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. 2018 Oct 11;113(6):43.
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  1 , Sapna Arjun  1 , Maryna V Basalay  1 , Robert M Bell  1 , Daniel I Bromage  2 , Hans Erik Bøtker  3 , Richard D Carr  1   4 , John Cunningham  5 , Arjun K Ghosh  1 , Gerd Heusch  6 , Borja Ibanez  7   8   9 , Petra Kleinbongard  6 , Sandrine Lecour  10 , Helen Maddock  11 , Michel Ovize  12 , Malcolm Walker  1 , Marlene Wiart  12   13 , Derek M Yellon  14
Affiliations

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 et al. Basic Res Cardiol. .

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.

Keywords: Anthracycline cardiotoxicity; Cardioprotection; Ischaemic stroke; Myocardial ischaemia; Neuroprotection; Reperfusion.

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Conflict of interest statement

Dr Richard Carr is an employee of MSD A/S, Copenhagen V, Denmark. There are no other conflicts of interest to declare.

Figures

Fig. 1
Fig. 1
In the brain, middle cerebral artery occlusion results in a gradient of reduction in cerebral blood flow from the ischaemic core (red) through the penumbra and oligaemia (blue) to normally perfused cortex (grey). No reflow may also occur from 5 to 10 min. In the heart, occlusion of the LAD followed by reperfusion results in an ischaemia area risk in which a transmural infarct slowly develops, followed by the appearance of a zone of no reflow within the infarct
Fig. 2
Fig. 2
MRI images of a rat subject to middle cerebral artery (MCA) occlusion and reperfusion, illustrating recruitment of the ischaemic penumbra in the infarct. The top panels confirm the complete occlusion of the MCA and show the perfusion-weighted and diffusion-weighted images, which when combined reveal the ischaemic penumbra. In the lower panel, after 24 h part of the penumbra has been recruited into the area of infarct, and brain swelling has caused a quantifiable shift of the midline
See this image and copyright information in PMC

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