This website uses cookies to store information on your computer. Some of these cookies are used for visitor analysis, others are essential to making our site function properly and improve the user experience. By using this site, you consent to the placement of these cookies. Click Accept to consent and dismiss this message or Deny to leave this website. Read our Privacy Statement for more.
Sign In   |   Register
News: Congress

Report from the Joint ESC/EAS Session: Can we really prevent atherosclerosis?

Tuesday 8 May 2018   (1 Comments)
Share |

Cardiovascular disease is a major cause of death and disability globally.1 Yet while there have been decreases in cardiovascular disease mortality in higher income regions, it is not the case in other less wealthy regions of the world. Indeed, the pandemics of obesity and type 2 diabetes have created a ‘perfect storm’ scenario in these regions, especially South Asia and the Middle East and North Africa regions, where rates of obesity have spiralled due to adoption of Western diets and increasingly sedentary lifestyles. 

Could atherosclerosis be prevented by targeting intervention earlier – - the primordial approach to prevention - and more comprehensively, including consideration of environmental factors, as well as novel preventive strategies?  This question was posed to experts at this Joint Session of the European Society of Cardiology (ESC)/EAS chaired by the President of the ESC Professor Jeroen Bax and the President of the EAS Professor Lale Tokgozoglu.

That is, of course not to disregard the constant need to improve goal attainment with aggressive lipid lowering strategies. However, there is clear evidence demonstrated in the EAS Consensus Panel paper on LDL causality that not only lower but earlier is better for cardiovascular disease prevention.2 According to Professor Alberico Catapano (University of Milan, Italy) as LDL has both a causal and cumulative effect on coronary risk, regression of atherosclerotic plaque may be possible with intensification of LDL cholesterol lowering; moreover, this may also promote compositional changes within the plaque leading to stabilisation of disease. In addition, knowledge of the genetic predisposition may help to individualise therapy and prevent the clinical complications of atherosclerotic cardiovascular disease.

Improving antithrombotic approaches is also relevant. As discussed by Professor Stephan Gielen (Martin-Luther-University, Halle-Wittenberg, Germany), in the acute coronary syndrome setting, dual antiplatelet therapy has been shown to significantly reduce mortality and non-fatal myocardial infarction.3 Certain patient groups with additional risk factors (for example, those who are older, with diabetes, multivessel or recurrent disease) are likely to benefit from a prolonged duration of intervention. In the primary prevention setting, aspirin is recommended in individuals with elevated risk where an aggressive approach is indicated.4  

However, what really attracted attention in this session was the need to change how we implement guidelines and cardiovascular preventive strategies. According to Professor Diederick Grobbee (University Medical Center Utrecht, the Netherlands) beyond the ‘usual’ suspects, we need to consider novel risk factors, especially the role of environmental factors, which have been shown to have important impact on cardiovascular risk. Advances in technology have allowed for the development of novel approaches to monitor the environment, including possibilities for remote and in situ sensing, smart home technology, as well as the use of social media. He suggested a novel term – the exposome – which uses an ‘omics’ approach to take account of the totality of exposures and their context.5 By definition this concept not only takes account of factors associated with the natural and social environment but also the effects of culture, economic activities, and social networks that may affect cardiovascular health by influencing access to healthcare, social cohesion, and socioeconomic status. For example, proximity to fast food outlets may be one issue to consider, as illustrated by a recent study from the Netherlands.6 Increased density of fast food outlets within 1000 m in an urban residential environment was associated with a significantly increased incidence of cardiovascular disease and coronary heart disease.

We already have strong evidence for established cardiovascular risk factors and guidelines provide evidence-based strategies for managing cardiovascular risk. It is increasingly recognised, however, that environmental factors also play a role in the propensity for development of cardiovascular disease, which may account for part of the residual risk independent of traditional factors.

We already know that more intensive management of established risk factors can provide additional clinical benefit, as evident by the PCSK9 inhibitor outcomes studies. Yet, it is apparent that we are lacking in implementation in already established treatments, as highlighted by Professor Ulrich Laufs (Leipzig University, Germany). This was highlighted by early data yesterday from EUROASPIRE V, an audit of the implementation of the 2016 Joint European Society of Cardiology/EAS lipid guidelines for secondary prevention patients. While most patients (84%) were receiving lipid lowering therapy (the majority statins), only about one in three of these patients (32%) attained the recommended LDL cholesterol goal of <1.8 mmol/L (<70 mg/dl) (Late Breaking Session, Monday). It is clear that clinicians need to ensure that high risk patients attain LDL cholesterol goals recommended by European guidelines.

However, given that atherosclerosis is a chronic inflammatory disease, we also need to think more about primordial intervention, targeting preventive strategies before the onset of disease. Additionally, knowledge about other factors, especially environmental factors that influence risk is highly relevant.  The use of ‘smart’ technological advances may make early primordial interventions more feasible and effective.

All of these considerations may help in the fight to truly prevent atherosclerosis in the future.



1. Joseph P, Leong D, McKee M et al. Reducing the Global Burden of Cardiovascular Disease, Part 1: The Epidemiology and Risk Factors. Circ Res 2017;121:677-694.

2. 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;38:2459-2472.

3. Bonaca MP, Bhatt DL, Steg PG et al. Ischaemic risk and efficacy of ticagrelor in relation to time from P2Y12 inhibitor withdrawal in patients with prior myocardial infarction: insights from PEGASUS-TIMI 54. Eur Heart J 2016;37:1133-42.

4. Guirguis-Blake JM, Evans CV, Senger CA et al. Aspirin for the Primary Prevention of Cardiovascular Events: A Systematic Evidence Review for the U.S. Preventive Services Task Force. Ann Intern Med 2016;164:804-13.

5. Riggs DW, Yeager RA, Bhatnagar A. Defining the Human Envirome: An Omics Approach for Assessing the Environmental Risk of Cardiovascular Disease. Circ Res 2018;122:1259-1275.

6. Poelman M, Strak M, Schmitz O et al. Relations between the residential fast-food environment and the individual risk of cardiovascular diseases in The Netherlands: A nationwide follow-up study. Eur J Prev Cardiol 2018. doi: 10.1177/2047487318769458. [Epub ahead of print]


William E. Feeman says...
Posted Thursday 2 August 2018
To borrow a line from the movie "Jurassic Park," just because you can do something doesn't mean you should. So it is interventional lipidology. The trick is to understand the pathophysiology of atherothrombotic disease (ATD) and that requires a knowledge of ATD risk factors because as the late William Kannel, MD stated, ATD "does not occur as a bolt out of the blue." Rather it is due to the presence of ATD risk factors, and that in the absence of those risk factors ATD is uncommon. That said, no one , if he/she lives long enough escapes some form of clinical ATD, so the trick is to identify the population at risk of ATD in the years prior to very old age. The risk factors are cigarette smoking, dyslipidemia, and hypertension, with some contribution by the very high blood sugar levels of uncontrolled diabetes. Dyslipidemia is best defined as a ratio between LDL- and HDL-cholesterol, particularly the Cholesterol Retention Fraction ([LDL-HDL]/LDL). See my poster at IAS2018.

Membership Software Powered by YourMembership  ::  Legal