The contemporary literature now contains numerous reports of the relationship between various biomarkers of inflammation and prospective cardiovascular risk, in apparently well individuals as well as in patients with coronary heart disease or heart failure. The clinical utility of a biomarker for risk prediction depends on practicability, ease, cost, and reproducibility of the measurement, and the ability to add to the predictability of existing biomarkers such as those incorporated in the Framingham algorithm. Many reviews have highlighted this fast-moving field (42). Among the many biomarkers of inflammation proposed for diagnostic use, myeloperoxidase, Lp-PLA2, pentraxin-3, cytokines such as IL-6, proteases such as matrix metalloproteinase-9, and C-reactive protein (CRP) measured by a highly sensitive assay (hsCRP) have generated considerable attention. For a variety of reasons, CRP has emerged as a leading biomarker of inflammation for clinical application. In well individuals without acute infections or inflammatory diseases (e.g., rheumatoid arthritis), levels of hsCRP remain stable over long periods of time with a year-to-year and decade-to-decade variability comparable to that of cholesterol (43- 44). CRP has considerable chemical stability, requires no special precautions for sampling, and has a relatively long half-life without the diurnal variation that plagues certain other biomarkers.