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Treatments targeting inotropy

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Treatments targeting inotropy : A position paper of the Committees on Translational Research and Acute Heart Failure of the Heart Failure Association (HFA) of the European Society of Cardiology (ESC). / Maack, Christoph; Eschenhagen, Thomas; Hamdani, Nazha; Heinzel, Frank R.; Lyon, Alexander R.; Manstein, Dietmar; Metzger, Joseph; Papp, Zoltán; Tocchetti, Carlo G; Yilmaz, Mehmet Birhan; Anker, Stefan D.; Balligand, Jean-Luc; Bauersachs, Johann; Brutsaert, Dirk; Carrier, Lucie; Chlopicki, Stefan; Cleland, John G.; de Boer, Rudolf A.; Dietl, Alexander; Fischmeister, Rodolphe; Harjola, Veli-Pekka; Heymans, Stephane; Hilfiker-Kleiner, Denise; Holzmeister, Johannes; de Keulenaer, Gilles; Limongelli, Giuseppe; Linke, Wolfgang A; Lund, Lars H.; Masip, Josef; Metra, Marco; Mueller, Christian; Pieske, Burkert; Ponikowski, Piotr; Ristic, Arsen; Ruschitzka, Frank; Seferovic, Petar M.; Skouri, Hadi; Zimmermann, Wolfram H.; Mebazaa, Alexandre.

In: EUR HEART J, 2018.

Research output: SCORING: Contribution to journal › SCORING: Review article › Research

Harvard

Maack, C, Eschenhagen, T, Hamdani, N, Heinzel, FR, Lyon, AR, Manstein, D, Metzger, J, Papp, Z, Tocchetti, CG, Yilmaz, MB, Anker, SD, Balligand, J-L, Bauersachs, J, Brutsaert, D, Carrier, L, Chlopicki, S, Cleland, JG, de Boer, RA, Dietl, A, Fischmeister, R, Harjola, V-P, Heymans, S, Hilfiker-Kleiner, D, Holzmeister, J, de Keulenaer, G, Limongelli, G, Linke, WA, Lund, LH, Masip, J, Metra, M, Mueller, C, Pieske, B, Ponikowski, P, Ristic, A, Ruschitzka, F, Seferovic, PM, Skouri, H, Zimmermann, WH & Mebazaa, A 2018, 'Treatments targeting inotropy: A position paper of the Committees on Translational Research and Acute Heart Failure of the Heart Failure Association (HFA) of the European Society of Cardiology (ESC)', EUR HEART J. https://doi.org/10.1093/eurheartj/ehy600

APA

Maack, C., Eschenhagen, T., Hamdani, N., Heinzel, F. R., Lyon, A. R., Manstein, D., Metzger, J., Papp, Z., Tocchetti, C. G., Yilmaz, M. B., Anker, S. D., Balligand, J-L., Bauersachs, J., Brutsaert, D., Carrier, L., Chlopicki, S., Cleland, J. G., de Boer, R. A., Dietl, A., ... Mebazaa, A. (2018). Treatments targeting inotropy: A position paper of the Committees on Translational Research and Acute Heart Failure of the Heart Failure Association (HFA) of the European Society of Cardiology (ESC). EUR HEART J. https://doi.org/10.1093/eurheartj/ehy600

Vancouver

Maack C, Eschenhagen T, Hamdani N, Heinzel FR, Lyon AR, Manstein D et al. Treatments targeting inotropy: A position paper of the Committees on Translational Research and Acute Heart Failure of the Heart Failure Association (HFA) of the European Society of Cardiology (ESC). EUR HEART J. 2018. https://doi.org/10.1093/eurheartj/ehy600

Bibtex

@article{5c5989cd41aa42c79b6e8dc41db43505,
title = "Treatments targeting inotropy: A position paper of the Committees on Translational Research and Acute Heart Failure of the Heart Failure Association (HFA) of the European Society of Cardiology (ESC)",
abstract = "Acute heart failure and in particular, cardiogenic shock are associated with high morbidity and mortality. A therapeutic dilemma is that the use of positive inotropic agents, such as catecholamines or phosphodiesterase-inhibitors, is associated with increased mortality. Newer drugs, such as levosimendan or omecamtiv mecarbil, target sarcomeres to improve systolic function putatively without elevating intracellular Ca2+. Although meta-analyses of smaller trialssuggested that levosimendan is associated with a better outcome than dobutamine, larger comparative trials failed to confirm this observation. For omecamtiv mecarbil, phase II clinical trials suggest a favorable hemodynamic profile in patients with acute and chronic heart failure, and a phase III morbidity/mortality trial in patients with chronic heart failure has recently begun. Here, we review the pathophysiological basis of systolic dysfunction in patients with heart failure and the mechanisms through which different inotropic agents improve cardiac function. Since adenosine triphosphate and reactive oxygen species production in mitochondria are intimately linked to the processes of excitation-contraction coupling, we also discuss the impactof inotropic agents on mitochondrial bioenergetics and redox regulation. Therefore, this position paper should help identify novel targets for treatments that could not only safely improve systolic and diastolic function acutely, but potentially also myocardial structure and function over a longer term.",
author = "Christoph Maack and Thomas Eschenhagen and Nazha Hamdani and Heinzel, {Frank R.} and Lyon, {Alexander R.} and Dietmar Manstein and Joseph Metzger and Zolt{\'a}n Papp and Tocchetti, {Carlo G} and Yilmaz, {Mehmet Birhan} and Anker, {Stefan D.} and Jean-Luc Balligand and Johann Bauersachs and Dirk Brutsaert and Lucie Carrier and Stefan Chlopicki and Cleland, {John G.} and {de Boer}, {Rudolf A.} and Alexander Dietl and Rodolphe Fischmeister and Veli-Pekka Harjola and Stephane Heymans and Denise Hilfiker-Kleiner and Johannes Holzmeister and {de Keulenaer}, Gilles and Giuseppe Limongelli and Linke, {Wolfgang A} and Lund, {Lars H.} and Josef Masip and Marco Metra and Christian Mueller and Burkert Pieske and Piotr Ponikowski and Arsen Ristic and Frank Ruschitzka and Seferovic, {Petar M.} and Hadi Skouri and Zimmermann, {Wolfram H.} and Alexandre Mebazaa",
year = "2018",
doi = "10.1093/eurheartj/ehy600",
language = "English",
journal = "EUR HEART J",
issn = "0195-668X",
publisher = "Oxford University Press",

}

RIS

TY - JOUR

T1 - Treatments targeting inotropy

T2 - A position paper of the Committees on Translational Research and Acute Heart Failure of the Heart Failure Association (HFA) of the European Society of Cardiology (ESC)

AU - Maack, Christoph

AU - Eschenhagen, Thomas

AU - Hamdani, Nazha

AU - Heinzel, Frank R.

AU - Lyon, Alexander R.

AU - Manstein, Dietmar

AU - Metzger, Joseph

AU - Papp, Zoltán

AU - Tocchetti, Carlo G

AU - Yilmaz, Mehmet Birhan

AU - Anker, Stefan D.

AU - Balligand, Jean-Luc

AU - Bauersachs, Johann

AU - Brutsaert, Dirk

AU - Carrier, Lucie

AU - Chlopicki, Stefan

AU - Cleland, John G.

AU - de Boer, Rudolf A.

AU - Dietl, Alexander

AU - Fischmeister, Rodolphe

AU - Harjola, Veli-Pekka

AU - Heymans, Stephane

AU - Hilfiker-Kleiner, Denise

AU - Holzmeister, Johannes

AU - de Keulenaer, Gilles

AU - Limongelli, Giuseppe

AU - Linke, Wolfgang A

AU - Lund, Lars H.

AU - Masip, Josef

AU - Metra, Marco

AU - Mueller, Christian

AU - Pieske, Burkert

AU - Ponikowski, Piotr

AU - Ristic, Arsen

AU - Ruschitzka, Frank

AU - Seferovic, Petar M.

AU - Skouri, Hadi

AU - Zimmermann, Wolfram H.

AU - Mebazaa, Alexandre

PY - 2018

Y1 - 2018

N2 - Acute heart failure and in particular, cardiogenic shock are associated with high morbidity and mortality. A therapeutic dilemma is that the use of positive inotropic agents, such as catecholamines or phosphodiesterase-inhibitors, is associated with increased mortality. Newer drugs, such as levosimendan or omecamtiv mecarbil, target sarcomeres to improve systolic function putatively without elevating intracellular Ca2+. Although meta-analyses of smaller trialssuggested that levosimendan is associated with a better outcome than dobutamine, larger comparative trials failed to confirm this observation. For omecamtiv mecarbil, phase II clinical trials suggest a favorable hemodynamic profile in patients with acute and chronic heart failure, and a phase III morbidity/mortality trial in patients with chronic heart failure has recently begun. Here, we review the pathophysiological basis of systolic dysfunction in patients with heart failure and the mechanisms through which different inotropic agents improve cardiac function. Since adenosine triphosphate and reactive oxygen species production in mitochondria are intimately linked to the processes of excitation-contraction coupling, we also discuss the impactof inotropic agents on mitochondrial bioenergetics and redox regulation. Therefore, this position paper should help identify novel targets for treatments that could not only safely improve systolic and diastolic function acutely, but potentially also myocardial structure and function over a longer term.

AB - Acute heart failure and in particular, cardiogenic shock are associated with high morbidity and mortality. A therapeutic dilemma is that the use of positive inotropic agents, such as catecholamines or phosphodiesterase-inhibitors, is associated with increased mortality. Newer drugs, such as levosimendan or omecamtiv mecarbil, target sarcomeres to improve systolic function putatively without elevating intracellular Ca2+. Although meta-analyses of smaller trialssuggested that levosimendan is associated with a better outcome than dobutamine, larger comparative trials failed to confirm this observation. For omecamtiv mecarbil, phase II clinical trials suggest a favorable hemodynamic profile in patients with acute and chronic heart failure, and a phase III morbidity/mortality trial in patients with chronic heart failure has recently begun. Here, we review the pathophysiological basis of systolic dysfunction in patients with heart failure and the mechanisms through which different inotropic agents improve cardiac function. Since adenosine triphosphate and reactive oxygen species production in mitochondria are intimately linked to the processes of excitation-contraction coupling, we also discuss the impactof inotropic agents on mitochondrial bioenergetics and redox regulation. Therefore, this position paper should help identify novel targets for treatments that could not only safely improve systolic and diastolic function acutely, but potentially also myocardial structure and function over a longer term.

U2 - 10.1093/eurheartj/ehy600

DO - 10.1093/eurheartj/ehy600

M3 - SCORING: Review article

JO - EUR HEART J

JF - EUR HEART J

SN - 0195-668X

ER -