Autonomic neuromodulation for cardiomyopathy associated with metabolic syndrome - Prevention of precursors for heart failure with preserved ejection fraction

Metabolic syndrome (MetS) induces a systemic inflammatory state which can lead to cardiomyopathy, manifesting clinically as heart failure (HF) with preserved ejection fraction (HFpEF). MetS components are intricately linked to the pathophysiologic processes of myocardial remodeling. Increased sympat...

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Bibliographic Details
Published in:Hypertension research 2024-12, Vol.47 (12), p.3318-3329
Main Authors: Nagai, Michiaki, Rommel, Karl-Philipp, Po, Sunny S., Dasari, Tarun W.
Format: Article
Language:English
Subjects:
Animals
Autonomic Nervous System - physiopathology
Cardiomyopathies - physiopathology
Cardiomyopathies - therapy
Geriatrics/Gerontology
Health Promotion and Disease Prevention
Heart Failure - complications
Heart Failure - physiopathology
Heart Failure - therapy
Humans
Internal Medicine
Medicine
Medicine & Public Health
Metabolic Syndrome - complications
Metabolic Syndrome - physiopathology
Metabolic Syndrome - therapy
Mini Review
Obstetrics/Perinatology/Midwifery
Public Health
Stroke Volume - physiology
Vagus Nerve Stimulation
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Description
Summary:Metabolic syndrome (MetS) induces a systemic inflammatory state which can lead to cardiomyopathy, manifesting clinically as heart failure (HF) with preserved ejection fraction (HFpEF). MetS components are intricately linked to the pathophysiologic processes of myocardial remodeling. Increased sympathetic nervous system activity, which is noted as an upstream factor of MetS, has been linked to adverse myocardial structural changes. Since renal denervation and vagus nerve stimulation have a sympathoinhibitory effect, attention has been paid to the cardioprotective effects of autonomic neuromodulation. In this review, the pathophysiology underlying the relationship between MetS and HF is elucidated, and the evidence regarding autonomic neuromodulation in HFpEF is summarized.
ISSN:0916-9636
1348-4214
1348-4214
DOI:10.1038/s41440-024-01886-2