Researchers in Europe have discovered that stabilising vulnerable plaques as part of secondary prevention could contribute to eliminating at least 50 % of coronary events. Published in the journal Thrombosis and Haemostasis, the position paper of the European Society of Cardiology (ESC) Working Group of Atherosclerosis and Vascular Biology suggests that research on the causes of plaque rupture, as well as the on development of improved diagnostics and treatments, should be intensified.
The position paper tackled the current state of knowledge concerning unstable plaques by investigating the role of inflammation, growth factors, platelets, chemokines, angiogenesis and smoking. Therapies including statins, antiplatelet and antihypertensive treatments were outlined in the paper, and the researchers assessed novel approaches to dealing with cardiovascular events. They also worked on identifying unstable plaques through genetic testing, biomarkers and imaging.
'We want more medical professionals to understand the concept that stabilising vulnerable plaques offers a fundamental approach to preventing cardiovascular events,' explains Seppo Ylä-Herttuala of the University of Eastern Finland in Kuopio, chairman of the position paper task force and lead author. Professor Ylä-Herttuala goes on to say that researchers have observed a drop in cardiovascular events during a number of statin trials for secondary prevention. Such events have also benefited from platelet therapies.
For his part, Dr Christian Weber of Ludwig-Maximilians-University Munich in Germany, a member of the working group, says: 'Widespread stabilisation of vulnerable plaques would also have important socioeconomic implications, dramatically reducing the need for invasive treatments.'
Experts say not all plaques are made equally; some plaques are strong and have the capacity to withstand coronary events while others are more vulnerable and have a tendency to rupture and trigger such events. The researchers point out that these plaques are not necessarily the same as those that cause symptoms such as angina.
Dr Weber says the theory behind vulnerable plaques is that inflammatory cells that emerge from ongoing inflammation destabilise the structure of the plaque. 'It is believed that they degrade the fibres that make the plaque stable, leading to a greater potential for the plaque to rupture,' the German researcher says.
Researchers began investigating plaque stabilisation to describe how the number of acute coronary events could drop when lipids are decreased, without the accompanying regression of coronary atherosclerosis seen using angiography.
The working paper, says Professor Ylä-Herttuala, could help guide general clinicians better. 'The whole field can be really confusing,' he remarks. 'After patients have been treated with statins for two or three years, family doctors can be really concerned that they see no changes on angiograms. In such cases, there's a danger that they may decide to stop life saving treatment,' he adds.
'The single most important advance that would help us to tackle vulnerable plaques would be to have a non-invasive imaging tool that would allow us to identify at risk patients before they suffer an event,' the Finnish researcher says.
As for what the future holds, the position paper suggests more translational research into biomarkers and imaging be carried out, and new treatments be developed.
Says Dr Weber: 'There is a real need to develop treatments specifically for the purpose of stabilising vulnerable plaques. At the moment, we only have treatments that were discovered to have a beneficial effect through serendipity.'
Experts from Denmark, the Netherlands, Poland, Turkey and the United Kingdom also contributed to this paper.