Abstract 12627: Myocardial Infarction Alters Neural Processing of Afferent Inputs in the Intrinsic Cardiac Nervous System
Introduction: The intrinsic cardiac nervous system (ICNS) is an important coordinator of cardiac function and its regulatory functions can be impacted by cardiac disease. Our aim was to characterize the neural remodeling that occurs in the ICNS in response to chronic myocardial infarction (MI).
Methods: Activity from intrinsic cardiac (IC) neurons in the ventral interventricular ganglionated plexus was recorded using a linear microelectrode array in 5 normal pigs and 6 pigs with chronic MI. Changes in neuron activity were evaluated in response to: (1) focal mechanotransduction (touch); transient occlusion of the (2) inferior vena cava (IVC) and (3) carotid arteries; and electrical stimulation of (4) cervical vagi and (5) stellate ganglia.
Results: A total of 72 IC neurons were identified in normal pigs and 63 neurons in MI pigs. The proportion of neurons that responded to epicardial touch at the left ventricular (LV) apex (i.e. infarct zone) was significantly decreased in MI (3.2%) compared to normal (23.2%) (p < 0.05) (Figure 1A). The response to IVC occlusion was also significantly decreased in MI (28.6%) compared to normal (56.9%) (p < 0.01) (Figure 1B). However, there was no significant difference in response to bilateral carotid artery occlusion or stimulation of cervical vagi or stellate ganglia between normal and MI: 38.6% in normal versus 28.0% in MI and 47.2% in normal versus 46.0% in MI, respectively.
Conclusions: Our results suggest chronic MI alters information processing in the ICNS. We observed a significant decrease in afferent signaling from the infarct zone to the ICNS. Although no change in evoked efferent signaling to the ICNS was observed, the integrated IC reflex response to IVC occlusion was significantly attenuated. These MI-induced alterations in information processing in the ICNS represent the ‘neural signature’ of altered cardiac afferent signaling, which initiates the pathophysiologic processes responsible for arrhythmias and heart failure.
Author Disclosures: P.S. Rajendran: None. M. Vaseghi: None. J. Armour: None. J.L. Ardell: Research Grant; Significant; Cyberonics. Consultant/Advisory Board; Significant; Cyberonics. K. Shivkumar: None.
- © 2014 by American Heart Association, Inc.