Serum amyloid P component and cardiovascular disease: is there a sensible link?

Atherosclerosis shows several features of an inflammatory process.1 There is ubiquitous presence of characteristic cells like monocytes/macrophages, and T cells that produce various mediators involved in local inflammation and these inflammatory molecules (cytokines, chemokines, growth factors) are found at the site of the plaque in the arterial vessel wall through all stages of the process, most pronounced during acute ischemic syndromes.2 Atherosclerosis is also accompanied by a systemic low-grade inflammatory response that can be detected by sensitive assays. Because of the importance of inflammation for the initiation and progression of the atherosclerotic process, and the occurrence of deleterious clinical events, interest has focused on a large number of potential biomarkers that have been tested prospectively in clinical and epidemiological studies. Most of them are part of the acute phase reaction and indeed have been found to predict clinical atherosclerosis end points, even after controlling for a variety of traditional risk factors.3 A particular large database has been build up for C-reactive protein (CRP), a member of the pentraxin family, and an exquisitely sensitive acute phase reactant, documenting its association with various cardiovascular disease (CVD) end points.4 In addition, in vitro studies and animal experiments have suggested a direct contribution of CRP to atherogenesis.5 However, such evidence6 and the issue of an incremental value of CRP and other emerging blood biomarkers to risk prediction over and above global risk assessment by risk scores using traditional risk factors, still represent a matter of controversy.7