Back to Search Start Over

Autonomic Nervous System: A Therapeutic Target for Cardiac End-Organ Damage in Hypertension.

Authors :
Gottlieb LA
Mahfoud F
Stavrakis S
Jespersen T
Linz D
Source :
Hypertension (Dallas, Tex. : 1979) [Hypertension] 2024 Oct; Vol. 81 (10), pp. 2027-2037. Date of Electronic Publication: 2024 Aug 13.
Publication Year :
2024

Abstract

More than 1.5 billion people worldwide have arterial hypertension. Hypertension increases the risks of death and cardiovascular disease, such as atrial fibrillation and heart failure. The autonomic nervous system plays an essential role in hypertension development and disease progression. While lifestyle factors, such as obesity and obstructive sleep apnea, predispose to hypertension by increasing sympathetic activity, hypertension itself maintains the autonomic nervous imbalance, providing the substrate for atrial fibrillation and heart failure. Therefore, autonomic nervous system modulation either by direct targeting or indirect treatment of comorbidities has the potential to treat both hypertension and related atrial and ventricular end-organ damage. We discuss interventions for the modulation of the autonomic nervous system for hypertension and related cardiac end-organ damage, including pharmacological adrenergic beta-receptor blockade, renal denervation, carotid baroreceptor stimulation, low-level vagal stimulation, and ablation of ganglionated plexuses. In summary, the literature suggests that targeting the autonomic nervous system potentially represents a therapeutic approach to prevent atrial and ventricular end-organ damage in patients with hypertension. However, clinical trials specifically designed to test the effect of autonomic modulation on hypertension-mediated cardiac end-organ damage are scarce.<br />Competing Interests: None.

Details

Language :
English
ISSN :
1524-4563
Volume :
81
Issue :
10
Database :
MEDLINE
Journal :
Hypertension (Dallas, Tex. : 1979)
Publication Type :
Academic Journal
Accession number :
39136127
Full Text :
https://doi.org/10.1161/HYPERTENSIONAHA.123.19460