Our mission is to become a worldwide reference for education in the field for all professionals involved in the process to disseminate knowledge & skills of Acute Cardiovascular Care.
Our mission is to promote excellence in clinical diagnosis, research, technical development, and education in cardiovascular imaging in Europe.
Our mission is to promote excellence in research, practice, education and policy in cardiovascular health, primary and secondary prevention.
Our mission is to reduce the burden of cardiovascular disease through percutaneous cardiovascular interventions.
Improving the quality of life and reducing sudden cardiac death by limiting the impact of heart rhythm disturbances.
Our mission is to improve quality of life and longevity, through better prevention, diagnosis and treatment of heart failure, including the establishment of networks for its management, education and research.
The ESC Working Groups' goal is to stimulate and disseminate scientific knowledge in different fields of cardiology.
The ESC Councils' goal is to share knowledge among medical professionals practising in specific cardiology domains.
OUR MISSION: TO REDUCE THE BURDEN OF CARDIOVASCULAR DISEASE
Prof. Michael Weis
Individualized immunosuppression after transplantation. New insights into pathogenesis and treatment of graft arteriosclerosis While major improvements have been made in the prevention and treatment of acute transplant rejection, accelerated cardiac allograft vasculopathy (CAV) still limits the long-term success of heart transplantation (HTx). This session gave us an outstanding overview concerning new experimental models, stem cell and immune pathways as well as on new treatment options with respect to CAV.
In the first presentation, Q. Xu (London, GB) demonstrated that (based on mouse models for vein grafts and CAV) stem cells identified in blood and bone marrow, as well as the vasculature, contribute to allograft atherosclerotic lesion formation. Moreover, he described that the alloimmune response induces chemokines that attract stem cells to the allograft. In the second presentation, A.G. Pockley (Sheffield, GB) indicated that extracellular stress proteins (like gp96) have immunostimulatory and immunosuppressive potential depending on the context in which they are encountered by the cellular immune-response network. He described that high dose gp96 treatment prolongs survival in animal transplant models, at least in part via modulation of T-cell function. In the third presentation, B. de Geest (Leuven, BE) described that human apoA-I gene transfer increases the number of circulating EPCs, enhances their incorporation into allografts, promotes endothelial regeneration, and attenuates neointima formation in a murine model of transplant arteriosclerosis. In addition, he showed that the HDL-induced effect on EPC migration depends on the receptor SRBI. Finally, S. Kofler (Munich, Germany) presented the current and future potential of immunosuppressive drugs and pointed out that individualized immunosuppression is needed. Calcineurin-inhibitor free protocols and the use of new costimulatory signal inhibitors are currently being studied.
Alloimmune-dependent and alloimmune-independent injuries in the context of impaired/ heightened repair mechanisms (reduced activity of endothelial cell progenitors, enhanced smooth muscle cell progenitors) are controlling the progression of graft arteriosclerosis. As individual responses to an allograft change over time, we need to develop assays for monitoring the recipient immune response as well as individualized methods for therapeutic immune modulation. The era of using standardized immunosuppressive protocols is over; immune tolerance appears on the horizon.
Graft arteriosclerosis: new insights
This congress report accompanies a presentation given at the ESC Congress 2008. Written by the author himself/herself, this report does not necessarily reflect the opinion of the European Society of Cardiology.
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