Remote ischemic conditioning: from experimental observation to clinical application: report from the 8th Biennial Hatter Cardiovascular Institute Workshop
posted on 2016-02-10, 15:20authored byJ. M. J. Pickard, H. E. Bøtker, G. Crimi, B. Davidson, S. M. Davidson, D. Dutka, P. Ferdinandy, R. Ganske, D. Garcia-Dorado, Z. Giricz, A. V. Gourine, G. Heusch, R. Kharbanda, P. Kleinbongard, R. MacAllister, C. McIntyre, P. Meybohm, F. Prunier, A. Redington, N. J. Robertson, M. S. Suleiman, Andrew Vanezis, S. Walsh, D. M. Yellon, D. J. Hausenloy
In 1993, Przyklenk and colleagues made the intriguing experimental observation that ‘brief ischemia in one vascular bed also protects remote, virgin myocardium from subsequent sustained coronary artery occlusion’ and that this effect ‘…. may be mediated by factor(s) activated, produced, or transported throughout the heart during brief ischemia/reperfusion’. This seminal study laid the foundation for the discovery of ‘remote ischemic conditioning’ (RIC), a phenomenon in which the heart is protected from the detrimental effects of acute ischemia/reperfusion injury (IRI), by applying cycles of brief ischemia and reperfusion to an organ or tissue remote from the heart. The concept of RIC quickly evolved to extend beyond the heart, encompassing inter-organ protection against acute IRI. The crucial discovery that the protective RIC stimulus could be applied non-invasively, by simply inflating and deflating a blood pressure cuff placed on the upper arm to induce cycles of brief ischemia and reperfusion, has facilitated the translation of RIC into the clinical setting. Despite intensive investigation over the last 20 years, the underlying mechanisms continue to elude researchers. In the 8th Biennial Hatter Cardiovascular Institute Workshop, recent developments in the field of RIC were discussed with a focus on new insights into the underlying mechanisms, the diversity of non-cardiac protection, new clinical applications, and large outcome studies. The scientific advances made in this field of research highlight the journey that RIC has made from being an intriguing experimental observation to a clinical application with patient benefit.
Funding
JMJP, DMY and DJH are funded by the British
Heart Foundation (grant numbers FS/10/039/28270 and FS 12/70/
30009), the Rosetrees Trust, and the National Institute for Health
Research University College London Hospitals Biomedical Research
Centre of which DMY is a Senior Investigator. GH is supported by
the German Research Foundation (He1320/18-3). PF and ZG are
funded by the Hungarian Scientific Research Fund (OTKA PD
109051, OTKA ANN 107803). ZG holds a ‘‘Ja´nosBolyai Fellowship’’
from the Hungarian Academy of Sciences. PF is a Szenta´gothai
Fellow of the Hungarian National Program of Excellence (TAMOP
4.2.4.A/2-11-1-2012-0001). RKK is supported by the Oxford Comprehensive
Biomedical Research Centre NIHR program. SD is funded
by the Medical Research Council (MR/K002066/1). PM is supported
by the German Research Foundation (ME 3559/1-1), the International
Anesthesia Research Society and the German Society of Anesthesiology
and Intensive Care Medicine. AVG is a Wellcome Trust Senior
Research Fellow. MSS is supported by The NIHR Bristol Biomedical
Research Unit in Cardiovascular Disease. HEB was supported by the
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Novo Nordic Foundation, Fondation Leducq (06CVD), the Danish
Research Council for Strategic Research (11-115818), the Danish
Research Council (11-108354). NJR was funded by the MRC (MR/
J00457X/1). Funded in part by the Cambridge NIHR Comprehensive
Biomedical Research Centre.