Crp a nonspecific marker of inflammation

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CRP rises in many inflammatory conditions, ranging from acute infections to chronic inflammatory diseases such as rheumatoid arthritis. This nonspecificity of CRP elevations could understandably engender skepticism regarding its utility as a risk marker for cardiovascular diseases. The very nonspecificity of CRP elevation, however, may explain why it appears useful for cardiovascular risk prediction. CRP serves as an overall barometer or

Oxidized LDL

compon

Inflamed Atheromata Visceral Adipose

Tissue

Cardiac Biomarkers Crp

Systemic

Infections Inflammatory Low HDL Diseases

Fig. 5. Multiple triggers can incite inflammation in CVDs. The first wave ofproinflammatory cytokines hypothesized in Fig. 4 may arise from a variety of vascular and extravascular stimuli. See text for explanation. HDL, high-density lipoprotein.

Inflamed Atheromata Visceral Adipose

Tissue

Systemic

Infections Inflammatory Low HDL Diseases

Fig. 5. Multiple triggers can incite inflammation in CVDs. The first wave ofproinflammatory cytokines hypothesized in Fig. 4 may arise from a variety of vascular and extravascular stimuli. See text for explanation. HDL, high-density lipoprotein.

integrator of inflammation in a given individual regardless of the source of that inflammation. The mix of proinflammatory stimuli that trigger the first wave of proinflammatory cytokines that ultimately elevate CRP levels likely differs among individuals. In some, chronic low-level infectious processes such as bronchitis or gingivitis may contribute to CRP elevation. In others, visceral adipose tissue may prevail as a stimulus for increased CRP levels. In others with widespread atherosclerotic plaques teeming with inflammatory activity, the atherosclerotic lesions themselves may contribute more to elevations in blood CRP levels. Since each ofthese diverse sources of initial inflammatory stimuli may augment atherogenesis or increase the risk of its thrombotic complications, CRP presents a simple gauge of inflammatory burden, whatever the mix of proximal stimuli that elicit the inflammatory response (Fig. 5).

The promise of clinical translation of inflammation biology depends on the availability of a practical test such as CRP measured by the high sensitivity assay (hsCRP). It also requires a substantial evidence base to merit incorporation into daily practice and practice guidelines. Many, though hardly all, agree that sufficient evidence supports the ability ofhsCRP to predict prospectively cardiovascular risk in primary prevention to encourage its consideration for clinical use. However, inclusion of CRP and other biomarkers of inflammation into clinically useful risk algorithms requires critical consideration. First, any biomarker, inflammatory or other, must demonstrate that it improves risk prediction beyond well-established and traditional risk factors such as those incorporated in the Framingham Risk Prediction Instrument. Chapter 16 contains full consideration of this point. In addition, a candidate biomarker must have a reproducible, available, and economical assay. The hsCRP assay fulfills such criteria. Optimally, adoption of a new risk marker should lead to cost-effective changes in therapy or management. Biomarkers of inflammation including hsCRP do not yet satisfy this criterion. The issue of the clinical

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