Cardiac Sensory Consequences of Low‐Amplitude Autonomic Regulation Therapy

Abstract

ObjectiveTo determine if vagus nerve stimulation (VNS) or spinal cord stimulation (SCS) affects the capacity of cardiac afferent neurons to transduce myocardial ischemia (MI).MethodsUsing extracellular recordings in anesthetized canines, cardiac‐related dorsal root (DRG; T1‐T3 spinal levels) or nodose ganglia neurons were identified by touch/chemical activation in their epicardial sensory fields located adjacent to the left anterior descending (LAD) coronary artery. Neuronal responses to 1 min LAD coronary artery occlusion (CAO) were then evaluated prior to and following SCS [T1‐T3 spinal level; 50Hz, 90% motor threshold; 20 min] or left cervical VNS [20 Hz; current amplitudes (CA): CA1 (1–1.9 mA) or CA2 (2–3.5 mA); 3 min].ResultsLAD CAO activated cardiac afferent neurons in nodose and DRG ganglia, enhancement that persisted for up to 30 min into reperfusion. Following SCS or CA2 VNS, LAD CAO failed to alter their neural activity. VNS at CA1 did not mitigate MI‐induced activation of nodose neurons.ConclusionsTransient myocardial ischemia activates primary afferent inputs to the central nervous system (CNS), responses that persist into reperfusion. Pre‐emptive VNS or SCS obtunds sensory transduction of the ischemic myocardium to the CNS, in part accounting for the anti‐anginal and broader cardioprotective effects of such therapy being evaluated clinically. (HL71830)