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Neurohormonal Activation in Heart Failure with Reduced Ejection Fraction

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Journal Nat Rev Cardiol
Date 2016 Oct 7
PMID 27708278
Citations 239
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Abstract

Heart failure with reduced ejection fraction (HFrEF) develops when cardiac output falls as a result of cardiac injury. The most well-recognized of the compensatory homeostatic responses to a fall in cardiac output are activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS). In the short term, these 'neurohormonal' systems induce a number of changes in the heart, kidneys, and vasculature that are designed to maintain cardiovascular homeostasis. However, with chronic activation, these responses result in haemodynamic stress and exert deleterious effects on the heart and the circulation. Neurohormonal activation is now known to be one of the most important mechanisms underlying the progression of heart failure, and therapeutic antagonism of neurohormonal systems has become the cornerstone of contemporary pharmacotherapy for heart failure. In this Review, we discuss the effects of neurohormonal activation in HFrEF and highlight the mechanisms by which these systems contribute to disease progression.

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References
1.
Packer M . The neurohormonal hypothesis: a theory to explain the mechanism of disease progression in heart failure. J Am Coll Cardiol. 1992; 20(1):248-54. DOI: 10.1016/0735-1097(92)90167-l. View

2.
Brilla C, Funck R, Rupp H . Lisinopril-mediated regression of myocardial fibrosis in patients with hypertensive heart disease. Circulation. 2000; 102(12):1388-93. DOI: 10.1161/01.cir.102.12.1388. View

3.
Izawa H, Murohara T, Nagata K, Isobe S, Asano H, Amano T . Mineralocorticoid receptor antagonism ameliorates left ventricular diastolic dysfunction and myocardial fibrosis in mildly symptomatic patients with idiopathic dilated cardiomyopathy: a pilot study. Circulation. 2005; 112(19):2940-5. DOI: 10.1161/CIRCULATIONAHA.105.571653. View

4.
Lymperopoulos A, Rengo G, Koch W . Adrenergic nervous system in heart failure: pathophysiology and therapy. Circ Res. 2013; 113(6):739-53. PMC: 3843360. DOI: 10.1161/CIRCRESAHA.113.300308. View

5.
Zannad F, Alla F, Dousset B, Perez A, Pitt B . Limitation of excessive extracellular matrix turnover may contribute to survival benefit of spironolactone therapy in patients with congestive heart failure: insights from the randomized aldactone evaluation study (RALES). Rales Investigators. Circulation. 2000; 102(22):2700-6. DOI: 10.1161/01.cir.102.22.2700. View