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Physicians depend greatly on imaging techniques that help them make clinical decisions. However, when a diagnosis is made on the basis of anatomical imaging alone, the disease process has often advanced beyond the point where preventative therapy can be applied. In many cardiovascular diseases, it is vital to detect pathological and normal processes at an early, subclinical stage, to enable early and improved diagnosis, prediction and treatment (figure 1A). This is particularly relevant to atherosclerosis, which can be clinically silent for decades and then manifest suddenly as an acute myocardial infarction (MI) or stroke.
The holy grail in cardiovascular prevention is to identify individuals at risk for MI or stroke. At present, structural imaging tools such as CT or intravascular ultrasound (IVUS) cannot reliably identify ‘vulnerable’ patients with a high risk plaque that will lead to thrombotic occlusion of a coronary or cerebral artery.w1 w2 Our current understanding of such plaques is largely defined by postmortem studies, but is limited by processing and only provides a single snapshot in the lifetime of a culprit lesion. These studies demonstrate that culprit lesions in acute MI demonstrate acute plaque rupture in ∼60% of cases, plaque erosion in ∼25%, and other mechanisms in the remainder of cases (calcified nodule, other). Plaque rupture is biologically driven by inflammatory cells (macrophages, lymphocytes), destabilising proteases (matrix metalloproteinases, cathepsins), reactive oxygen species, fragile …