Key result
A novel computational approach demonstrated that complex re-entrant excitation patterns and spontaneous sub-cellular calcium release events may be bi-directionally coupled, promoting arrhythmia.
Why the study?
Multi-scale mechanisms of how spontaneous sub-cellular calcium release events develop into arrhythmia triggers and dynamically interact with tissue substrates remain elusive due to the challenge of simultaneous study across nanometre to centimetre scales.
A novel multi-scale computational framework demonstrates that complex re-entrant excitation patterns and spontaneous sub-cellular calcium release events are bi-directionally coupled, promoting arrhythmia perpetuation.
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Hypothesis-generating for calcium-reentry coupling in arrhythmia; leaves open translation to human therapies.
Michael A. Colman (2019) studied Cardiac arrhythmias. Computational modeling was evaluated. A novel computational approach demonstrated that complex re-entrant excitation patterns and spontaneous sub-cellular calcium release events may be bi-directionally coupled, promoting arrhythmia.
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