10 Molecular MRI of Atherosclerosis

Atherosclerosis and its consequences contribute to more than 50% of mortality in Europe, the United States of America and many developed or developing countries (Schafers et al., 2010). The main pathologic substrate in atherosclerosis is the atherosclerotic lesion. The classical high-risk plaque is characterized by a large lipid core, a thin fibrous cap and many macrophages in the shoulder regions of the plaque (Falk et al., 1995; Stary et al., 1995). Rupture of the fibrous cap or, more subtle, erosion leads to exposure of the thrombogenic sub-endothelial matrix to blood leading to thrombus formation. Recurrent thrombosis or major atherothrombosis may lead to an acute cardiovascular event via sub(total) occlusion of the vessel of interest. Macrophages are the key mediators of plaque inflammation and progression (Lusis, 2000; Ross, 1999). Inflammatory activity can be evaluated at the cellular (macrophages and neutrophils) or sub-cellular (secreted enzymes, membrane-bound proteins) level. Sensitive and specific biomarkers of plaque inflammation and instability are highly desired for more accurate definition of high-risk plaques in high risk patient populations. At present, serologic markers do not accomplish this need sufficiently. Therefore, there is a need for noninvasive imaging techniques for identification and quantification of local plaque biomarkers, which can direct interventional cardiologists and vascular surgeons to diseased sites and can monitor therapeutic response.