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Neurohormones and death in systolic heart failure: keep your friends close, but your enemies closer
  1. Josip A Borovac1,2,3
  1. 1 Department of Pathophysiology, University of Split School of Medicine, Split, Croatia
  2. 2 Institute of Emergency Medicine of Split-Dalmatia County, Split, Croatia
  3. 3 Working Group on Heart Failure of Croatian Cardiac Society, Zagreb, Croatia
  1. Correspondence to Dr Josip A Borovac, Department of Pathophysiology, University of Split School of Medicine, Split 21000, Croatia; jborovac{at}mefst.hr

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During the past several decades, our scientific journey to understand the aetiology, progression and treatment of heart failure (HF) has been marked by a series of grand successes and bitter defeats. Although diverse types of insults to cardiomyocytes, of which injury due to myocardial infarction is the most common, can precipitate poor contractility and subsequent pump failure, it became evident that there is more to HF than only mechanical issues could account for. In earlier times, it was thought that correction of haemodynamic abnormalities will abrogate HF symptoms and progression of the disease. However, while therapeutic interventions that increased contractility or decreased peripheral vasoconstriction were often able to ameliorate symptoms and improve the haemodynamic status of a patient in a short term, the long-term outcomes remained abysmal marked by high rates of progression to end-stage disease and death. As a physiological response to impaired pump function, a complex network of peripheral arterial baroreceptors, chemoreceptors and ergoreceptors can detect circulatory deficits and activate a series of compensatory mechanisms that synergistically work to maintain cardiovascular homeostasis by augmenting cardiac contractility and heart rate, promoting water and salt retention and constricting peripheral blood vessels.1 This compensation is characterised by the activation of several systems such as sympathetic (adrenergic) nervous system (SNS), renin–angiotensin–aldosterone system (RAAS) and cytokine-mediated innate immunity adaptations that all contribute to cardiac repair and remodelling through endocrine, paracrine or autocrine release of biologically active molecules—neurohormones. This coordinated response of neurohormones to restore cardiac output of the failing heart is beneficial in the short term; however, they impose deleterious effects and drive progression and exacerbation of HF.

Historically, the major work in understanding compensatory mechanisms in HF was undertaken during the 1960s and 1970s, when investigators described the Frank-Starling principle, myocardial hypertrophy, increased sympathoadrenal activity and peripheral resistance vessel constriction as …

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  • Contributors I declare that I am the sole author of this work and I wrote this piece in its entirety.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

  • Provenance and peer review Commissioned; externally peer reviewed.

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