Engström raises the question whether “elevated CRP level is attributable to CHD risk factors” or whether “CHD risk factors are attributable to low-grade inflammation.”1(p2063) If elevated CRP level is attributable to CHD risk factors, one would predict that therapies aimed at improving the CHD risk profile would also favorably influence CRP levels. In fact, this has been well documented following treatment of obesity, diabetes mellitus, hypertension, and dyslipidemia.2-4 In contrast, it is considerably less plausible to believe that CHD risk factors such as cigarette smoking or physical inactivity would be “caused” by inflammation. Moreover, the concept that “CRP measurements may have limited clinical utility as a screening tool beyond other known risk factors”1(p2063) gained further support recently when the Framingham Heart Study found that CRP level added no additional value in predicting CHD events beyond that derived from traditional risk factors.5 In view of the aforementioned, we agree with Engström that there are “reasons to remain doubtful about the utility of CRP level as a screening tool.” Rather, the clinical significance of CRP level should be more thoroughly evaluated using statistical tools such as the receiver operating characteristic curve to more appropriately express the low impact of this biomarker in CHD risk assessment.6 In the meantime, we should focus our attention on improving the prevention and control of traditional risk factors.
Miller M, Havas S. The Role of Inflammation for Heart Disease Risk Cannot Be Determined by Correlations Between C-Reactive Protein and Risk Factors—Reply. Arch Intern Med. 2006;166(9):1040–1041. doi:https://doi.org/10.1001/archinte.166.9.1040-b
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