Intraplaque Hemorrhage: An Imaging Marker for Atherosclerotic Plaque Destabilization?

Luminal thrombosis by rupture of the vulnerable atherosclerotic plaque is considered the main pathological substrate of the acute cerebral and coronary syndrome. The traditional definition of the vulnerable plaque has been based on cross-sectional postmortem observations and is reflected by a thin capped atheromatous lesion hiding different types of inflammatory cells that degrade the fibrous tissue. More recently the role of intraplaque hemorrhage (IPH) in atherosclerotic disease progression has gained serious interest.1 IPHs are caused by neocapillary rupture and relate to angiogenesis from the adventitia toward the plaque. The density of neovessel formation is positively correlated with the extent of necrotic core formation and inflammatory infiltrates, suggesting that vessel formation appears to be linked to the evolution of atherosclerosis from early stage to a complicated lesion.2 The clinical and biological importance of IPHs has long been neglected, because the majority of biological studies focused on lipid metabolism and the inflammatory responses that are evident in atherosclerotic disease initiation and progression. The presence of intraplaque extravasation or bleeding is no longer considered an innocent bystander but regarded as a feature that contributes to local lipid deposition and acts as a source for proinflammatory responses.1 It has been shown that lipid-rich …