The 10th Biennial Hatter Cardiovascular Institute workshop: cellular protectionevaluating new directions in the setting of myocardial infarction, ischaemic stroke, and cardio-oncology
2018
Davidson, S. M. | Arjun, S. | Basalay, M. V. | Bell, R. M. | Bromage, D. I. | Botker, H. E. | Carr, R. D. | Cunningham, J. | Ghosh, A. K. | Heusch, G. | Ibanez, B. | Kleinbongard, P. | Lecour, S. | Maddock, H. | Ovize, Michel | Walker, M. | Wiart, Marlène | Yellon, D. M.
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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