As elegantly outlined by Drs Verma and Yeh in their article, accumulating data suggest a potential direct proinflammatory role for C-reactive protein (CRP) in atherogenesis. Although these laboratory data are intriguing, the clinical relevance of these effects remains unproven. We concur that circulating levels of CRP may not accurately reflect local tissue concentrations at the vascular endothelium, making direct correlation between plasma levels of CRP used for risk prediction and local concentrations required to elicit pro-atherogenic effects difficult. Nonetheless, the clinical utility of CRP as a robust predictor of incident cardiovascular events may also relate to its favorable analytic properties, such as lack of circadian rhythm, relatively long half-life (18 h), and stability over time.
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