Recent evidence has shown that inflammation plays a pivotal role in the inception and progression of atherosclerosis, and population studies have demonstrated a strong and independent association between baseline concentrations of inflammatory biomarkers and future coronary events. Because the majority of individuals who develop coronary events are not in a high-risk group according to the Framingham risk assessment of traditional risk factors for coronary heart disease (CHD),2 and because one half of those who suffer myocardial infarctions have normal lipid values, measurement of inflammatory markers has been suggested as an adjunct to lipid testing to better identify individuals at increased risk (1). Of the inflammatory markers evaluated by a CDC and American Heart Association (AHA) Panel in 2002(2)(3), only C-reactive protein (CRP) met the analytical requirements for outpatient clinical use and, therefore, has been studied intensely over the past decade. More than 25 prospective epidemiologic studies have shown that CRP is a strong and independent predictor of future myocardial infarction, ischemic stroke, peripheral arterial disease, and sudden cardiac death in apparently healthy men and women (4). Furthermore, 9 studies to date have demonstrated that CRP provides additional prognostic value to the Framingham Risk Score(4). Guidelines regarding the potential usefulness of CRP in primary and secondary prevention settings have been issued by the CDC and AHA(2). Physicians have become accustomed to use of the “high-sensitivity CRP (hsCRP)” terminology when considering measurement of CRP for vascular disease risk stratification, as opposed to the use of standard CRP assays that monitor infections and other inflammatory conditions. To assess CHD risk, CRP must …