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      Chronic vagal stimulation for the treatment of low ejection fraction heart failure: results of the NEural Cardiac TherApy foR Heart Failure (NECTAR-HF) randomized controlled trial.

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          Abstract

          The neural cardiac therapy for heart failure (NECTAR-HF) was a randomized sham-controlled trial designed to evaluate whether a single dose of vagal nerve stimulation (VNS) would attenuate cardiac remodelling, improve cardiac function and increase exercise capacity in symptomatic heart failure patients with severe left ventricular (LV) systolic dysfunction despite guideline recommended medical therapy.

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          Nicotinic acetylcholine receptor alpha7 subunit is an essential regulator of inflammation.

          Hong. Wang, Man Yu, Mahendar Ochani … (2003)
          Excessive inflammation and tumour-necrosis factor (TNF) synthesis cause morbidity and mortality in diverse human diseases including endotoxaemia, sepsis, rheumatoid arthritis and inflammatory bowel disease. Highly conserved, endogenous mechanisms normally regulate the magnitude of innate immune responses and prevent excessive inflammation. The nervous system, through the vagus nerve, can inhibit significantly and rapidly the release of macrophage TNF, and attenuate systemic inflammatory responses. This physiological mechanism, termed the 'cholinergic anti-inflammatory pathway' has major implications in immunology and in therapeutics; however, the identity of the essential macrophage acetylcholine-mediated (cholinergic) receptor that responds to vagus nerve signals was previously unknown. Here we report that the nicotinic acetylcholine receptor alpha7 subunit is required for acetylcholine inhibition of macrophage TNF release. Electrical stimulation of the vagus nerve inhibits TNF synthesis in wild-type mice, but fails to inhibit TNF synthesis in alpha7-deficient mice. Thus, the nicotinic acetylcholine receptor alpha7 subunit is essential for inhibiting cytokine synthesis by the cholinergic anti-inflammatory pathway.
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            Vagal nerve stimulation markedly improves long-term survival after chronic heart failure in rats.

            Meihua Li, Can Zheng, Takayuki Sato … (2004)
            Diminished cardiac vagal activity and higher heart rate predict a high mortality rate of chronic heart failure (CHF) after myocardial infarction. We investigated the effects of chronic electrical stimulation of the vagus nerve on cardiac remodeling and long-term survival in an animal model of CHF after large myocardial infarction. Two weeks after the ligation of the left coronary artery, surviving rats were randomized to vagal- and sham-stimulated groups. Using an implantable miniature radio-controlled electrical stimulator, we stimulated the right vagal nerve of CHF rats for 6 weeks. The intensity of electrical stimulation was adjusted for each rat, so that the heart rate was lowered by 20 to 30 beats per minute. The treated rats had significantly lower left ventricular end-diastolic pressure (17.1+/-5.9 versus 23.5+/-4.2 mm Hg, P<0.05) and higher maximum dp/dt of left ventricular pressure (4152+/-237 versus 2987+/-192 mm Hg/s, P<0.05) than the untreated rats. Improvement of cardiac pumping function was accompanied by a decrease in normalized biventricular weight (2.75+/-0.25 versus 3.14+/-0.22 g/kg, P<0.01). Although the 140-day survival of the untreated group was only half, vagal stimulation markedly improved the survival rate (86% versus 50%, P=0.008). Vagal stimulation therapy achieved a 73% reduction in a relative risk ratio of death. Vagal nerve stimulation markedly improved the long-term survival of CHF rats through the prevention of pumping failure and cardiac remodeling.
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              Pharmacological Stimulation of the Cholinergic Antiinflammatory Pathway

              Thomas R. Bernik, Steven G. Friedman, Mahendar Ochani … (2002)
              Efferent activity in the vagus nerve can prevent endotoxin-induced shock by attenuating tumor necrosis factor (TNF) synthesis. Termed the “cholinergic antiinflammatory pathway,” inhibition of TNF synthesis is dependent on nicotinic α-bungarotoxin-sensitive acetylcholine receptors on macrophages. Vagus nerve firing is also stimulated by CNI-1493, a tetravalent guanylhydrazone molecule that inhibits systemic inflammation. Here, we studied the effects of pharmacological and electrical stimulation of the intact vagus nerve in adult male Lewis rats subjected to endotoxin-induced shock to determine whether intact vagus nerve signaling is required for the antiinflammatory action of CNI-1493. CNI-1493 administered via the intracerebroventricular route was 100,000-fold more effective in suppressing endotoxin-induced TNF release and shock as compared with intravenous dosing. Surgical or chemical vagotomy rendered animals sensitive to TNF release and shock, despite treatment with CNI-1493, indicating that an intact cholinergic antiinflammatory pathway is required for antiinflammatory efficacy in vivo. Electrical stimulation of either the right or left intact vagus nerve conferred significant protection against endotoxin-induced shock, and specifically attenuated serum and myocardial TNF, but not pulmonary TNF synthesis, as compared with sham-operated animals. Together, these results indicate that stimulation of the cholinergic antiinflammatory pathway by either pharmacological or electrical methods can attenuate the systemic inflammatory response to endotoxin-induced shock.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): Eur. Heart J.
                Title: European heart journal
                Publisher: Oxford University Press (OUP)
                ISSN (Electronic): 1522-9645
                ISSN (Print): 0195-668X
                Publication date (Electronic): Feb 14 2015
                Volume: 36
                Issue: 7
                Affiliations
                [1 ] Inserm, CIC 1433, Centre Hospitalier Universitaire, Department of Cardiology, Nancy University, Université de Lorraine, Nancy, France f.zannad@chu-nancy.fr.
                [2 ] Department of Cardiology and Cardiovascular Clinical Research Center, Fondazione IRCCS, Policlinico San Matteo, Pavia, Italy.
                [3 ] Department of Cardiology, University Medical Center, Utrecht, The Netherlands.
                [4 ] Department of Cardiology, Liverpool Heart and Chest, Liverpool, UK.
                [5 ] Thorax Institute, Hospital Clinic, Barcelona, Spain.
                [6 ] Heart Centre Brandenburg Hospital, Bernau, Germany.
                [7 ] Division of Cardiology, Otto-von-Guericke Universität Magdeburg, Magdeburg, Germany.
                [8 ] Boston Scientific Corporation, St. Paul, MN, USA.
                [9 ] Guidant Europe, Diegem, Belgium.
                [10 ] Department of Cardiology, Homolka Hospital, Prague, Czech Republic.
                [11 ] Department of Cardiology, Catharina Hospital, Eindhoven, The Netherlands.
                [12 ] Azienda Ospedaliera dei Colli - Monaldi, Napoli, Italy.
                [13 ] Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
                Article
                Publisher Item ID: ehu345
                DOI: 10.1093/eurheartj/ehu345
                PMC ID: 4328197
                PubMed ID: 25176942
                SO-VID: bd78fd5a-e740-4b37-a6cd-f54ab64d9103
                History

                Keywords: Autonomic nervous system,Heart failure,Vagal stimulation
                Data availability:
                Keywords: Autonomic nervous system, Heart failure, Vagal stimulation

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