Chronic inflammatory changes of the arterial wall are inherent in the genesis of atherosclerosis ( 1 Ross R Atherosclerosis: an inflammatory disease. N Engl J Med. 1999; 340: 115-126 Crossref PubMed Scopus (19069) Google Scholar ). Despite the inhomogeneous makeup of atherosclerotic plaque, it is assumed that atherosclerotic changes originate from fatty streaks that occur early in life and tend to progress to advanced lesions ( 2 Berliner JA Navab M Fogelman AM et al. Atherosclerosis: basic mechanisms—oxidation, inflammation, and genetics. Circulation. 1995; 91: 2488-2496 Crossref PubMed Scopus (1574) Google Scholar , 3 Ross R The pathogenesis of atherosclerosis: a perspective for the 1990s. Nature. 1993; 362: 801-809 Crossref PubMed Scopus (9929) Google Scholar ). Particular plaque configurations yield high risks for thrombosis independent of the degree of associated luminal narrowing ( 4 Fuster V Badimon L Badimon JJ Chesebro JH The pathogenesis of coronary artery disease and the acute coronary syndromes (1). N Engl J Med. 1992; 326: 242-250 Crossref PubMed Scopus (2899) Google Scholar ). Whereas conventional angiographic techniques display luminal narrowing, the presented strategy aims at the detection of atherosclerosis-associated inflammatory changes in the vessel wall, based on the observation that ultrasmall superparamagnetic iron oxide (USPIO) particles undergo phagocytosis by cells of the mononuclear phagocytic system ( 5 Saini S Stark DD Hahn PF Wittenberg J Brady TJ Ferrucci Jr, JT Ferrite particles: a superparamagnetic MR contrast agent for the reticuloendothelial system. Radiology. 1987; 162: 211-216 Crossref PubMed Scopus (237) Google Scholar ).