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Prof. Cetin Erol ,
Liapis defined vulnerable plaque as a “future culprit plaque” and described its features: thin fibrous cap, large necrotic lipid core and inflammation. Then he stressed the importance of detection. Imaging technologies are perfect but they are invasive, expensive and not available everywhere. So biomarkers are an alternative option, there are many of them that could be used. Biomarkers predict natural history of carotid and cerebrovascular disease, predict perioperative risk and guide medical treatment. However, there is no gold standard among biomarkers.
By using High Definition Ultrasonography with computer assisted Plaque Analysis, active carotid plaques could be identified by measuring degree of stenosis, activity index and image based Risk Prediction Score. Homogenous and heterogeneous plaque differentiation should be done. Then he also mentioned the 3D construction of the plaque.
Fernandes first gave the general overview of renal artery stenosis, then why it should be treated. The reasons for treatment are: to control blood pressure and save renal function, then treatment choices are medical or interventional. Recent studies comparing medical and interventional therapies were summarised. According to the recent trend, medical treatment should be given as a first choice to these patients.
Narula drew the attention of the audience to the diversity between plaque rupture and the severity of stenosis. Also, no correlation has been found between the high risk plaque and the severity of stenosis. He stressed that more necrotic core means a thin fibrous cap, which can possibly predict major cardiovascular outcomes. Attenuation of the plaque seen by CT may herald the slow flow after PCI and Napkin Ring Type imaging shows the cholesterol burden. Stent implantation for a vulnerable plaque could end with no endothelisation. So a new type of stent would be preferable. Overall, the symposium was very useful for understanding the importance of the vulnerable plaque and the new developments in this issue.
Identification of vulnerable atherosclerotic plaques and impact on treatment decision
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