laboratory of Urban Water Resource and Environment, Harbin Institute of TechnologyHarbin, China.
3
Biological Physics Group, School of Physics and Astronomy, University of ManchesterManchester, UK.
4
Space Institute of Southern ChinaShenzhen, China.

Abstract

Acidosis has complex electrophysiological effects, which are associated with a high recurrence of ventricular arrhythmias. Through multi-scale cardiac computer modeling, this study investigated the mechanisms underlying the emergence of post-acidosis arrhythmia at the tissue level. In simulations, ten Tusscher-Panfilov ventricular model was modified to incorporate various data on acidosis-induced alterations of cellular electrophysiology and intercellular electrical coupling. The single cell models were incorporated into multicellular one-dimensional (1D) fiber and 2D sheet tissue models. Electrophysiological effects were quantified as changes of action potential profile, sink-source interactions of fiber tissue, and the vulnerability of tissue to the genesis of unidirectional conduction that led to initiation of re-entry. It was shown that acidosis-induced sarcoplasmic reticulum (SR) calcium load contributed to delayed afterdepolarizations (DADs) in single cells. These DADs may be synchronized to overcome the source-sink mismatch arising from intercellular electrotonic coupling, and produce a premature ventricular complex (PVC) at the tissue level. The PVC conduction can be unidirectionally blocked in the transmural ventricular wall with altered electrical heterogeneity, resulting in the genesis of re-entry. In conclusion, altered source-sink interactions and electrical heterogeneity due to acidosis-induced cellular electrophysiological alterations may increase susceptibility to post-acidosis ventricular arrhythmias.

KEYWORDS:

delayed afterdepolarization; post acidosis arrhythmias; premature ventricular complexes; sink-source mismatch; transmural dispersion of repolarization; ventricular tachycardia

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