ABSTRACT
C-reactive protein (CRP) is a nonspecific acute phase protein that has been used as an inflammatory marker for decades. More recently, it has been proposed as a predictor of cardiovascular disease (myocardial infarction, stroke, peripheral artery disease and sudden heart death). Physiologic functions of CRP as an anti-inflammatory scavenger molecule have begun to emerge. CRP binds to damaged lipoproteins and facilitates their removal by phagocytes, partially activating the complement cascade. Increased levels of CRP may result in direct effects on vascular cells, including the induction of cytokines and prothrombotic factors. Although previous studies suggested a potent independent association of CRP levels with cardiac events, the strength of this association has been shown to be weaker than previously reported in a recent large meta-analysis and in prospective studies. Therapy with statins in patients with coronary artery disease has been found to reduce adverse outcomes in association with reductions of CRP levels, independently of their effects on the lipid profile.