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Review
. 2024 Mar;29(2):355-365.
doi: 10.1007/s10741-023-10345-y. Epub 2023 Sep 14.

The sympathetic nervous system in heart failure revisited

Filippos Triposkiadis  1 , Alexandros Briasoulis  2 , Takeshi Kitai  3 , Dimitrios Magouliotis  4 , Thanos Athanasiou  5 , John Skoularigis  6 , Andrew Xanthopoulos  6
Affiliations
Review

The sympathetic nervous system in heart failure revisited

Filippos Triposkiadis et al. Heart Fail Rev. 2024 Mar.

Abstract

Several attempts have been made, by the scientific community, to develop a unifying hypothesis that explains the clinical syndrome of heart failure (HF). The currently widely accepted neurohormonal model has substituted the cardiorenal and the cardiocirculatory models, which focused on salt-water retention and low cardiac output/peripheral vasoconstriction, respectively. According to the neurohormonal model, HF with eccentric left ventricular (LV) hypertrophy (LVH) (systolic HF or HF with reduced LV ejection fraction [LVEF] or HFrEF) develops and progresses because endogenous neurohormonal systems, predominantly the sympathetic nervous system (SNS) and the renin-angiotensin-aldosterone system (RAAS), exhibit prolonged activation following the initial heart injury exerting deleterious hemodynamic and direct nonhemodynamic cardiovascular effects. However, there is evidence to suggest that SNS overactivity often preexists HF development due to its association with HF risk factors, is also present in HF with preserved LVEF (diastolic HF or HFpEF), and that it is linked to immune/inflammatory factors. Furthermore, SNS activity in HF may be augmented by coexisting noncardiac morbidities and modified by genetic factors and demographics. The purpose of this paper is to provide a contemporary overview of the complex associations between SNS overactivity and the development and progression of HF, summarize the underlying mechanisms, and discuss the clinical implications as they relate to therapeutic interventions mitigating SNS overactivity.

Keywords: Ejection fraction; Heart failure; Hypertrophy; Renin–angiotensin–aldosterone system; Sympathetic nervous system.

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References

    1. Braunwald E (1997) Shattuck lecture–cardiovascular medicine at the turn of the millennium: triumphs, concerns, and opportunities. N Engl J Med 337(19):1360–1369 - PubMed - DOI
    1. Giannoni A, Mirizzi G, Aimo A, Emdin M, Passino C (2015) Peripheral reflex feedbacks in chronic heart failure: is it time for a direct treatment? World J Cardiol 7(12):824–828 - PubMed - PMC - DOI
    1. Packer M (1995) Evolution of the neurohormonal hypothesis to explain the progression of chronic heart failure. Eur Heart J 16 Suppl F:4–6
    1. Grassi G, Seravalle G, Quarti-Trevano F, Dell’Oro R, Bolla G, Mancia G (2003) Effects of hypertension and obesity on the sympathetic activation of heart failure patients. Hypertension 42(5):873–877 - PubMed - DOI
    1. Badrov MB, Mak S, Floras JS (2021) Cardiovascular autonomic disturbances in heart failure with preserved ejection fraction. Can J Cardiol 37(4):609–620 - PubMed - DOI

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