{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,2]],"date-time":"2026-11-02T20:26:43Z","timestamp":1793651203627,"version":"4.5.1"},"reference-count":65,"publisher":"Oxford University Press (OUP)","issue":"Supplement_E","license":[{"start":{"date-parts":[[2022,8,17]],"date-time":"2022-08-17T00:00:00Z","timestamp":1660694400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2022,8,17]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Sympathetic activation has been long appreciated exclusively as a fundamental compensatory mechanism of the failing heart and, thus, welcome and to be supported. In the initial clinical phases of heart failure (HF), the sympathetic nervous system overdrive plays a compensatory function aimed at maintaining an adequate cardiac output despite the inotropic dysfunction affecting the myocardium. However, when the sympathetic reflex response is exaggerated it triggers a sequence of unfavourable remodelling processes causing a further contractile deterioration that unleashes major adverse cardiovascular consequences, favouring the HF progression and the occurrence of fatal events. Eventually, the sympathetic nervous system in HF was demonstrated to be a \u2018lethality factor\u2019 and thus became a prominent therapeutic target. The existence of an effective highly specialized intracardiac neuronal network immediately rules out the old concept that sympathetic activation in HF is merely the consequence of a drop in cardiac output. When a cardiac damage occurs, such as myocardial ischaemia or a primary myocardial disorder, the adaptive capability of the system may be overcame, leading to excessive sympatho-excitation coupled with attenuation till to abolishment of central parasympathetic drive. Myocardial infarction causes, within a very short time, both a functional and anatomical remodelling with a diffuse up-regulation of nerve growth factor (NGF). The subsequent nerve sprouting signal, facilitated by a rise in the levels of NGF in the left stellate ganglion and in the serum, triggers an increase in cardiac nerve density in both peri-infarct and non-infarcted areas. Finally, NFG production decreases over time, supposedly as an adaptative response to the prolonged exposure to sympathetic overactivity, leading in the end to a reduction in sympathetic nerve density. Accordingly, NGF levels were markedly reduced in patients with severe congestive heart failure. The kidney is the other key player of the sympathetic response to HF as it indeed reacts to under-perfusion and to loop diuretics to preserve filtration at the cost of many pathological consequences on its physiology. This vicious loop ultimately participates to the chronic and disruptive sympathetic overdrive.<\/jats:p>\n                  <jats:p>In conclusion, sympathetic activation is the natural physiological consequence to life stressors but also to any condition that may harm our body. It is the first system of reaction to any potential life-threatening event. However, in any aspect of life over reaction is never effective but, in many instances, is, actually, life threatening. One for all is the case of ischaemia-related ventricular fibrillation which is, strongly facilitated by sympathetic hyperactivity. The take home message? When, in a condition of harm, everybody is yelling failure is just around the corner.<\/jats:p>","DOI":"10.1093\/eurheartjsupp\/suac030","type":"journal-article","created":{"date-parts":[[2022,8,17]],"date-time":"2022-08-17T14:19:16Z","timestamp":1660745956000},"page":"E4-E11","source":"Crossref","is-referenced-by-count":73,"title":["Sympathetic activation in heart failure"],"prefix":"10.1093","volume":"24","author":[{"given":"E","family":"Gronda","sequence":"first","affiliation":[{"name":"U.O.C. Nefrologia, Dialisi e Trapianto Renale dell\u2019Adulto, Programma Cardiorenale, Dipartimento di Medicina e Specialit\u00e0 Mediche, Fondazione IRCCS Ca\u2019 Granda, Ospedale Maggiore Policlinico , Milano , Italy"},{"name":"Area Cardiorenale Metabolica Associazione nazionale Medici Cardiologi Ospedalieri Italia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"V","family":"Dusi","sequence":"additional","affiliation":[{"name":"Cardiology Division, Department of Medical Sciences, University of Turin , Torino , Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E","family":"D\u2019Elia","sequence":"additional","affiliation":[{"name":"Cardiovascular Department, Papa Giovanni XXIII Hospital , Bergamo , Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M","family":"Iacoviello","sequence":"additional","affiliation":[{"name":"Area Cardiorenale Metabolica Associazione nazionale Medici Cardiologi Ospedalieri Italia"},{"name":"S.C. Cardiologia, AOU Policlinico Riuniti di Foggia, Dipartimento di Scienze Mediche e Chirurgiche, Universit\u00e0 degli Studi , Foggia , Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E","family":"Benvenuto","sequence":"additional","affiliation":[{"name":"Area Cardiorenale Metabolica Associazione nazionale Medici Cardiologi Ospedalieri Italia"},{"name":"U.O.C. di Cardiologia-UTIC-Emodinamica PO \u2018G. Mazzini\u2019 Teramo , Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E","family":"Vanoli","sequence":"additional","affiliation":[{"name":"Department of Molecular Medicine, University of Pavia , Pavia , Italy"},{"name":"Department of Medicine, Cardiology and Rehabilitation Sacra Famiglia Hospital , Erba , Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2022,8,17]]},"reference":[{"key":"2022081718190996500_suac030-B1","doi-asserted-by":"crossref","first-page":"1675","DOI":"10.1016\/j.jacc.2004.07.041","article-title":"Ephedrine increases ventricular arrhythmias in conscious dogs after myocardial infarction","volume":"44","author":"Adamson","year":"2004","journal-title":"J Am Coll Cardiol"},{"key":"2022081718190996500_suac030-B2","doi-asserted-by":"crossref","first-page":"1374","DOI":"10.1016\/S0140-6736(79)92010-5","article-title":"Prolongation of survival in congestive cardiomyopathy during treatment with beta-receptor blockade","volume":"1","author":"Swedberg","year":"1979","journal-title":"Lancet"},{"key":"2022081718190996500_suac030-B3","doi-asserted-by":"crossref","first-page":"1349","DOI":"10.1056\/NEJM199605233342101","article-title":"The effect of carvedilol on morbidity and mortality in patients with chronic heart failure. 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