The 10th Biennial Hatter Cardiovascular Institute workshop: cellular protection—evaluating new directions in the setting of myocardial infarction, ischaemic stroke, and cardio-oncology

Sean M. Davidson; Sapna Arjun; Maryna V. Basalay; Robert M. Bell; Daniel I. Bromage; Hans Erik Bøtker; Richard D. Carr; John Cunningham; Arjun K. Ghosh; Gerd Heusch; Borja Ibanez; Petra Kleinbongard; Sandrine Lecour; Helen Maddock; Michel Ovize; Malcolm Walker; Marlene Wiart; Derek M. Yellon

doi:10.1007/s00395-018-0704-z

The 10th Biennial Hatter Cardiovascular Institute workshop: cellular protection—evaluating new directions in the setting of myocardial infarction, ischaemic stroke, and cardio-oncology

Sean M. Davidson, Sapna Arjun, Maryna V. Basalay, Robert M. Bell, Daniel I. Bromage, Hans Erik Bøtker, Richard D. Carr, John Cunningham, Arjun K. Ghosh, Gerd Heusch, Borja Ibanez, Petra Kleinbongard, Sandrine Lecour, Helen Maddock, Michel Ovize, Malcolm Walker, Marlene Wiart, Derek M. Yellon

Research output: Contribution to journal › Conference article › peer-review

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Abstract

Due to its poor capacity for regeneration, the heart is particularly sensitive to the loss of contractile cardiomyocytes. The onslaught of damage caused by ischaemia and reperfusion, occurring during an acute myocardial infarction and the subsequent reperfusion therapy, can wipe out upwards of a billion cardiomyocytes. A similar program of cell death can cause the irreversible loss of neurons in ischaemic stroke. Similar pathways of lethal cell injury can contribute to other pathologies such as left ventricular dysfunction and heart failure caused by cancer therapy. Consequently, strategies designed to protect the heart from lethal cell injury have the potential to be applicable across all three pathologies. The investigators meeting at the 10th Hatter Cardiovascular Institute workshop examined the parallels between ST-segment elevation myocardial infarction (STEMI), ischaemic stroke, and other pathologies that cause the loss of cardiomyocytes including cancer therapeutic cardiotoxicity. They examined the prospects for protection by remote ischaemic conditioning (RIC) in each scenario, and evaluated impasses and novel opportunities for cellular protection, with the future landscape for RIC in the clinical setting to be determined by the outcome of the large ERIC-PPCI/CONDI2 study. It was agreed that the way forward must include measures to improve experimental methodologies, such that they better reflect the clinical scenario and to judiciously select combinations of therapies targeting specific pathways of cellular death and injury.

Original language	English
Number of pages	11
Journal	Basic Research in Cardiology
Volume	113
Issue number	43
Early online date	11 Oct 2018
DOIs	https://doi.org/10.1007/s00395-018-0704-z
Publication status	Published - 1 Nov 2018

Bibliographical note

This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

Keywords

Anthracycline cardiotoxicity
Cardioprotection
Ischaemic stroke
Myocardial ischaemia
Neuroprotection
Reperfusion

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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Cite this

Davidson, S. M., Arjun, S., Basalay, M. V., Bell, R. M., Bromage, D. I., Bøtker, H. E., Carr, R. D., Cunningham, J., Ghosh, A. K., Heusch, G., Ibanez, B., Kleinbongard, P., Lecour, S., Maddock, H., Ovize, M., Walker, M., Wiart, M., & Yellon, D. M. (2018). The 10th Biennial Hatter Cardiovascular Institute workshop: cellular protection—evaluating new directions in the setting of myocardial infarction, ischaemic stroke, and cardio-oncology. Basic Research in Cardiology, 113(43). https://doi.org/10.1007/s00395-018-0704-z

The 10th Biennial Hatter Cardiovascular Institute workshop: cellular protection—evaluating new directions in the setting of myocardial infarction, ischaemic stroke, and cardio-oncology. / Davidson, Sean M.; Arjun, Sapna; Basalay, Maryna V. et al.
In: Basic Research in Cardiology, Vol. 113, No. 43, 01.11.2018.

Research output: Contribution to journal › Conference article › peer-review

Davidson, SM, Arjun, S, Basalay, MV, Bell, RM, Bromage, DI, Bøtker, HE, Carr, RD, Cunningham, J, Ghosh, AK, Heusch, G, Ibanez, B, Kleinbongard, P, Lecour, S, Maddock, H, Ovize, M, Walker, M, Wiart, M & Yellon, DM 2018, 'The 10th Biennial Hatter Cardiovascular Institute workshop: cellular protection—evaluating new directions in the setting of myocardial infarction, ischaemic stroke, and cardio-oncology', Basic Research in Cardiology, vol. 113, no. 43. https://doi.org/10.1007/s00395-018-0704-z

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title = "The 10th Biennial Hatter Cardiovascular Institute workshop: cellular protection—evaluating new directions in the setting of myocardial infarction, ischaemic stroke, and cardio-oncology",

abstract = "Due to its poor capacity for regeneration, the heart is particularly sensitive to the loss of contractile cardiomyocytes. The onslaught of damage caused by ischaemia and reperfusion, occurring during an acute myocardial infarction and the subsequent reperfusion therapy, can wipe out upwards of a billion cardiomyocytes. A similar program of cell death can cause the irreversible loss of neurons in ischaemic stroke. Similar pathways of lethal cell injury can contribute to other pathologies such as left ventricular dysfunction and heart failure caused by cancer therapy. Consequently, strategies designed to protect the heart from lethal cell injury have the potential to be applicable across all three pathologies. The investigators meeting at the 10th Hatter Cardiovascular Institute workshop examined the parallels between ST-segment elevation myocardial infarction (STEMI), ischaemic stroke, and other pathologies that cause the loss of cardiomyocytes including cancer therapeutic cardiotoxicity. They examined the prospects for protection by remote ischaemic conditioning (RIC) in each scenario, and evaluated impasses and novel opportunities for cellular protection, with the future landscape for RIC in the clinical setting to be determined by the outcome of the large ERIC-PPCI/CONDI2 study. It was agreed that the way forward must include measures to improve experimental methodologies, such that they better reflect the clinical scenario and to judiciously select combinations of therapies targeting specific pathways of cellular death and injury.",

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AU - Yellon, Derek M.

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N2 - Due to its poor capacity for regeneration, the heart is particularly sensitive to the loss of contractile cardiomyocytes. The onslaught of damage caused by ischaemia and reperfusion, occurring during an acute myocardial infarction and the subsequent reperfusion therapy, can wipe out upwards of a billion cardiomyocytes. A similar program of cell death can cause the irreversible loss of neurons in ischaemic stroke. Similar pathways of lethal cell injury can contribute to other pathologies such as left ventricular dysfunction and heart failure caused by cancer therapy. Consequently, strategies designed to protect the heart from lethal cell injury have the potential to be applicable across all three pathologies. The investigators meeting at the 10th Hatter Cardiovascular Institute workshop examined the parallels between ST-segment elevation myocardial infarction (STEMI), ischaemic stroke, and other pathologies that cause the loss of cardiomyocytes including cancer therapeutic cardiotoxicity. They examined the prospects for protection by remote ischaemic conditioning (RIC) in each scenario, and evaluated impasses and novel opportunities for cellular protection, with the future landscape for RIC in the clinical setting to be determined by the outcome of the large ERIC-PPCI/CONDI2 study. It was agreed that the way forward must include measures to improve experimental methodologies, such that they better reflect the clinical scenario and to judiciously select combinations of therapies targeting specific pathways of cellular death and injury.

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The 10th Biennial Hatter Cardiovascular Institute workshop: cellular protection—evaluating new directions in the setting of myocardial infarction, ischaemic stroke, and cardio-oncology

Abstract

Bibliographical note

Keywords

UN SDGs

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