Cardiac Spinal Deafferentation Reduces the Susceptibility to Sustained Ventricular Tachycardia in Conscious Rats by Reducing Cardiac Metabolic Demand

The response to myocardial ischemia is complex and involves the cardio‐cardiac sympathetic reflex. Specifically, cardiac spinal (sympathetic) afferents are excited by ischemic metabolites and elicit a cardio‐cardiac sympathetic reflex which plays a major role in the genesis of ventricular arrhythmias. Clinical work with patients and experimental work with animals document that disruption of this reflex protects against ischemia‐induced ventricular arrhythmias. Therefore, we tested the hypothesis that cardiac spinal deafferentation reduces the susceptibility to sustained ventricular tachycardia by reducing cardiac metabolic demand. To test this hypothesis, we measured the susceptibility to ventricular tachy‐arrhythmias produced by occlusion of the left main coronary artery in two groups of conscious rats: 1) deafferentation (excision of the T1–T5 dorsal root ganglia) and 2) sham deafferentation. The ventricular arrhythmia threshold (VAT) was defined as the time from coronary occlusion to sustained ventricular tachycardia resulting in a reduction in arterial pressure. Results document a significantly higher VAT in the deafferentation group (7.1 ± 0.7 min) relative to sham deafferentation (4.7 ± 0.1 min) rats. The decreased susceptibility to tachyarrhythmias with deafferentation was associated with a reduced cardiac metabolic demand (lower rate‐pressure product and ST‐segment elevation) during ischemia. Supported by NIH HL088615