ABSTRACT
The importance of acute phase molecules as risk factors for human cardiovascular disease has been emphasized in a number of reports.1-7 The principal acute phase protein, C-reactive protein (CRP), named for its capacity to precipitate the somatic C-polysaccharide of Streptococcus pneumoniae, has been linked to atherosclerosis and its complications. The biological characteristics of CRP have been reviewed by Pepys and Hirschfield.8 Briefly, CRP consists of five identical non-glycosylated 23 kDa subunits, is mainly synthesized by hepatocytes under interleukin-6 (IL-6) control, is highly stable, and its serum concentration of less than 1 mg/l can increase 10 000-fold during the acute phase response.9,10 Over the past decade, multiple clinical studies have associated CRP with an increased risk of developing myocardial infarction, stroke, peripheral arterial disease, cardiovascular events, and sudden death.1-7,11-23 In addition to predicting cardiovascular events in patients with atherosclerotic disease, elevated levels of CRP are among the strongest predictors of progressive vascular disease21 and future cardiovascular events in apparently healthy men and women.4,5,11 Accumulating evidence indicates that CRP is directly involved in biological processes that contribute to the pathogenesis of atherosclerotic disease.
