Who gets the heart attack: noninvasive imaging markers of plaque instability

Excerpt

Acute coronary events result from thrombotic occlusion of the coronary artery.1-5 The occlusion is secondary to rupture of an atherosclerotic plaque in up to three-fourths of subjects; plaque erosion is seen in most of the remaining subjects who have died of an acute coronary event.2 Plaque rupture is associated with traditional risk factors, whereas erosion is generally associated with smoking and is commonly observed in women or younger subjects. Upon histopathological examination, the plaques that are prone to rupture and result in an acute event are almost always large.1-5 Such plaques also demonstrate large necrotic cores that occupy a large proportion of the plaque area. These necrotic cores are often associated with intraplaque neovascularization and hemorrhage, and adventitial vasa vasorum proliferation. 6,7 The necrotic cores are covered by rather attenuated fibrous cap, which are intensely inflamed. Therefore, an imaging strategy designed to identify rupture-prone plaques would target the enormity of plaque and necrotic core volumes, positive remodeling, and plaque inflammation.4,5 The morphological characteristics of such plaques can be identified by CT angiography of coronary arteries.4,8 Magnetic resonance has been employed for morphologic characterization of carotids and can also identify intraplaque hemorrhage.9,10 Contrast-enhanced ultrasound examination has revealed plaque neovascularization and vasa vasorum proliferation.11,12 Assessment of the fibrous cap thickness needs intravascular imaging techniques such as the optical coherence tomography.13 Plaque inflammation has been successfully assessed by PET imaging using fluorodeoxyglucose (FDG).14,15 Newer molecular imaging strategies have targeted upregulation of receptors on infiltrating monocyte or cytokine production.5 …