The hypothesis that atherosclerosis is largely an inflammatory disease is barely a decade old. As a result, even for basic research, relationships are still hazy between coronary artery inflammation and ischemic heart disease. Not only is inflammatory risk multifactorial, but the two major end points of ischemic heart disease—chronic atherosclerosis and acute coronary syndromes—differ in their pathogenesis: 70% of myocardial infarcts follow the sudden occlusion of an artery with no previous flow-limiting stenosis. Prognostic tests using systemic markers of inflammation, such as C-reactive protein, have yielded some striking correlations, epidemiologically and clinically, notably over the short term in unstable patients, but it is still premature and simplistic to expect them to reflect the general risk of two only partially related end points...