Evaluation of percutaneous valves. 01/01/2014 - 31/12/2023

Abstract

This project represents a formal research agreement between UA and on the other hand the client. UA provides the client research results mentioned in the title of the project under the conditions as stipulated in this contract.

Researcher(s)

Research team(s)

Project type(s)

  • Research Project

01/07/2012 - 30/06/2016

Abstract

Researcher(s)

Research team(s)

    Project type(s)

    • Research Project

    Coronary hemodynamics after a myocardial infarction. 01/10/2005 - 30/09/2007

    Abstract

    Cardiovascular morbidity and mortality is one of the major health issues in the Western world. It is known that myocardial infarction can severely affect the prognosis of a patient. More research in this area is needed. Miniaturisation of the technology has made it possible to perform measurements in the human coronary circulation. This technological development offers an unique opportunity to study pathophysiological processes in humans. The vasoreactivity of the microcirculation can for instance be assessed by measuring the flow in basal and hyperemic conditions. Furthermore it is possible to perform simultaneous pressure-flow measurements. With the use of adapted software these signals can be combined and a pressure-flow loop of the coronary circulation can be made. Extrapolation of the diastolic pressure-flowrelation to the pressure-axis (X-axis) can give us an estimation of the zero flow pressure. The slope of this diastolic relation can also learn us something about the conductance of the coronary circulation. Nowadays one has realised that myocardial infarction triggers an inflammatory cascade which is accompanied by the release of numerous cytokines. Their prognostic implications can no longer be denied. The mechanisms that relate acute phase proteins to short and long term prognosis are unclear. New data suggest that impairment of the endothelial function by an inflammatory response creates a link between systemic inflammation and ischemic coronary syndromes. The purpose of this project is to gain more insight in the pathophysiology of the coronary circulation after infarction by perfoming intracoronary measurements and by measuring inflammatory cytokines.

    Researcher(s)

    Research team(s)

      Project type(s)

      • Research Project

      Coronary hemodynamics after a myocardial infarction. 01/10/2003 - 30/09/2005

      Abstract

      Cardiovascular morbidity and mortality is one of the major health issues in the Western world. It is known that myocardial infarction can severely affect the prognosis of a patient. More research in this area is needed. Miniaturisation of the technology has made it possible to perform measurements in the human coronary circulation. This technological development offers an unique opportunity to study pathophysiological processes in humans. The vasoreactivity of the microcirculation can for instance be assessed by measuring the flow in basal and hyperemic conditions. Furthermore it is possible to perform simultaneous pressure-flow measurements. With the use of adapted software these signals can be combined and a pressure-flow loop of the coronary circulation can be made. Extrapolation of the diastolic pressure-flowrelation to the pressure-axis (X-axis) can give us an estimation of the zero flow pressure. The slope of this diastolic relation can also learn us something about the conductance of the coronary circulation. Nowadays one has realised that myocardial infarction triggers an inflammatory cascade which is accompanied by the release of numerous cytokines. Their prognostic implications can no longer be denied. The mechanisms that relate acute phase proteins to short and long term prognosis are unclear. New data suggest that impairment of the endothelial function by an inflammatory response creates a link between systemic inflammation and ischemic coronary syndromes. The purpose of this project is to gain more insight in the pathophysiology of the coronary circulation after infarction by perfoming intracoronary measurements and by measuring inflammatory cytokines.

      Researcher(s)

      Research team(s)

        Project type(s)

        • Research Project

        Prevention of in-stent restenosis by the use of anti-proliferative drugs. 01/01/2003 - 31/12/2005

        Abstract

        In-stent restenosis remains a limitation of the percutaneous treatment modalities of coronary atherosclerosis. This project aims to develop 'single-component' and 'multi-component' directly coated drug eluting stents. Selective modulation of oxidative stress, smooth muscle cell migration and proliferation and endothelial cell regeneration are investigated, by single molecules, or combinations of locally delivered molecules. The used methodology consists of stenttechnology, farmacokinetic evaluations, in-vitro and in-vivo biological research.

        Researcher(s)

        Research team(s)

          Project type(s)

          • Research Project

          Development, farmacokinetic, in-vitro and in-vivo evaluation of 'multi-component', directly coated drug eluting stents 01/01/2003 - 31/12/2004

          Abstract

          In-stent restenosis remains a limitation of the percutaneous treatment modalities of coronary atherosclerosis. This project aims to develop 'single-component' and 'multi-component' directly coated drug eluting stents. Selective modulation of oxidative stress, smooth muscle cell migration and proliferation and endothelial cell regeneration are investigated, by single molecules, or combinations of locally delivered molecules. The used methodology consists of stenttechnology, farmacokinetic evaluations, in-vitro and in-vivo biological research.

          Researcher(s)

          Research team(s)

            Project type(s)

            • Research Project

            Medtronic experiment Cytochalasin D coated stents. 01/11/2001 - 30/10/2002

            Abstract

            Researcher(s)

            Research team(s)

              Project type(s)

              • Research Project