Am J Physiol Regul Integr Comp Physiol 285: R1258, 2003;
doi:10.1152/ajpregu.00483.2003
0363-6119/03 $5.00
POINT-COUNTERPOINT
Response to S. Verma and E. T. H. Yeh: C-reactive protein and atherothrombosis—Beyond a biomarker: an actual partaker of lesion formation
Gavin J. Blake and
Paul M. Ridker
Cardiovascular Division and the Center for Cardiovascular Disease Prevention, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02215
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.
FOOTNOTES
Address for reprint requests and other correspondence: P. M. Ridker, Center for Cardiovascular Disease Prevention, Brigham and Women's Hospital, 900 Commonwealth Ave. East, Boston, MA 02215 (E-mail: pridker{at}partners.org).
Copyright © 2003 by the American Physiological Society.
