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Published on: May 22, 2018
Neuroendocrine effects on the heart and targets for therapeutic manipulation in heart failure
Parminder S Chaggar1, Chris J Malkin, Steven M Shaw
1Northwest Heart and Transplant Centre, Wythenshawe Hospital, Manchester M23 9LT, UK. pchaggar@doctors.org.uk
Insights
Chronic heart failure (CHF) causes metabolic problems, including hormonal imbalances that worsen the condition and increase mortality. This review explores neuroendocrine treatments to address these catabolic and anabolic defects in CHF patients.
Area of Science:
- Cardiology
- Endocrinology
- Metabolic Medicine
Background:
- Chronic heart failure (CHF) is characterized by neurohormonal axis dysfunction.
- This dysfunction leads to a procatabolic state and wasting syndrome, increasing mortality.
- Key abnormalities include elevated catecholamines/glucocorticoids and deficiencies in sex steroids, with insulin and growth hormone (GH) resistance.
Purpose of the Study:
- To review the current understanding of metabolic derangements in CHF.
- To highlight potential neuroendocrine treatment strategies for CHF.
Main Methods:
- Literature review of studies on neuroendocrine axes in CHF.
- Analysis of pilot studies augmenting anabolic axes (testosterone, GH, IGF-1, GH secretagogues).
Main Results:
- Metabolic abnormalities in CHF are linked to increased morbidity and mortality.
- Pilot studies using anabolic agents in CHF have shown varied results.
- Some treatments demonstrated improvements in surrogate endpoints.
Conclusions:
- Neuroendocrine dysregulation significantly impacts CHF pathophysiology and outcomes.
- Targeting anabolic axes presents a potential therapeutic strategy for CHF.
- Further research is needed to optimize neuroendocrine treatments for CHF.
Abstract:
Chronic heart failure (CHF) involves derangements in multiple neurohormonal axes leading to a procatabolic state and wasting syndrome associated with significant mortality. Catabolic abnormalities include excess catecholamines and glucocorticoids. Anabolic defects include deficiencies of sex steroids, insulin resistance, and growth hormone (GH) resistance. These abnormalities are also correlated with increased morbidity and mortality in CHF. Anabolic axes have been augmented in pilot studies in CHF with testosterone, GH, insulin-like growth factor-1, and GH secretagogues. Results have been varied although some treatments have been associated with improved surrogate endpoints. This review article explores the current understanding of metabolic derangements in CHF and highlights potential neuroendocrine treatment strategies.
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