Electrically stabilizing the myocardial border zone with vagal nerve stimulation (VNS) may offer a new mechanism for reducing arrhythmia.
Electrically stabilizing the myocardial border zone with vagal nerve stimulation (VNS) may offer a new mechanism for reducing arrhythmia. A University of California Los Angeles team is due to report Sunday, March 15 at the 2015 annual meeting of the American College of Cardiology in San Diego, CA.
Marmar Vaseghi, MD, a cardiologist at Ronald Reagan Medical Center, reported on an assessment of the regional electrophysiological effects of vagal nerve stimulation, bilateral stellate ganglia stimulation (SGS), and neurotransmitter content after myocardial infarction.
She looked at 15 infarcted and 7 normal pig hearts. VNS and SGS were performed and the inducibility of ventral tachycardia (VT) was assessed. The team then looked at activation recovery interval (ARI) recordings from both scarred and viable areas.
The researchers also analyzed acetylcholine (Ach) and norepinephrine content.
The results showed that VNS prolonged global ARI of infarcted more thannormal hearts. ACH content was greatin the border zone and viable regions of the infarcted hearts. VNS prolonged border zone ARI more than scar or viable areas and reduced border zone dispersion of repolarization significantly compared to other regions.
SGS shortened scar ARI as well as that in the border zone and viable myocardium and increased dispersion in all regions. VNS decreased VT inducibility from 60% to 30%.
“The greater response of VNS and Ach content of viable and border zone myocardium in infarcted hearts suggests a decrease in parasympathetic drive,” the researchers concluded, indicating that electrical stabilization of the border zone “is a novel mechanism for arrhythmia reduction with VNS.”