Key result
Acute MI in mice triggers a ~5-fold increase in peri-infarct nerve density lasting months.
Acute myocardial infarction in mice induces immediate and sustained upregulation of neurotrophic factors and nerve sprouting, particularly in the peri-infarct areas, which may contribute to arrhythmogenesis.
May implicate early nerve sprouting in post-MI arrhythmogenesis in mice; leaves open translational relevance to human arrhythmia prevention.
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Oh et al. (2007) studied Acute Myocardial Infarction (n=32). Acute Myocardial Infarction (left coronary artery ligation) vs. Normal control mice was evaluated on Nerve density (GAP-43 immunopositive nerve fibers) (>5 times control level at peri-infarct area, p=<0.0001). Acute myocardial infarction in mice induced immediate upregulation of neurotrophic factors and increased nerve sprouting activity that peaked at 3 hours and persisted for at least 2 months.
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