Jean-Louis Vanoverschelde
Mayo Clinic
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Publication
Featured researches published by Jean-Louis Vanoverschelde.
Journal of the American College of Cardiology | 2013
Jozef Bartunek; Atta Behfar; Dariouch Dolatabadi; Marc Vanderheyden; Miodrag Ostojic; Jo Dens; Badih El Nakadi; Marko Banovic; Branko Beleslin; Mathias Vrolix; Victor Legrand; C. Vrints; Jean-Louis Vanoverschelde; Ruben Crespo-Diaz; Christian Homsy; Michal Tendera; Scott A. Waldman; William Wijns; Andre Terzic
We appreciate the interest of Dr. Mielewczik and colleagues in the C-CURE (Cardiopoietic stem Cell therapy in heart failURE) trial. As outlined in our paper [(1)][1], feasibility and safety were the primary endpoints in this first-in-man study that assessed cardiogenically-oriented, autologous bone
Archive | 1996
Jacques Melin; Jean-Louis Vanoverschelde; Bernhard Gerber; Christian Michel; William Wijns; Anne Bol
Several tracer approaches have been proposed for the assessment of myocardial perfusion with positron emission tomography (PET) in the clinical setting. These include nitrogen-13 (13N) labelled ammonia, oxygen-15 (15O) labelled water, rubidium-82 (82Rb) and potassium-38 (38K). These tracers require a local cyclotron for production, except for 82Rb which may be delivered directly to the patient from an on-site generator. There are two specific clinical applications of PET that have been proposed for the evaluation of patients with coronary artery disease (CAD) [1-3]. The first is the noninvasive detection of CAD and estimation of the severity of the disease. This is performed using a PET perfusion agent at rest and during pharmacologic vasodilation. A unique application of PET is the noninvasive calculation of absolute regional myocardial perfusion at rest and during vasodilation in humans using [15O]water or [13N]ammonia. However, most centers rely on the qualitative interpretation of 82Rb or [13N]ammonia images for the detection of CAD and the assessment of its severity. The second clinical application of PET is the assessment of myocardial viability in CAD patients with left ventricular dysfunction. The most common approach is to determine whether metabolic activity assessed by 2-[18F]fluoro-2-deoxy-D-glucose ([18F]FDG) is preserved in regions with reduced perfusion, thus indicating tissue viability.
Journal of the American College of Cardiology | 2015
Marie-Annick Clavel; Christophe Tribouilloy; Jean-Louis Vanoverschelde; Rodolfo Pizarro; Rakesh M. Suri; Catherine Szymanski; Siham Lazam; Maurice Enriquez-Sarano
Plasma B-type natriuretic peptide (BNP) varies with age and sex. However normalized values in patients with organic mitral regurgitation (OMR) remain unknown. The aim of this study was to assess the impact of an increase in BNP compared to normal upon mortality in a large population of OMR. In 1,
Archive | 2003
Jean-Louis Vanoverschelde; Agnes Pasquet
In adults with valvular heart disease, valve replacement and repair are the only therapeutic options that consistently improve symptoms and increase life expectancy. The assessment of the severity of a valvular lesion traditionally relies on the evaluation of valvular anatomy and on the demonstration of resting hemodynamic disturbances, attributable to the valve problem. In patients with stenotic lesions, this is usually achieved by measuring the transstenotic pressure difference and by calculating the surface of the stenotic orifice. In patients with regurgitant lesions, assessment of lesion severity requires that the degree of volume overload imposed on the heart chambers be determined. In many instances, however, discrepancies are found between the severity of the valvular lesion and either the symptoms or the hemodynamic impairment. A provocative maneuver to unmask the true severity of the valvular lesion may then be useful.
Archive | 1998
Jean-Louis Vanoverschelde; Bernhard Gerber; Jacques Melin
The term “hibernation” was employed for the first time by Diamond et al. in 1978 1 to describe the chronic wall motion abnormalities of patients with coronary artery disease but no previous myocardial infarction and their reversibility upon revascularization. The overall concept of myocardial hibernation was subsequently developed by Rahimtoola23 and popularized by Braunwald and Rutherford.4 In his 1989 description of the syndrome, Rahimtoola postulated that myocardial hibernation resulted from the “relatively uncommon response to reduced myocardial blood flow at rest whereby the heart downgrades its myocardial function to the extent that blood flow and function are once again in equilibrium, and as a result, neither myocardial necrosis or ischemic symptoms are present.” 2
Circulation (Baltimore) | 1994
Jean-Louis Vanoverschelde; Jacques Melin; Christophe Depre; M. Borgers; R. Dion; William Wijns
76th Annual Scientific Session of the American-Heart-Association | 2003
David Vancraeynest; Claude Hanet; Joelle Kefer; Agnes Pasquet; Bernhard Gerber; Christophe Beauloye; Jean-Louis Vanoverschelde
80th Annual Scientific Session of the American-Heart-Association | 2007
Jean-Benoît Le Polain De Waroux; Bernhard Gerber; Gebrine El Khoury; Jean-Louis Vanoverschelde; Anne-Catherine Pouleur; Céline Goffinet; David Vancraeynest; Agnes Pasquest; P. Noirhomme
Circulation (Baltimore) | 1993
Jean-Louis Vanoverschelde; Jacques Melin; Thomas Marwick; Anne-Marie D'hondt; T. Baudhuin; William Wijns
European Heart Journal (English Edition) | 2006
J.B. Le Polain De Waroux; Anne-Catherine Pouleur; Agnes Pasquet; Bernhard Gerber; Gebrine El Khoury; Philippe Noirhomme; Annie Robert; Jean-Louis Vanoverschelde