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- Professor of Cellular Cardiology
- Hatter Cardiovascular Institute
- Institute of Cardiovascular Science
- Faculty of Population Health Sciences
Derek M Yellon PhD, DSc, FRCP (Hon), FACC, FESC, FAHA, is Professor of Molecular & Cellular Cardiology at University College London (UCL). He is Head of the Research Department for Cardiovascular Medicine at UCL as well as Head of the Centre for Cardiology and Director of the Hatter Cardiovascular Institute at UCL Hospitals & Medical School.
In 1993 he was appointed Professor of Molecular & Cellular Cardiology at University College London. He is a Fellow of the Royal College of Physicians; the American College of Cardiology; the European Society of Cardiology; the International Society for Heart Research and the American Heart Association.In 1994 he was awarded a DSc for his “substantial contribution to the knowledge of cardiovascular disease and treatment”. He is Vice President of the British Cardiovascular Society and is past Chairman of the Cellular Biology Working
Group of the European Society of Cardiology as well as past member of the World Council of the International Society for Heart Research. He was recently elected to Department of Health’s National Institute for Health Research (NIHR) as a Senior Investigator as well as a member of the College of Senior Investigators.Professor Yellon was instrumental in establishing a second Hatter Cardiovascular Institute at the Medical School of the University of Cape Town to which he is also a Director and Chairman of the Institute Board. In recognition of these achievements he was, in 1997, made an Hon Professor of Medicine in the Department of Medicine at the University of Cape Town. He also holds Honorary Chairs at the University of South Alabama in the USA, and the North China Coal Medical University in China.
He is on the editorial board of a number of major Cardiovascular Journals and has published in excess of 400 full papers and edited 17 books. He runs a translational research Institute with his main area of interest including; myocardial protection, the pathophysiology of cardioprotection in setting of diabetes, ischaemia/reperfusion injury, molecular aspects of adaptation to ischaemic injury and myocardial pre and postconditioning in both the basic and clinical arena.
Coronary heart disease (CHD) is the leading cause of death in the UK, accounting for 105,000 deaths in 2004 and costing the UK economy in excess of £7.9 billion a year. Innovative treatment strategies are required to improve health outcomes in patients with CHD. The Hatter Cardiovascular Institute at UCL has been undertaking translational studies to try and address this issue. In this regard experimental basic laboratory studies have identified two novel targets for cardioprotection: (a) the mitochondrial permeability transition pore (mPTP), a mitochondrial channel whose opening induces cardiomyocyte death at the onset of myocardial reperfusion but can be prevented using the immunosupressent cyclopsorine-A in animals & man (b) the Reperfusion Injury Salvage Kinase (RISK) pathway, a group of endogenous pro-survival protein kinases which when activated at the onset of reperfusion, reduce myocardial injury. In addition our experimental studies have also identified specific pharamcological agents which directly target the RISK pathway and the mPTP.
Our clinical research programme, emanating from our basic science studies, cross-cuts the research themes of Cardiovascular and Imaging, and involves active collaborations across the Academic Health Sciences Partnership and other London hospital Trustee below. Based directly on our preclinical observations, we are currently investigating new and specific treatment strategies for reducing myocardial injury and improving clinical outcomes in patients with CHD, focusing on those AMI patients undergoing percutaneous coronary intervention (PCI) and patients undergoing coronary artery bypass graft (CABG) surgery. These new treatment strategies include: (1) Remote ischaemic conditioning (RIC), which describes the cardioprotection obtained from inducing brief ischaemia-reperfusion to the upper limb, using a blood pressure cuff applied to the upper arm. Paramedics from LAS have been administering the RIC protocol to AMI patients in the ambulance. We have recently demonstrated that RIC reduces myocardial injury in CABG patients - we now intend to determine whether RIC can improve clinical outcomes in CABG patients in a London-wide multicentred study; (2) Erythropoietin (EPO), a haemopoietic agent, which is capable of reducing myocardial infarct size by 40-50% through the activation of the RISK pathway. (3) Cyclosporin-A (CsA). We are organising an Europe-wide multi-centred clinical study to determine whether CsA can improve clinical outcomes in AMI patients undergoing PPCI. We will be assessing cardioprotection in AMI patients in terms of myocardial infarct size, microvascular obstruction, and LV function using cardiac MRI.
|01-JAN-2009||Head of the Research Department of Cardiovascular Medicine||Medicine||UCL, United Kingdom|
|01-OCT-1992||Director of the Centre for Cardiology||Medicine||UCL, United Kingdom|
|01-JAN-1990||Director of Hatter Cardiovascular Institute||Medicine||UCL, United Kingdom|
|2000||FRCP||Fellow of the Royal College of Physicians|
|1994||DSC||Doctor of Science||University of Bath|
|1978||PhD||Doctor of Philosophy||University of Bath|