Abstract
The cardiac autonomic nervous system (ANS) is a crucial component in physiological and pathological responses of the cardiovascular system. Through its 2 branches, the sympathetic nervous system (SNS) and the parasympathetic nervous system (PNS) nervous systems, as well as effector molecules including norepinephrine (NE) and acetylcholine, the ANS orchestrates many events that allow for appropriate blood pressure (BP), heart rate (HR), and vasoregulatory responses to routine daily stimuli. Dysregulation of this system due to aging, acute and chronic stress, organic and idiopathic and other causes contributes to cardiovascular pathology, including hypertension, ischemic heart disease, arrhythmias, and congestive heart failure, and often contributes to fatal outcomes. Heart failure with reduced ejection fraction (HFrEF) is characterized by neurohumoral activation mediated by the SNS and renin-angiotensin system (1). Sympathetic hyperactivity is evident by increased central sympathetic outflow and plasma NE levels, with NE spillover of up to 50-fold compared to that in controls (2,3). Even in HF patients with preserved EF (HFpEF), sympathetic hyperactivity represented by increased skeletal muscle nerve activity may contribute to the development of diastolic dysfunction (4). 123I-labeled metaiodobenzylguanidine (MIBG) cardiac nuclear imaging assesses cardiac adrenergic nerve function and provides prognostic information for risk stratifying patients with HF (5).
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