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Structural heterogeneity promotes triggered activity, reflection and arrhythmogenesis in cardiomyocyte monolayers
Author(s) -
Auerbach David S.,
Grzȩda Krzysztof R.,
Furspan Philip B.,
Sato Priscila Y.,
Mironov Sergey,
Jalife José
Publication year - 2011
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2010.200576
Subject(s) - heartbeat , reflection (computer programming) , cardiac arrhythmia , medicine , sodium channel , mechanism (biology) , cardiology , cardiac muscle , optical mapping , neuroscience , chemistry , sodium , biology , physics , computer science , organic chemistry , programming language , computer security , quantum mechanics , atrial fibrillation
Non‐technical summary The heartbeat depends on the spread of electrical waves through the cardiac muscle. If that spread becomes disturbed, arrhythmias and death may ensue. Patients with heart disease are predisposed to cardiac arrhythmias by unidentified mechanisms. Using both experiments and computer models we demonstrate that structural defects in the heart leading to contiguous areas of physical narrowing and expansion of the musculature can alter the spread of the waves, in such a way that some waves may return abnormally along the same narrow pathway as the original electrical wave (reflection), leading to extra beats and arrhythmia initiation. The possibility of reflection is enhanced when structural defects combine with alterations in the sodium channels responsible for the electrical waves, such as seen in inherited and acquired cardiac electrical diseases. Our results provide a novel mechanism whereby a substrate (structural heterogeneity) and a trigger (abnormal sodium channel activity) combine to promote life‐threatening arrhythmia initiation.