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EAS2019 - Highlights from the EAS 2019 Opening Ceremony 

Monday 27 May 2019  
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87th Congress of the European Atherosclerosis Society opens

After 24 years, the 87th Congress of the European Atherosclerosis Society returned to the Netherlands, opening proceedings in Maastricht last night. The location is most appropriate, given its unique position at the centre of Europe and as the birthplace of the European Union. Maastricht is important for much more, however, in particular its strong cardiovascular research community, with four top Universities within a radius of 30 kilometres.

This year’s Congress attracted more than 2,000 delegates from 70 countries, a reflection of the global presence of the EAS. Opening the Congress, EAS President Professor Lale Tokgözoğlu (Hacettepe University, Ankara, Turkey) highlighted the role of the Society in research, education and collaboration. The new Joint Dyslipidaemia Guidelines with the European Society of Cardiology are eagerly anticipated later this year, in the light of recent findings from major trials of innovative therapies. Added to this, Professor Tokgözoğlu confirmed that three new EAS Consensus Panel publications are anticipated in the near future, focusing on 1) pathophysiological evidence for the causality of apolipoprotein B-containing lipoproteins, a much anticipated follow-up to the first low-density lipoprotein (LDL) causality statement,1 2) rare lipid disorders, and 3) a new approach to cardiovascular risk estimation. In addition, advanced lipid courses, courses in rare lipid disorders, and the EAS Academy are just some examples of the role of the EAS in education.

The EAS has built on its mentoring role, with the initiation of the Young Scientists and Young Fellows programmes, the latter involving 50 leading young researchers, selected on merit, who will be offered training with top scientists in the field, as the experts of the future. Professor Tokgözoğlu also presented the 2019 Young Investigator Awards to Tom Seijkens, Amsterdam UMC, Amsterdam, the Netherlands (Basic Science) and Antonio J. Vallejo-Vaz, Imperial Centre for Cardiovascular Disease Prevention Imperial College London, UK (Clinical Science) (refer to the EAS website for further details).    

The EAS Familial Hypercholesterolaemia Studies Collaboration (FHSC) is an important example of the Society’s global position in atherosclerosis research. Currently, 68 countries have entered 59,600 FH cases in this Registry. The EAS FH Studies Registry has recently announced a collaboration with the patient representative network, FH Europe, to ensure that there is now one voice for FH in Europe. And collaboration extends further, with recent moves with the International Atherosclerosis Society and the World Heart Federation, aiming to ensure that the importance of high cholesterol is recognised by the World Health Organisation as part of the Non-Communicable Disease programme. Recent findings from the EAS FHSC Registry will be discussed at Monday’s Advanced Clinical Seminar: Genetically determined dyslipidemias.

‘The Congress registration, involving delegates from over 70 countries, reaffirms that the EAS Congress is truly a global meeting that is highly valued whether delegates are from Asia, Latin America, the Pacific and North America.’EAS President Professor Lale Tokgözoğlu

International Atherosclerosis Society President Professor Raul Santos (University of Sao Paulo Medical School Hospital and Hospital Israelita Albert Einstein, Sao Paulo, Brazil) reinforced the joint goals of both the EAS and the IAS in tackling the major issue facing all regions- poor attainment of LDL cholesterol goal in high risk patients. ‘The EAS offers an amazing opportunity for education, science and collaboration in joining forces to address this major challenge across the globe.’

In addition, the Congress Chairs, Professor Erik Biessen (University of Maastricht), and Professor Erik Stroes (Amsterdam Medical Centre, University of Amsterdam), welcomed delegates on behalf of the Dutch Cardiovascular Society. Vice Mayor of Maastricht, Dr. V. Heijnen, and the Maastricht University President, Dr. M. Paul, also welcomed the EAS Congress to Maastricht.


The pinnacle of the Opening Ceremony, however, is the Anitschkow Lecture, which this year was given by Anitschkow Award recipient, Professor Helen Hobbs, an international leader in research defining the genetic determinants of plasma lipid levels and cardiovascular risk.  Professor Hobbs’ lecture was a tour de force of her research career, illustrating the value of the rare genetic concept, initially from work within the Dallas Heart Study, a ‘human biology laboratory’2 and latterly, extending to collaborations across the globe. This approach has not only identified critical variants conferring protection from atherosclerotic cardiovascular disease but has also driven the development of novel therapeutic approaches. A key example is identification of the role of PCSK9 (proprotein convertase subtilisin/kexin type 9) in cholesterol homeostasis,3 which has led to novel therapeutic approaches to lowering LDL cholesterol with important implications for public health. The First Late Breaking Session on Monday afternoon highlights new insights from the trials of novel PCSK9-targeted therapies, specifically inclisiran and LIB003.

With a changing landscape for cardiometabolic risk, fuelled by the escalating obesity pandemic, Professor Hobbs turned her attention to the genetics of fatty liver disease. Insights from the Dallas Heart Study, together with international collaborations, identified two key variants that play a crucial role in the progression of both non-alcoholic and alcoholic fatty liver disease. The first of these is PNPLA3 (patatin-like phospholipase domain-containing protein 3) a missense variant of a lipid droplet protein that disrupts the conversion of triglycerides to fatty acids,4,5 and the second is TM6SF2 (transmembrane 6 superfamily member 2), a splice variant in an endoplasmic reticulumR/Golgi Body protein, that disrupts the secretion of very low-density lipoproteins.6

In concluding remarks, Professor Hobbs noted that both the development of atherosclerosis and fatty liver disease represent the culmination of long-term exposure to excess lipids (cholesterol or triglycerides, respectively). Genetics can help in the search for novel targets with therapeutic potential; in the case of fatty liver disease, recent identification of a novel variant HSD17B13 (hydroxysteroid 17-beta dehydrogenase 13), has indicated the possibility of preventing progressive liver damage in hepatosteatosis.7

References

1. Ference BA, Ginsberg HN, Graham I, et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel. Eur Heart J 2017;38:2459-72.

2. Cohen JC, Kiss RS, Pertsemlidis A, et al. Multiple rare alleles contribute to low plasma levels of HDL cholesterol. Science 2004;305:869-72.

3. Cohen JC, Boerwinkle E, Mosley TH Jr, Hobbs HH. Sequence variations in PCSK9, low LDL, and protection against coronary heart disease. N Engl J Med 2006;354:1264-72.

4. BasuRay S, Wang Y, Smagris E, et al. Accumulation of PNPLA3 on lipid droplets is the basis of associated hepatic steatosis. Proc Natl Acad Sci U S A 2019;116:9521-6.

5. BasuRay S, Smagris E, Cohen JC, Hobbs HH. The PNPLA3 variant associated with fatty liver disease (I148M) accumulates on lipid droplets by evading ubiquitylation. Hepatology 2017;66:1111-24.

6. Smagris E, Gilyard S, BasuRay S, et al. Inactivation of Tm6sf2, a gene defective in fatty liver disease, impairs lipidation but not secretion of very low density lipoproteins. J Biol Chem 2016;291:10659-76.

7. Abul-Husn NS, Cheng X, Li AH, Xin Y, et al. A protein-truncating HSD17B13 variant and protection from chronic liver disease. N Engl J Med 2018;378:1096-106.



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