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Cardiac Mitochondria and Heart Failure: The Chicken or the Egg?

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Annual Update in Intensive Care and Emergency Medicine 2011

Part of the book series: Annual Update in Intensive Care and Emergency Medicine 2011 ((AUICEM,volume 1))

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Abstract

Current medical therapies for heart failure are aimed at suppressing the neurohormonal activation (e.g., angiotensin converting enzyme [ACE] inhibitors, angiotensin II receptor antagonists, beta-adrenergic receptor antagonists, aldosterone receptor antagonists) and/or treating fluid volume overload and hemodynamic symptoms (diuretics, digoxin, inotropic agents) [1, 2]. Evidence suggests that intense suppression of the neurohormonal systems does not provide further benefit compared with more modest therapy. There is a need for novel therapies for heart failure that are independent of the neurohormonal axis and can improve cardiac performance and prevent the progression of heart failure and heart remodeling [3]. Modulation of mitochondrial metabolism and the oxidative status of the myocardium may represent a new approach to the treatment of heart failure and could work additively with standard medical therapy while not exerting negative hemodynamic effects [4].

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Scolletta, S., Biagioli, B., Giomarelli, P. (2011). Cardiac Mitochondria and Heart Failure: The Chicken or the Egg?. In: Vincent, JL. (eds) Annual Update in Intensive Care and Emergency Medicine 2011. Annual Update in Intensive Care and Emergency Medicine 2011, vol 1. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-18081-1_18

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  • DOI: https://doi.org/10.1007/978-3-642-18081-1_18

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-18080-4

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