It is generally accepted that the majority of acute coronary events are precipitated by the rupture of a vulnerable atherosclerotic plaque in the coronary system, and subsequent thrombogenesis.
1–3 The thin-cap fibroatheroma is currently hypothesised to be the most likely class of arterial wall pathology to constitute a vulnerable plaque.
4,5 The key to plaque vulnerability is still elusive,
7 even though recent technological advances in intravascular imaging technology have enabled the collection of a wealth of data on unstable atherosclerosis in all its stages of development,
8 both in clinical and in
ex vivo settings. It appears very likely that combined information on physiological, anatomical, chemical, and mechanical parameters
9–11 is needed for a reliable assessment of the proneness of a specific lesion to rupture. Some of these parameters may be accessible through intravascular imaging methods.
12–16 In addition, plaque type and morphology prior to intervention significantly influence the long-term procedure outcome.
17 The parameters that influence plaque vulnerability include the thickness of the fibrous cap overlying the necrotic core, inflammation, intraplaque haemorrhage, and composition.
10,18 Data on plaque composition and stability, complementing the image, may inform the decision on if and how to treat a particular section of coronary artery. …
