This review highlights the anatomical and functional pathways of the autonomic nervous system in the heart and how their disruption by myocardial infarction may contribute to arrhythmogenesis.
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MI-induced neural disruption may heighten postinfarct arrhythmia risk; leaves open targeted neuromodulation trials.
The purpose of this report is to present a brief overview of the concepts concerned with the potential effects of the autonomic nervous system on the genesis of cardiac arrhythmias. First, we present data indicating the functional importance of presynaptic and postsynaptic vagal modulation of adrenergic neurotransmission on electrical activity in sinus and A-V nodes, and contractile activity of canine cardiac Purkinje fibers. Second, we indicate the possible intraventricular adrenergic and vagal pathways to the ventricles, suggesting that sympathetic fibers travel in the epicardium while vagal fibers appear to cross the A-V groove in the epicardium but then take an intramural route for part of their course. Finally, we demonstrate that a lesion such as a myocardial infarction can interrupt neural fibers traveling through the infarction to affect noninfarcted myocardium distal to the infarction. These factors may play a role in the genesis of some cardiac arrhythmias.
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Zipes et al. (1983) studied this question.
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