Cardiac sympathetic afferent denervation improves cardiac post-ischemic remodeling by maintaining autonomic tone

The autonomic imbalance can negatively affect left ventricular (LV) remodeling following a myocardial infarction (MI). Ganglionated plexi (GP) play a crucial role in autonomic nervous system imbalance. Cardiac sympathetic afferent denervation (CSAD) has been shown to have beneficial effects in addressing this imbalance.

This study aimed to evaluate the effects of the ablation of cardiac sympathetic sensory neurons on LV remodeling. Resiniferatoxin (RTX), a neurotoxic transient receptor potential vanilloid (TRPV1) antagonist, was used to achieve it.

A total of 31 beagle dogs were randomly assigned to three groups: MI group (n = 12), CSAD group (MI with CSAD; n = 10), and Control group (sham surgery without CSAD; n = 9). In the CSAD group, RTX was injected into the anterior right ganglionated plexi (ARGP) only once. After a 4-week follow-up period, CSAD treatment resulted in a significant decrease in left stellate ganglion (LSG) activity, improved LSG remodeling, reduced LV dilation, and improved LV function. Furthermore, CSAD treatment significantly attenuated LV remodeling in post-MI LV tissue. The treatment also showed positive effects on high-sensitivity C-reactive protein (hs-CRP), norepinephrine (NE), N-terminal prohormone of brain natriuretic peptide (NT-proBNP) and Neuropeptide Y (NPY) levels.

In conscious dogs with healed MI, CSAD led to a reduction in cardiac sympathetic tone and an improvement in ventricular remodeling. This suggests that targeting cardiac sympathetic sensory neurons through CSAD may have therapeutic benefits in managing LV remodeling after MI.