Figure 2.

ANS-Related Pathophysiology of HF

Heart failure (HF) is associated with significant neural remodeling characterized by increased sympathetic and reduced parasympathetic nerve activity. The central panel shows that the autonomic nervous system (ANS) remodeling contributes to the pathophysiology of heart failure and affects the clinical outcomes. The left panel, adapted from Goldstein (201) shows a concept diagram relating stress to chronic disorders such as heart failure that involve autonomic effectors. Stress is a condition in which a homeostatic comparator senses a discrepancy between afferent information to the brain about a monitored variable and a set point or other instructions for responding. The error signal drives effectors including components of the autonomic nervous system in a manner that reduces the discrepancy. Cumulative wear and tear (allostatic load) decreases effector efficiency, eventually precipitating dyshomeostatic vicious cycles. Feed-forward anticipatory processes shift input–output curves determined by the “Regulator.” The right panel shows major types of sensory afferent nerves and the corresponding abnormalities in autonomic reflexes observed in heart failure are illustrated. Sympathoexcitatory afferents are shown in green; sympathoinhibitory afferents in blue. Examples of underlying mechanisms acting at sensory, central, efferent, and effector organ sites that contribute to the reflex cardiovascular/respiratory dysregulation are noted. Aff = afferent; DRG = dorsal root ganglia; HR = heart rate; ParaSNA = parasympathetic nerve activity; SNA = sympathetic nerve activity.