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Myocardial infarction remains the commonest cause of premature death worldwide with coronary atherosclerotic plaque rupture often initiating the event. Despite an ever-expanding repertoire of cardiovascular imaging techniques, the race is still on to identify atherosclerotic lesions at high-risk of rupture: the so-called vulnerable plaque. Conventional imaging modalities such as stress testing and coronary angiography have consistently failed to identify such plaques, leading to the increasing appreciation that plaque rupture relates to factors other than just the degree of luminal stenosis. Indeed the focus has recently shifted to molecular imaging, in an attempt to directly target the pathological disease processes leading to rupture and thereby localize high-risk lesions. Histological data indicate that inflammation, necrosis and early stage microcalcification are key imaging targets by which to achieve this aim. Here, we discuss how these processes are related, focusing on the rationale and evidence supporting 18F-fluoride positron emission tomography as a novel non-invasive imaging technique for the identification of vulnerable atherosclerotic plaque.

Original publication




Journal article


Curr cardiol rep

Publication Date





Coronary Artery Disease, Fluorine Radioisotopes, Humans, Multimodal Imaging, Myocardial Infarction, Plaque, Atherosclerotic, Positron-Emission Tomography, Radiopharmaceuticals, Risk Assessment, Sodium Fluoride, Tomography, X-Ray Computed, Vascular Calcification