Myocardial infarction (MI) leads to pathological changes in the cardiac sympathetic innervation. The distribution and density of sympathetic fibers are altered, along with regional changes in neurotransmitter synthesis. The resulting spatial heterogeneity of sympathetic transmission is implicated in the development of arrhythmias and sudden cardiac death. Despite the clinical importance of sympathetic dysfunction, the underlying causes are not well understood. We have investigated the molecular basis for these changes in sympathetic function, and have identified roles for gp130 inflammatory cytokines and neurotrophins/proneurotrophins in regulating region-specific denervation, hyperinnervation, and altered neurotransmitter production in the heart after ischemia-reperfusion. Recent studies revealed that the cardiac infarct remains denervated following ischemia-reperfusion due to blockade of axon regeneration by inhibitory chondroitin sulfate proteoglycans within the infarct. New data from telemetry and ex vivo electrical mapping suggest that promoting reinnervation of the infarct decreases arrhythmia susceptibility. Cardiac denervation and aberrant nerve sprouting in humans has been directly linked to cardiac pathology and sudden cardiac death, suggesting that strategies to ameliorate these pathological changes may be beneficial for human health.
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Received: May 15, 2013
© 2013 Published by Elsevier Inc.