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

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 bil...

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Detalles Bibliográficos
Autores: Davidson, Sean M., Arjun, Sapna, Basalay, Maryna V., Bell, Robert M., Bromage, Daniel I., Botker, Hans Erik, Carr, Richard D., Cunningham, John, Ghosh, Arjun K., Heusch, Gerd, Ibáñez, Borja, Kleinbongard, Petra, Lecour, Sandrine, Maddock, Helen, Ovize, Michel, Walker, Malcolm, Wiart, Marlene, Yellon, Derek M.
Tipo de recurso: artículo
Fecha de publicación:2018
País:España
Institución:Instituto de Salud Carlos III (ISCIII)
Repositorio:Repisalud
Idioma:inglés
OAI Identifier:oai:repisalud.isciii.es:20.500.12105/6528
Acceso en línea:http://hdl.handle.net/20.500.12105/6528
Access Level:acceso abierto
Palabra clave:Anthracycline cardiotoxicity
Cardioprotection
Ischaemic stroke
Myocardial ischaemia
Neuroprotection
Reperfusion
MITOCHONDRIAL PERMEABILITY TRANSITION
ST-SEGMENT ELEVATION
PERCUTANEOUS CORONARY INTERVENTION
RANDOMIZED CONTROLLED-TRIAL
ARTERY-BYPASS SURGERY
HEART POSITION PAPER
NO-REFLOW PHENOMENON
REPERFUSION INJURY
WORKING GROUP
CEREBRAL-ISCHEMIA
Descripción
Sumario: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.