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1. Early remote ischaemic preconditioning leads to sustained improvement in allograft function after live donor kidney transplantation: long-term outcomes in the REnal Protection Against Ischaemia–Reperfusion in transplantation (REPAIR) randomised trial

Author

Veighey, Kristin V., Nicholas, Jennifer M., Clayton, Tim, Knight, Rosemary, Robertson, Steven, Dalton, Neil, Harber, Mark, Watson, Christopher J.E., De Fijter, Johan W., Loukogeorgakis, Stavros, and MacAllister, Raymond

Published
2019
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2. Clinical applications of remote ischaemic preconditioning in native and transplant acute kidney injury

Author

Veighey, Kristin and MacAllister, Raymond

Subjects
Acute kidney failure -- Care and treatment -- Patient outcomes -- Research, Kidney transplantation -- Physiological aspects -- Research, Health
Abstract

Ischaemia-reperfusion (IR) injury is a composite of the injury sustained during a period of reduced or absent blood flow to a tissue or organ and the additional insult sustained upon reperfusion that limits the amount of tissue that can be salvaged. IR injury plays a central role in both native and transplant acute kidney injury (AKI). Native AKI is associated with increased morbidity and mortality in hospital inpatients, and transplant AKI contributes to graft dysfunction, ultimately limiting graft longevity. In this review, we discuss the potential therapeutic benefits of a cost-effective and low-risk intervention, remote ischaemic preconditioning (RIPC), and its applicability in the prevention and reduction of AKI., Author(s): Kristin Veighey[sup.1] [sup.2] , Raymond MacAllister[sup.1] Author Affiliations: (1) UCL Centre for Clinical Pharmacology & Therapeutics, University College London, The Rayne Building, University Street, WC1E 6JJ, London, UK (2) [...]

Published
2015
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3. Improving the odds of drug development success through human genomics: modelling study

Author

Hingorani, Aroon D., primary, Kuan, Valerie, additional, Finan, Chris, additional, Kruger, Felix A., additional, Gaulton, Anna, additional, Chopade, Sandesh, additional, Sofat, Reecha, additional, MacAllister, Raymond J., additional, Overington, John P., additional, Hemingway, Harry, additional, Denaxas, Spiros, additional, Prieto, David, additional, and Casas, Juan Pablo, additional

Published
2019
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4. Irbesartan in Marfan syndrome (AIMS): a double-blind, placebo-controlled randomised trial

Author

Mullen, Michael, primary, Jin, Xu Yu, additional, Child, Anne, additional, Stuart, A Graham, additional, Dodd, Matthew, additional, Aragon-Martin, José Antonio, additional, Gaze, David, additional, Kiotsekoglou, Anatoli, additional, Yuan, Li, additional, Hu, Jiangting, additional, Foley, Claire, additional, Van Dyck, Laura, additional, Knight, Rosemary, additional, Clayton, Tim, additional, Swan, Lorna, additional, Thomson, John D R, additional, Erdem, Guliz, additional, Crossman, David, additional, Flather, Marcus, additional, Dean, John, additional, Was, Bartosz, additional, Gow, Heather, additional, Murray, Jane, additional, D'Allessandro, Mariella, additional, Christie, Michael, additional, Cooper, Patricia, additional, Booth, Philip, additional, Burns, Sharon, additional, Paterson, Yvonne, additional, Chikermane, Ashish, additional, Assing, Anthony, additional, Cotter, Catherine, additional, Atkins, Gillian, additional, Williamson, Helen, additional, Barclay, Justin, additional, Jennison, Alan, additional, Henderson, Alex, additional, McSkeane, Anna, additional, Fairlamb, Helen, additional, Kelly, Julie, additional, Kelsall, Nicola, additional, Prentice, Scott, additional, O'Sullivan, John, additional, Head-Baister, Alison, additional, Phillipson, Angela, additional, Johnson, Anna, additional, Crossland, D, additional, Oliver, Jack, additional, Davison, Jade, additional, Wake, Jill, additional, Quinn, Louise, additional, Foreman, Maureen, additional, Wealleans, Vera, additional, Walker, Niki, additional, Duncan, Alexis, additional, Tibbs, Evelyn, additional, Kelly, Ruth, additional, Khambadkone, Sachin, additional, Zotti, Bridget, additional, Brady, Cassie, additional, Cervi, Elena, additional, Field, Ella, additional, Szepezvary, Eszter, additional, Mantey, Florence, additional, Riley, Gillian, additional, Titmus, Heather, additional, Bo, Ilaria, additional, Kaski, Juan Pablo, additional, Green, Loren, additional, Jones, Nigel, additional, Banks, Rebecca, additional, Kiesewetter, Christopher, additional, Mathur, Sujeev, additional, Frigiola, Alessandra, additional, Savis, Alex, additional, Belfield, Holly, additional, Guzman, Josephine, additional, Harris, Julia, additional, Wilson, Karen, additional, Peacock, Kelly, additional, Gibson, Kirsty, additional, Wellman, Paul, additional, Simpson, John, additional, Kabir, Saleha, additional, Mushemi, Sitali, additional, Stewart, Michael, additional, Atkinson, Bev, additional, Richardson, Cath, additional, Leng, Elaine, additional, Brennan, Paul, additional, Nixon, Annabel, additional, Spencer, Collette, additional, Oliver, James, additional, Forster, Jan, additional, Turner, Louise, additional, Bainbridge, Samantha, additional, Choy, Anna Maria, additional, Dawson, Adelle, additional, Kiddie, Gwen, additional, Kerr, Heather, additional, Mordi, Ify, additional, Duff, Jackie, additional, Dunlop, Jacqueline, additional, Berg, Jonathan, additional, Armory, Pauline, additional, Freeman, Leisa, additional, Anwar, Amir, additional, Graham, Charles, additional, London, Clare, additional, Healey, Gail, additional, Gallagher, Ian, additional, Ilsley, Mary, additional, Ahmed, Rizwan, additional, Wood, Sheila, additional, Wheeldon, Nigel, additional, Mason, Cecilia, additional, Nassim, Farook, additional, Middle, Janet, additional, Adams, Justin, additional, Angelini, Karen, additional, Housley, Kay, additional, Ryalls, Kim, additional, Agyemang, Michael, additional, Walker, Rachel, additional, Batigan, Robina, additional, Bennett, Tina, additional, Clift, Paul, additional, Alvior, Amor Mia, additional, Nilsson, Annette, additional, Green, Carole, additional, Crook, Charlotte, additional, Palmer, Connie Becani, additional, Dwenger, Elizabeth, additional, Doherty, Phillipa, additional, Igbokwe, Rebecca, additional, Sharif, Saba, additional, MacDonald, Sonia, additional, West, Cathy, additional, Kirby, Kevin, additional, Naqvi, Nitha, additional, Welch, Sophie, additional, Warsama, Suad, additional, Li, Wei, additional, Farzad, Zohreh, additional, Smith, Ben, additional, Murday, Victoria, additional, Murtagh, Eamonn, additional, Adams, Emma, additional, Armour, Lesley, additional, Lilley, Stuart, additional, Pandya, Bejal, additional, Richards, Amy, additional, Andiapen, Mervyn, additional, Macrae, Rebecca, additional, Tome, Maite, additional, Hutchinson, Carmel, additional, Angulo, Kameka, additional, Kauppayamootoo, Rooba, additional, Gati, Sabiha, additional, Cruddas, Elizabeth, additional, Newman, William G, additional, Breen, Catherine, additional, Kumar, Dhavendra, additional, Wilson, Dirk G, additional, Farrugia, Adele, additional, Fraser, Alan, additional, Sumers, Jayne, additional, Powell, Jessie, additional, Edwards, Julie, additional, Hale, Terese, additional, Boult, Zoe, additional, Carroll, Aisling, additional, Veldtman, Gruschen, additional, Ho, Andrew, additional, Black, David, additional, Fletcher, Lisa, additional, Mapstone, Sue, additional, Bharucha, Tara, additional, Marsh, Gary, additional, Jones, Joanne, additional, Sheehan, Karen, additional, Selway, Kathleen, additional, Stevenson, Kirsty, additional, Nelson, Martin, additional, Fairweather, Rebecca, additional, Curtis, Stephanie, additional, Simpson, Sue, additional, Denvir, Martin, additional, White, Audrey, additional, Steven, Jill, additional, Munro, Joanna, additional, Lam, Wayne, additional, Toff, William, additional, Petrou, Mario, additional, Silcocks, Paul, additional, and MacAllister, Raymond, additional

Published
2019
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5. Neprilysin inhibition for pulmonary arterial hypertension: a randomized, double‐blind, placebo‐controlled, proof‐of‐concept trial

Author

Hobbs, Adrian J., primary, Moyes, Amie J., additional, Baliga, Reshma S., additional, Ghedia, Dipa, additional, Ochiel, Rachel, additional, Sylvestre, Yvonne, additional, Doré, Caroline J., additional, Chowdhury, Kashfia, additional, Maclagan, Kate, additional, Quartly, Harriet L., additional, Sofat, Reecha, additional, Smit, Angelique, additional, Schreiber, Benjamin E., additional, Coghlan, Gerry J., additional, and MacAllister, Raymond J., additional

Published
2019
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6. Resistant Hypertension

Author

George, Marc J., primary, Marks, Daniel J.B., additional, Rezk, Tamer, additional, Breckenridge, Ross, additional, Sofat, Reecha, additional, Martin, John, additional, MacAllister, Raymond, additional, Touyz, Rhian M., additional, Staessen, Jan A., additional, Bursztyn, Michael, additional, Lappin, David, additional, Barigou, Mohammed, additional, and Hingorani, Aroon, additional

Published
2018
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7. Potent Anti-Inflammatory and Pro-Resolving Effects of Anabasum in a Human Model of Self-Resolving Acute Inflammation

Author

Motwani, Madhur P., primary, Bennett, Frances, additional, Norris, Paul C., additional, Maini, Alexander A., additional, George, Marc J., additional, Newson, Justine, additional, Henderson, Alice, additional, Hobbs, Adrian J., additional, Tepper, Mark, additional, White, Barbara, additional, Serhan, Charles N., additional, MacAllister, Raymond, additional, and Gilroy, Derek W., additional

Published
2018
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8. Scleroderma and related disorders: 223. Long Term Outcome in a Contemporary Systemic Sclerosis Cohort

Author

Nihtyanova, Svetlana, Ong, Voon, Black, Carol, Denton, Chris, Lutalo, Pamela, Shattles, Warren, Jones, Hugh, Nouri, Reem, Hepburn, Alastair, Chard, Michael, Horwood, Natalie, Lynn, Myo, Duke, Oliver, Kiely, Patrick, Zouita, Louisa, Davies, Ursula, Hughes, Rod, Lloyd, Mark, Nikitorowicz Buniak, Joanna, Shiwen, Xu, Abraham, David, Stratton, Richard, Hügle, Thomas, Schuetz, Philipp, Daikeler, Thomas, Tyndall, Alan, Matucci-Cerinic, Marco, Walker, Ulrich A., van Laar, Jacob M., Pauling, John D., Flower, Victoria, McHugh, Neil, Liu, Shangxi, Leask, Andrew, Aden, Nima, Khan, Korsa, Hoyles, Rachel, Bhagat, Shweta, Drummond, Tom, Goh, Cyndi, Busch, Robert, Hall, Frances, Meyer, Paul, Moinzadeh, Pia, Krieg, Thomas, Hellmich, Martin, Brinckmann, Juergen, Neumann, Elena, Mueller-Ladner, Ulf, Kreuter, Alexander, Dumitresco, Daniel, Rosenkranz, Stefan, Hunzelmann, Nicolas, Binai, Nadine, Huegle, Thomas, van Laar, Jaap, Sonnylal, S., Tam, A., Jones, H., Leask, A., Norman, J., Denton, C., de Crombrugghe, B., Abraham, D., Chighizola, Cecilia B., Luigi Meroni, Pier, Coghlan, Gerry, Newton, Florence, Derrett-Smith, Emma C., Dooley, Audrey, Baliga, Reshma, Hobbs, Adrian, MacAllister, Raymond, Futema, Marta, Pantelidis, Panagiotis, Renzoni, Elizabeth, Schreiber, Benjamin E., Coghlan, Gerry J., Wells, Athol U., Welsh, Ken, Fonseca, Carmen, Ponticos, Markella, Wells, Athol, Guillevin, Loic, Schwierin, Barbara, Rosenberg, Daniel, Silkey, Mariabeth, Parapuram, Sunil, Shi-wen, Xu, Denton, Christopher, Ahmed Abdi, Bahja, Xu, Shiwen, Nihtyanova, Svetlana, Ong, Voon, Black, Carol, Denton, Chris, Lutalo, Pamela, Shattles, Warren, Jones, Hugh, Nouri, Reem, Hepburn, Alastair, Chard, Michael, Horwood, Natalie, Lynn, Myo, Duke, Oliver, Kiely, Patrick, Zouita, Louisa, Davies, Ursula, Hughes, Rod, Lloyd, Mark, Nikitorowicz Buniak, Joanna, Shiwen, Xu, Abraham, David, Stratton, Richard, Hügle, Thomas, Schuetz, Philipp, Daikeler, Thomas, Tyndall, Alan, Matucci-Cerinic, Marco, Walker, Ulrich A., van Laar, Jacob M., Pauling, John D., Flower, Victoria, McHugh, Neil, Liu, Shangxi, Leask, Andrew, Aden, Nima, Khan, Korsa, Hoyles, Rachel, Bhagat, Shweta, Drummond, Tom, Goh, Cyndi, Busch, Robert, Hall, Frances, Meyer, Paul, Moinzadeh, Pia, Krieg, Thomas, Hellmich, Martin, Brinckmann, Juergen, Neumann, Elena, Mueller-Ladner, Ulf, Kreuter, Alexander, Dumitresco, Daniel, Rosenkranz, Stefan, Hunzelmann, Nicolas, Binai, Nadine, Huegle, Thomas, van Laar, Jaap, Sonnylal, S., Tam, A., Jones, H., Leask, A., Norman, J., Denton, C., de Crombrugghe, B., Abraham, D., Chighizola, Cecilia B., Luigi Meroni, Pier, Coghlan, Gerry, Newton, Florence, Derrett-Smith, Emma C., Dooley, Audrey, Baliga, Reshma, Hobbs, Adrian, MacAllister, Raymond, Futema, Marta, Pantelidis, Panagiotis, Renzoni, Elizabeth, Schreiber, Benjamin E., Coghlan, Gerry J., Wells, Athol U., Welsh, Ken, Fonseca, Carmen, Ponticos, Markella, Wells, Athol, Guillevin, Loic, Schwierin, Barbara, Rosenberg, Daniel, Silkey, Mariabeth, Parapuram, Sunil, Shi-wen, Xu, Denton, Christopher, Ahmed Abdi, Bahja, and Xu, Shiwen

Abstract

Background: We have previously compared outcome in two groups of systemic sclerosis (SSc) patients with disease onset a decade apart and we reported data on 5 year survival and cumulative incidence of organ disease in a contemporary SSc cohort. The present study examines longer term outcome in an additional cohort of SSc followed for 10 years. Methods: We have examined patients with disease onset between years 1995 and 1999 allowing for at least 10 years of follow-up in a group that has characteristics representative for the patients we see in contemporary clinical practice. Results: Of the 398 patients included in the study, 252 (63.3%) had limited cutaneous (lc) SSc and 146 (36.7%) had diffuse cutaneous (dc) SSc. The proportion of male patients was higher among the dcSSc group (17.1% v 9.9%, p = 0.037) while the mean age of onset was significantly higher among lcSSc patients (50 ± 13 v 46 ± 13 years ± SD, p = 0.003). During a 10 year follow-up from disease onset, 45% of the dcSSc and 21% of the lcSSc subjects developed clinically significant pulmonary fibrosis, p < 0.001. Among them approximately half reached the endpoint within the first 3 years (23% of dcSSc and 10% of lcSSc) and over three quarters within the first 5 years (34% and 16% respectively). There was a similar incidence of pulmonary hypertension (PH) in the two subsets with a steady rate of increase over time. At 10 years 13% of dcSSc and 15% of lcSSc subjects had developed PH (p=0.558), with the earliest cases observed within the first 2 years of disease. Comparison between subjects who developed PH in the first and second 5 years from disease onset demonstrated no difference in demographic or clinical characteristics, but 5-year survival from PH onset was better among those who developed this complication later in their disease (49% v 24%), with a strong trend towards statistical significance (p = 0.058). Incidence of SSc renal crisis (SRC) was significantly higher among the dcSSc patients (12% v 4%

Published
2017

9. Remote ischemic preconditioning provides early and late protection against endothelial ischemia-reperfusion injury in humans: Role of the autonomic nervous system

Author

Loukogeorgakis, Stavros P., Panagiotidou, Anna T., Broadhead, Michael W., Donald, Ann, Deanfield, John E., and MacAllister, Raymond J.

Abstract

ObjectivesThe aim of this study was to characterize the time course and neuronal mechanism of remote ischemic preconditioning (RIPC) of the vasculature in humans.BackgroundNon-lethal ischemia of internal organs induces local (ischemic preconditioning) and systemic (RIPC) resistance to lethal ischemia-reperfusion (IR) injury. Experimental RIPC has two temporal components, is neuronally mediated, is induced by limb ischemia, and reduces infarct size. In humans, RIPC prevents IR-induced vascular injury. Determining the time course and mechanism is a prelude to clinical outcome studies of RIPC.MethodsEndothelial IR injury was induced by arm ischemia (20 min) and reperfusion, and measured by flow-mediated dilation. To establish if there are early and late phases, RIPC (three 5-min cycles of ischemia of the contralateral arm) was applied immediately, 4, 24, and 48 h before IR. To determine neuronal involvement, trimetaphan (autonomic ganglion blocker; 1 to 6 mg/min intravenous) was infused during the application of the RIPC stimulus.ResultsFlow-mediated dilation was reduced by IR (8.7 ± 1.1% before IR, 4.9 ± 1.2% after IR; p < 0.001), but not when preceded by RIPC (8.0 ± 0.8% after IR; p = NS); RIPC did not protect after 4 h (4.9 ± 1.1% after IR; p < 0.001), but protected at 24 (8.7 ± 1.1% after IR; p = NS) and 48 h (8.8 ± 1.4% after IR; p = NS). Trimetaphan attenuated early (8.3 ± 1.1% before IR, 4.2 ± 0.9% after IR; p < 0.05) and delayed (7.3 ± 1.0% before IR, 2.3 ± 0.6% after IR, p < 0.001) RIPC.ConclusionsRemote ischemic preconditioning in humans has two phases of protection against endothelial IR injury; an early (short) and late (prolonged) phase, both of which are neuronally mediated. The potential for late phase RIPC to provide prolonged protection during clinical IR syndromes merits investigation.

Published
2016

10. Endogenous opioids contribute to insensitivity to pain in humans and mice lacking sodium channel Nav1.7

Author

Minett, Michael, Pereira, Vanessa, Sikandar, Shafaq, Matsuyama, Ayako, Lolignier, Stéphane, Kanellopoulos, Alexandros, Mancini, Flavia, Iannetti, Gian, Bogdanov, Yury, Santana-Varela, Sonia, Millet, Queensta, Baskozos, Giorgios, Macallister, Raymond, Cox, James, Zhao, Jing, Wood, John, Wolfson Institute for Biomedical Research (WIBR), and University College of London [London] (UCL)

Subjects
Adult, Male, Mice, Knockout, Pain Insensitivity, Congenital, Sensory Receptor Cells, NAV1.7 Voltage-Gated Sodium Channel, Sensation, Enkephalins, Article, Mice, [SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/Pharmacology, Animals, Humans, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Female
Abstract

Loss-of-function mutations in the SCN9A gene encoding voltage-gated sodium channel Nav1.7 cause congenital insensitivity to pain in humans and mice. Surprisingly, many potent selective antagonists of Nav1.7 are weak analgesics. We investigated whether Nav1.7, as well as contributing to electrical signalling, may have additional functions. Here we report that Nav1.7 deletion has profound effects on gene expression, leading to an upregulation of enkephalin precursor Penk mRNA and met-enkephalin protein in sensory neurons. In contrast, Nav1.8-null mutant sensory neurons show no upregulated Penk mRNA expression. Application of the opioid antagonist naloxone potentiates noxious peripheral input into the spinal cord and dramatically reduces analgesia in both female and male Nav1.7-null mutant mice, as well as in a human Nav1.7-null mutant. These data suggest that Nav1.7 channel blockers alone may not replicate the analgesic phenotype of null mutant humans and mice, but may be potentiated with exogenous opioids., Nav1.7 channels are known to regulate pain perception in humans and mice. Here, the authors provide evidence that Nav1.7 deletion leads to transcriptional upregulation of opioid peptides in sensory neurons, and that treatment with the opioid blocker naloxone helps reverse analgesia in mice and human Nav1.7 nulls.

Published
2015

11. Flipping the odds of drug development success through human genomics

Author

Hingorani, Aroon D., primary, Kuan, Valerie, additional, Finan, Chris, additional, Kruger, Felix A., additional, Gaulton, Anna, additional, Chopade, Sandesh, additional, Sofat, Reecha, additional, MacAllister, Raymond J., additional, Overington, John P., additional, Hemingway, Harry, additional, Denaxas, Spiros, additional, Prieto, David, additional, and Casas, Juan Pablo, additional

Published
2017
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13. Remote ischemic conditioning: from experimental observation to clinical application: report from the 8th Biennial Hatter Cardiovascular Institute Workshop

Author

Pickard, Jack M J, Bøtker, Hans Erik, Crimi, Gabriele, Davidson, Brian, Davidson, Sean M, Dutka, David, Ferdinandy, Peter, Ganske, Rocky, Garcia-Dorado, David, Giricz, Zoltan, Gourine, Alexander V, Heusch, Gerd, Kharbanda, Rajesh, Kleinbongard, Petra, MacAllister, Raymond, McIntyre, Christopher, Meybohm, Patrick, Prunier, Fabrice, Redington, Andrew, Robertson, Nicola J, Suleiman, M Saadeh, Vanezis, Andrew, Walsh, Stewart, Yellon, Derek M, and Hausenloy, Derek J

Subjects
Physiology, Medizin, Myocardial Reperfusion Injury, Review, Ventricular Function, Left, european-society, Ischemia, Physiology (medical), Humans, Organ protection, bypass graft-surgery, Aldehyde Dehydrogenase, Mitochondrial, percutaneous coronary intervention, Remote ischemic conditioning, Acute Kidney Injury, Aldehyde Dehydrogenase, preconditioning protects, induced nephropathy, elevation myocardial-infarction, cellular biology, Reperfusion Injury, randomized controlled-trial, Reperfusion, Ischemic Preconditioning, Myocardial, Cardiology and Cardiovascular Medicine, Signal Transduction
Abstract

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.

Published
2014

14. Resistant Hypertension: Trials and Tribulations.

Author

George, Marc J., Marks, Daniel J. B., Rezk, Tamer, Breckenridge, Ross, Sofat, Reecha, Martin, John, Macallister, Raymond, Touyz, Rhian M., Staessen, Jan A., Bursztyn, Michael, Lappin, David, Barigou, Mohammed, and Hingorani, Aroon

Abstract

The article presents a case study of a 62-year old white woman diagnosed with hypertension.

Published
2018
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16. Remote ischemic conditioning: from experimental observation to clinical application: report from the 8th Biennial Hatter Cardiovascular Institute Workshop.

Author

Pickard, Jack, Bøtker, Hans, Crimi, Gabriele, Davidson, Brian, Davidson, Sean, Dutka, David, Ferdinandy, Peter, Ganske, Rocky, Garcia-Dorado, David, Giricz, Zoltan, Gourine, Alexander, Heusch, Gerd, Kharbanda, Rajesh, Kleinbongard, Petra, MacAllister, Raymond, McIntyre, Christopher, Meybohm, Patrick, Prunier, Fabrice, Redington, Andrew, and Robertson, Nicola

Subjects
ISCHEMIA, CONFERENCES & conventions, ARTERIAL occlusions, CORONARY disease, REPERFUSION injury, BLOOD pressure
Abstract

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. [ABSTRACT FROM AUTHOR]

Published
2015
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