2026-08-29T13:16:56Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/65282024-09-27T08:17:56Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605
Repisalud
author
Davidson, Sean M.
author
Arjun, Sapna
author
Basalay, Maryna V.
author
Bell, Robert M.
author
Bromage, Daniel I.
author
Botker, Hans Erik
author
Carr, Richard D.
author
Cunningham, John
author
Ghosh, Arjun K.
author
Heusch, Gerd
author
Ibáñez, Borja
author
Kleinbongard, Petra
author
Lecour, Sandrine
author
Maddock, Helen
author
Ovize, Michel
author
Walker, Malcolm
author
Wiart, Marlene
author
Yellon, Derek M.
funder
British Heart Foundation
funder
Deutsche Forschungsgemeinschaft (Alemania)
2018-10-26T07:59:24Z
2018-10-26T07:59:24Z
2018
Basic Res Cardiol. 2018; 113(6):43
10.1007/s00395-018-0704-z
1435-1803
0300-8428
Basic Research in Cardiology
30310998
http://hdl.handle.net/20.500.12105/6528
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.
eng
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
The 10th Biennial Hatter Cardiovascular Institute workshop: cellular protectionevaluating new directions in the setting of myocardial infarction, ischaemic stroke, and cardio-oncology
journal article
URL
https://repisalud.isciii.es/bitstreams/841c1302-37a7-4ed0-b8a4-3d4694940eda/download
File
MD5
3d743cf29332c6abc5197dec38e07532
955328
application/pdf
The10thBiennialHatter _2018.pdf
URL
https://repisalud.isciii.es/bitstreams/cbb6905f-2658-40e1-9067-ddac98ef2da8/download
File
MD5
de7caa1af94172f2098d54c13aa336f5
61984
text/plain
The10thBiennialHatter _2018.pdf.txt