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Chemohypersensitivity and Autonomic Modulation of Venous Capacitance in the Pathophysiology of Acute Decompensated Heart Failure

  • Pathophysiology: Neuroendocrine, Vascular, and Metabolic Factors (SD Katz, Section Editor)
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Abstract

Heart failure is increasing in prevalence around the world, with hospitalization and re-hospitalization as a result of acute decompensated heart failure (ADHF) presenting a huge social and economic burden. The mechanism for this decompensation is not clear. Whilst in some cases it is due to volume expansion, over half of patients with an acute admission for ADHF did not experience an increase in total body weight. This calls into question the current treatment strategy of targeting salt and water retention in ADHF. An alternative hypothesis proposed by Fallick et al. is that an endogenous fluid shift from the splanchnic bed is implicated in ADHF, rather than an exogenous fluid gain. The hypothesis states further that this shift is triggered by an increase in sympathetic tone causing vasoconstriction in the splanchnic bed, a mechanism that can translocate blood rapidly into the effective circulating volume, generating the raised venous pressure and congestion seen in ADHF. This hypothesis encourages a new clinical paradigm which focuses on the underlying mechanisms of congestion, and highlights the importance of fluid redistribution and neurohormonal activation in its pathophysiology. In this article, we consider the concept that ADHF is attributable to episodic sympathetic hyperactivity, resulting in fluid shifts from the splanchnic bed. Chemosensitivity is a pathologic autonomic mechanism associated with mortality in patients with systolic heart failure. Tonic and episodic activity of the peripheral chemoreceptors may underlie the syndrome of acute decompensation without total body salt and water expansion. We suggest in this manuscript that chemosensitivity in response to intermittent hypoxia, such as experienced in sleep disordered breathing, may explain the intermittent sympathetic hyperactivity underlying renal sodium retention and acute volume redistribution from venous storage sites. This hypothesis provides an alternative structure to guide novel diagnostic and treatment strategies for ADHF.

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Conflict of Interest

Amy E. Burchell declares she has no conflict of interest.

Paul A. Sobotka has received compensation for serving as Chief Medical Officer of Cibiem, Inc.; compensation for serving as a consultant for Medtronic, Inc.; payment for lectures including service on speakers bureaus from Medtronic, Inc.; compensation for patents from Cibiem, Inc. (device to modulate the carotid body) and Medtronic, Inc. (applications related to renal denervation); royalties from Medtronic, Inc. for the Symplicity Renal Denervation System; compensatory stock options from Cibiem, Inc., Rox, Inc., and Ardelyx, Inc. for services rendered; reimbursement for travel/accommodations/meeting expenses from Medtronic, Inc.

Emma C. Hart has received compensation from Cibiem, Inc. for serving as a consultant in a clinical trial associated with developing a new intervention for improving prognosis of heart failure.

Angus K. Nightingale has received compensation from Novartis for serving as a member of the United Kingdom Advisory Board on Serelaxin; supported by a grant from Cibiem, Inc. for a study on carotid body modulation in hypertension; payment for lectures including service on speakers bureaus from Servier; reimbursement for travel/accommodations/meeting expenses from Novartis and Servier; payment to Bristol Heart Institute from Medtronic, Inc. for training of physicians and other staff in renal denervation.

Mark E. Dunlap has received compensation for serving as a consultant for Medtronic/Ardian, Inc.; supported by grants from BioControl Medical, Inc. and Medtronic/Ardian, Inc.; payment for lectures including service on speakers bureaus from BioControl Medical, Inc.

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Authors and Affiliations

  1. Bristol CardioNomics Group, Bristol Heart Institute, Bristol Royal Infirmary, Bristol, BS2 8HW, UK

    Amy E. Burchell, Emma C. Hart & Angus K. Nightingale

  2. Paul A. Sobotka, The Ohio State University, Columbus, OH, UK

    Paul A. Sobotka

  3. Heart and Vascular Center H350, MetroHealth Campus of Case Western Reserve University, 2500 MetroHealth Dr., Cleveland, OH, 44109, USA

    Mark E. Dunlap

  4. School of Clinical Sciences, University of Bristol, Research Floor Level 7, Queens Building, Bristol Royal Infirmary, Marlborough Street, Bristol, BS2 8HW, UK

    Amy E. Burchell

  5. School of Physiology and Pharmacology, University of Bristol, Medical Sciences Building, University Walk, Bristol, BS8 1TD, UK

    Emma C. Hart

  6. Cardiology Department, Bristol Heart Institute, University Hospitals Bristol NHS Foundation Trust, Bristol, BS2 8HW, UK

    Angus K. Nightingale

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  1. Amy E. Burchell
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  2. Paul A. Sobotka
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Correspondence to Mark E. Dunlap.

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Burchell, A.E., Sobotka, P.A., Hart, E.C. et al. Chemohypersensitivity and Autonomic Modulation of Venous Capacitance in the Pathophysiology of Acute Decompensated Heart Failure. Curr Heart Fail Rep 10, 139–146 (2013). https://doi.org/10.1007/s11897-013-0135-y

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