Sensitive markers of inflammation make it possible to study the chronic process: the rise of interest in low levels of C-reactive protein.

Increases in baseline levels of C-reactive protein (CRP) have been consistently identified as an independent risk indicator of cardiovascular events. The measurement of the low level is robust and well established. Increases in low levels of CRP can mark low-grade continuous inflammation and hyperresponse in acute situations. In addition, CRP can exert various actions on vascular cells and activates complement thus participating in infarction pathogenesis. Various cardiovascular drugs, notably statins, can induce a marked decrease in low levels of CRP, which is indicative of their beneficial effect on inflammation. Future studies need to demonstrate whether increases in baseline levels of CRP can become a useful practical addition to risk recognition strategies and possibly may also serve as an additional surrogate endpoint in cardiovascular disease treatments.