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.
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 practicing in specific cardiology domains.
Joint consensus document of the European Society of Cardiology (ESC) Working Groups “Atherosclerosis & Vascular Biology” and “Thrombosis”
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Authors: C. Weber, E. Shantsila, M. Hristov, G. Caligiuri, T. Guzik, G. H. Heine, I. E. Hoefer, C. Monaco, K. Peter, E. Rainger, A. Siegbahn, S. Steffens, J. Wojta, G. Y. H. Lip
References: Thrombosis and Haemostasis; 0340-6245; doi:10.1160/TH16-02-0091; Ahead of Print: 2016-07-14
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Authors: Imo E. Hoefer, Sabine Steffens, Mika Ala-Korpela, Magnus Bäck, Lina Badimon, Marie-Luce Bochaton-Piallat, Chantal M. Boulanger, Giuseppina Caligiuri, Stefanie Dimmeler, Jesus Egido, Paul C. Evans, Tomasz Guzik, Brenda R. Kwak, Ulf Landmesser, Manuel Mayr, Claudia Monaco, Gerard Pasterkamp, Jose Tuñón, Christian Weber on behalf of the ESC Working Group Atherosclerosis and Vascular Biology.
Eur Heart J (2015) 36, 2635–2642 doi:10.1093/eurheartj/ehv236 First published online: 6 June 2015
Authors: Seppo Yla-Herttuala, Jacob Fog Bentzon, Mat Daemen, Erling Falk, Hector M. Garcia-Garcia, Joerg Herrmann, Imo Hoefer, Suvi Jauhiainen7, J.Wouter Jukema, Rob Krams, Brenda R. Kwak, Nikolaus Marx, Marek Naruszewicz, Andrew Newby, Gerard Pasterkamp, PatrickW.J.C. Serruys, Johannes Waltenberger, Christian Weber, and Lale Tokgozoglu, ESC Working Group of Atherosclerosis and Vascular Biology
References: Eur Heart J (2013) doi: 10.1093/eurheartj/eht301 First published online: 21 August 2013
Position Paper of The European Society Of Cardiology Working Group on Atherosclerosis and Vascular Biology
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Authors: S. Ylä-Herttuala, J. F. Bentzon, M. Daemen, E. Falk, H. M. Garcia-Garcia, J. Herrmann, I. Hoefer, J. W. Jukema, R. Krams, B. R. Kwak, N. Marx, M. Naruszewicz, A. Newby, G. Pasterkamp, P. W. J. C. Serruys, J. Waltenberger, C. Weber, L. Tokgözoglu
Reference: Thrombosis and Haemostasis 2011 106 DOI: 10.1160/TH10-12-0784 First Published online: 14 June 2011
Summary: Plaque rupture and subsequent thrombotic occlusion of the coronary artery account for as many as three-quarters of myocardial infarctions. The concept of plaque stabilisation emerged about 20 years ago to explain the discrepancy between the reduction of cardiovascular events in patients receiving lipid-lowering therapy and the small decrease seen in angiographic evaluation of atherosclerosis. Since then, the concept of a vulnerable plaque has received a lot of attention in basic and clinical research leading to a better understanding of the pathophysiology of the vulnerable plaque and acute coronary syndromes. From pathological and clinical observations, plaques that have recently ruptured have thin fibrous caps, large lipid cores, exhibit outward remodelling and invasion by vasa vasorum. Ruptured plaques are also focally inflamed and this may be a common denominator of the other pathological features. Plaques with similar characteristics, but which have not yet ruptured, are believed to be vulnerable to rupture. Experimental studies strongly support the validity of anti-inflammatory approaches to promote plaque stability. Unfortunately, reliable non-invasive methods for imaging and detection of such plaques are not yet readily available. There is a strong biological basis and supportive clinical evidence that low-density lipoprotein lowering with statins is useful for the stabilisation of vulnerable plaques. There is also some clinical evidence for the usefulness of antiplatelet agents, beta blockers and renin-angiotensin-aldosterone system inhibitors for plaque stabilisation. Determining the causes of plaque rupture and designing diagnostics and interventions to prevent them are urgent priorities for current basic and clinical research in the cardiovascular area.
Read the Press Release related to this position paperESC calls for research into vulnerable plaques: Widespread stabilisation of vulnerable plaque would dramatically reduce the need for invasive treatment
Our mission: To reduce the burden of cardiovascular disease
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