Disturbed Connexin43 gap junction distribution correlates with reentrant VT circuit locations in healing canine infarcts, suggesting it plays a role in VT susceptibility.
Hypothesis-generating for gap junction remodeling as VT substrate in infarct models; leaves open human translation and therapeutic targeting.
Altered gap-junctional distribution is part of the early remodeling of myocardium after infarction, and by defining the location of the common central pathway of the reentrant VT circuits, it may be a determinant of VT susceptibility.
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Peters et al. (1997) studied this question.
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