Autonomic Nervous System: A Therapeutic Target for Cardiac End-Organ Damage in Hypertension.
arterial hypertension
atrial fibrillation
autonomic nervous system
ganglionated plexuses
heart failure
renal denervation
Journal
Hypertension (Dallas, Tex. : 1979)
ISSN: 1524-4563
Titre abrégé: Hypertension
Pays: United States
ID NLM: 7906255
Informations de publication
Date de publication:
13 Aug 2024
13 Aug 2024
Historique:
medline:
13
8
2024
pubmed:
13
8
2024
entrez:
13
8
2024
Statut:
aheadofprint
Résumé
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.
Identifiants
pubmed: 39136127
doi: 10.1161/HYPERTENSIONAHA.123.19460
doi:
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM