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Neurohormonal activation in heart failure with reduced ejection fraction
Justin Hartupee1, Douglas L Mann1
1Center for Cardiovascular Research, Division of Cardiology, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Nature Reviews. Cardiology
|October 7, 2016
Summary
Neurohormonal systems like the sympathetic nervous system and renin-angiotensin-aldosterone system (RAAS) initially compensate for heart failure with reduced ejection fraction (HFrEF). Chronic activation, however, drives disease progression, making their antagonism key in HFrEF treatment.
Area of Science:
- Cardiology
- Physiology
- Pharmacology
Background:
- Heart failure with reduced ejection fraction (HFrEF) results from decreased cardiac output due to cardiac injury.
- Compensatory responses include activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS).
Purpose of the Study:
- To review the effects of neurohormonal activation in HFrEF.
- To highlight mechanisms by which these systems contribute to heart failure progression.
Main Methods:
- This is a review article.
- It synthesizes current understanding of neurohormonal pathways in HFrEF.
Main Results:
- Short-term neurohormonal activation aids cardiovascular homeostasis.
- Chronic activation leads to hemodynamic stress and detrimental effects on the heart and circulation.
- Neurohormonal activation is a primary driver of HFrEF progression.
Conclusions:
- Therapeutic antagonism of neurohormonal systems is central to current HFrEF pharmacotherapy.
- Understanding these mechanisms is crucial for developing effective HFrEF treatments.
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