An elevated level of C-reactive protein (CRP), an acute phase protein, is one of many downstream indicators of inflammation. Physiologically, CRP enhances cell-mediated immunity by promoting phagocytosis, accelerating chemotaxis, and activating platelets. The purposes of this article are (1) to review the clinical data implicating serum CRP level as a systemic marker of focal inflammation and (2) to explore serum CRP level as a reflection of the inflammatory component of atherogenesis. Our findings indicate that CRP levels serve as an early marker of the magnitude of inflammation in events as dissimilar as appendicitis and myocardial infarction. The level of circulating CRP correlates with endovascular disease and may serve to identify otherwise asymptomatic patients at sufficient cardiovascular risk to warrant aggressive therapy. Determining whether CRP has a direct pathologic role in the vascular wall itself may have the most clinical relevance.