Editorial
Computed tomography for detection of vulnerable coronary plaque – A Cassandra's dream?

The majority of acute coronary syndromes occur without warning due to rupture of coronary atherosclerotic plaques. Coronary lesions prone to rupture reveal several high-risk features that can be identified before the development of devastating clinical events, using modern imaging modalities. Recent advances in coronary computed tomography angiography (CCTA) allow the identification, quantification, and risk stratification of coronary plaques. Unquestionably, attempts to identify high-risk plaques by CCTA provide a unique opportunity to implement targeted preventive measures and improve prognosis. This review highlights insights into the ability of CCTA for the identification of vulnerable plaque and prediction of future coronary events that might affect future diagnosis and management of coronary artery disease.

The concept of vulnerable plaque

The concept of vulnerable plaque is based on the premise that certain coronary plaques are more prone to disruption or thrombosis than others, leading to a symptomatic acute coronary event [1]. Histological investigations have revealed two main features of coronary plaques associated with acute thrombus formation, i.e. plaque rupture (in about 70% of cases) and plaque erosion (in about 30% of cases) [1, 2]. Ruptured plaques are characterised by a large lipid pool of cholesterol-rich necrotic core covered by a thin layer of fibrous cap infiltrated with macrophages and T-lymphocytes. These plaques are supplied by an abundant vasa vasorum penetrating into the plaque intima from the adventitia [2]. Conversely, the more infrequent plaque erosion is characterised by an absent or disrupted endothelial lining and greater proliferation of smooth muscle than inflammatory cells. Of note, plaque erosions often lack the large lipid pool and/or thin fibrous cap, and appear to be more common in younger women [2].
It is assumed that plaques vulnerable to rupture share the same morphological features as ruptured plaques, but with an intact thin fibrous cap of < 65 µm [3]. These lesions are termed thin-cap fibroatheroma (TCFA) and are considered to be the requisite precondition for subsequent plaque rupture [1]. Interestingly, a serial angiographic study showed that the actual size of plaques responsible for the infarction was only moderate, with the majority of lesions having less than 50% luminal narrowing before the event (which does not necessarily imply that high-grade stenoses are always “innocent” and...


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