The Autonomic Nervous System (ANS) employs several modes of regulation over the cardiovascular system including chronotropic, dromotropic, inotropic, and lusitropic effects. Sympathetic activity is associated with “fight or flight”, and leads to an increase in heart rate, contractility, and vasoconstriction. Whereas parasympathetic activity is associated with “rest and digest”, and leads to a decrease in heart rate and contractility, along with an increase in vasodilation. Cardiac innervation is remodeled structurally and functionally in pathological states. This pathological process makes the ANS a logical target for treatment and intervention. Cervicothoracic sympathectomy, or Bilateral Cardiac Sympathetic Denervation (BCSD) is a procedure in which the lower half of the stellate ganglion is removed along with T2-T4 on both sides of the thorax. This severs most of the sympathetic innervation to the myocardium. In patients with severe ventricular arrhythmia, where conventional treatment such as antiarrhythmic medications, beta blockers, and cardiac ablation have failed, this surgery provides antiarrhythmic benefits. While it is known that BCSD imparts antiarrhythmic benefits, it remains unknown exactly how. Changes in autonomic reflexes as a result of BCSD are also unknown.
The goal of this study is to assess changes to the ANS before and after BCSD, in order to better understand how BCSD affects ANS signaling, in comparison to control subjects.
Autonomic reflex activity in healthy control subjects, cardiomyopathy patients pre-BCSD, and post-BCSD, were tested by the introduction of an autonomic challenge, posture change task (PTASK). As this stressor was introduced hemodynamic and autonomic readouts were obtained. A non-invasive blood pressure machine was used to obtain Systolic Blood Pressure(SBP), Diastolic Blood Pressure (DBP), and Mean Arterial Pressure (MAP). Finger plethysmography was utilized to measure changes in finger pulse volume (FPV). Also obtained was the galvanic skin response (GSR), and an ECG was used to gather data on heart rate (HR).
The study population consists of 12 healthy control subjects (HCs); 12 cardiomyopathy (CMY) patients with severe arrhythmia pre-BCSD and the same 12 CMY patients post-BCSD. First, hemodynamic and autonomic measurements were obtained at rest, and there was no significant difference between MAP, DBP, or GSR in HCs compared to CMY patients. However, resting SBP (P= 0.0078) and FPV (p= 0.0011) were significantly lower in CMY patients at rest. Additionally, CMY patients demonstrated a reduced response to autonomic stressor PTASK, compared to HCs. While HCs displayed a significant change in FPV (p= 0.0261), and HR (p= 0.0312) when this stressor was introduced to CMY patients, they displayed no significant changes. When the same patients were introduced to PTASK post-BCSD, there was no significant change in SBP, DBP, HR, or MAP, compared to Pre-BCSD. However, there was a significant decrease in the percent change of GSR (p<.005) and FPV (p<.005) response to PTASK Post-BCSD.
This study shows that CMY patients pre-BCSD had a blunted response to an autonomic stressor, PTASK. When those same patients were introduced to PTASK Post-BCSD there was no significant change in hemodynamic measurements. This suggests that BCSD did not significantly impact the autonomic reflexes necessary for orthostatic cardiovascular control. These results also suggest that ANS reflex activity is not restored post-BCSD, and therefore restoration of ANS reflex activity is not the mechanism via which anti-arrhythmic benefits are imparted to patients.