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Atherosclerosis and Vascular Biology

Position papers and consensus documents from the ESC Working Group on Atherosclerosis and Vascular Biology

Role and analysis of monocyte subsets in cardiovascular disease

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

Summary: Monocytes as cells of the innate immunity are prominently involved in the development of atherosclerotic lesions. The heterogeneity of blood monocytes has widely been acknowledged by accumulating experimental and clinical data suggesting a differential, subset-specific contribution of the corresponding subpopulations to the pathology of cardiovascular and other diseases. This document re-evaluates current nomenclature and summarises key findings on monocyte subset biology to propose a consensus statement about phenotype, separation and quantification of the individual subsets.

Novel methodologies for biomarker discovery in atherosclerosis

No longer available

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 

Stabilization of atherosclerotic plaques: an update

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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 

Stabilisation of atherosclerotic plaques

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 paper
ESC calls for research into vulnerable plaques: Widespread stabilisation of vulnerable plaque would dramatically reduce the need for invasive treatment