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© The European Society of Cardiology 2006. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Plaque stability and plaque regression: new insights

Diethelm Tschoepe and Bernd Stratmann

Diabetes Center, Bad Oeynhausen, Heart and Diabetes Center, North Rhine Westfalia, University Clinic, Ruhr University Bochum, Georg Str. 11, 32545 Bad Oeynhausen, Germany

Corresponding author. Tel: +49 5731 972292. E-mail address: ieickhoff{at}hdz-nrw.de

Patients with prior cardiovascular disease and/or diabetes are at the highest risk of a myocardial infarction or stroke. Thus, the majority of morbid cardiovascular events arise in the large population of patients with qualifying risk factors, according to standard risk factor scoring techniques. Angiography studies suggest that a substantial proportion of myocardial infarctions arise in vessels without severe atherosclerotic stenosis on initial examination. The rupture of the fibrous cap of the mature atherosclerotic plaque usually initiates intra-arterial thrombosis and is rendered more likely by additional factors such as inflammation, hyperglycaemic spikes, and mechanical or shear stress in the artery wall. The vulnerability of plaques to rupture is therefore an important determinant of outcome, and treatment strategies in patients with cardiovascular disease should address this issue. Continuing improvements in cardiac-imaging techniques raise the possibility of routine assessment of plaque stability in the future, which will facilitate the identification of vulnerable plaques and the delivery of appropriate treatment. Recent evidence from a large observational study suggests that low HDL-cholesterol not only drives atherosclerosis progression but also increases plaque vulnerability. Correcting low HDL-cholesterol, for example, with nicotinic acid or a fibrate, appears a rational strategy for addressing the continuing burden of atherothrombotic disease.

Key Words: Atherosclerosis • Diabetes • Dyslipidaemia • Cardiovascular risk factors • HDL-cholesterol • Metabolic syndrome


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