Education
Director of Anesthesia and critical care Residency Program (2015-20)
Professor of Anaesthesia and Critical Care, University of Bordeaux (2011)
Ph. D., Université of Paris (2006)
National board of cardiopulmonary bypass, University of Paris (2005)
National board of Perioperative Echocardiography, University of Paris (2003)
National Board of Anaesthesiologist, University of Poitiers (2000)
M.D Medicine, University of Poitiers (2000)
Master of Science, Cardiovascular Physiology and Biology, University of Paris (1999)
Professional training
2004 - 2000 Anaesthesiology Resident
Department of Anaesthesiology, Jean Bernard Hospital, Poitiers and Pitié-Salpêtrière Hospital, Paris, France
1998 - 1999 Research Fellow
Laboratory of Anaesthesiology, Department of Anaesthesiology, University Pierre et Marie Curie, Paris, France
2001 - 2003 Anaesthesiology Fellow
Cardiovascular Anaesthesia, Department of Anaesthesiology (Pitié-Salpêtrière Hospital), University Pierre et Marie Curie, Paris, France
2003 - 2009 Staff Anaesthesiologist
Cardiovascular Anaesthesia, Department of Anaesthesiology (Pitié-Salpêtrière Hospital), University Pierre et Marie Curie, Paris, France
2009 - 2011 Assistant Professor
Cardiovascular Anaesthesia, Department of Anaesthesiology (Haut-Lévêque Hospital), University Bordeaux Segalen, Bordeaux, France
2010 Professor / Chairman of Department of Anaesthesiology and Critical Care
CHU de Bordeaux, France
2013 - 2018 Associated Editor for Anaesthesia and Critical Care Pain Medicine
Five to 10% of patients presenting with acute myocardial infarction develop cardiogenic shock. Despite the early myocardial revascularization, optimal pharmacological treatment and the use of short-term mechanical circulatory support, the mortality of cardiogenic shock complicating acute myocardial infarction remains abnormally high. Insights into cardiogenic shock’s pathophysiology remain crucial to the development of new therapeutic approaches. In this context, large animal models may provide a heuristic methodology to test pathophysiological hypotheses and thus new therapies. Our group developed a stable and reproductible closed chest sheep’s model of severe cardiogenic shock due to myocardial infarction. Percutaneous closed-chest models present the advantage to profoundly limit the huge trauma of thoracotomy, thus respecting cardiac and whole-body physiology and favouring recovery. Consequently, our model presents a high rate of survival after the induction of CS. Our experimental set-up could lead to a better understanding of mechanical interaction between short-term mechanical circulatory support and an acutely failing ventricle. The potential usefulness or harmfulness of vasoactive and inotropic drugs in patients assisted with those devices might also be explored in this model. Moreover, the impact of ventricular support on early remodelling of non-ischemic territory could be more fully investigated.