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(Circulation. 2007;115:e476.)
© 2007 American Heart Association, Inc.

Correspondence

Response to Letter Regarding Article, "The Inflammatory Hypothesis: Any Progress in Risk Stratification and Therapeutic Targets?"

Stefan Blankenberg, MD

Department of Medicine II, Johannes Gutenberg University, Mainz, Germany

Salim Yusuf, DPhil, FRCPC, FRSC

McMaster University and Hamilton General Hospital, Hamilton, Canada

An extract of the first 250 words of the full text is provided, because this article has no abstract.

We thank Drs Ridker and Everett for their interest in our work,¹ and we commend Ridker’s pioneering work describing an association between C-reactive protein (CRP) and the risk of myocardial infarction or stroke. Subsequent studies have both confirmed and refuted these original observations. The former studies "controlled" or "adjusted" for fewer other risk factors; when they did so, they dichotomized variables (a weaker approach) rather than using them as continuous variables. By contrast, the latter studies have incorporated adjustments for other markers (especially of abdominal obesity, because visceral fat is a source of various cytokines or N-terminal-pro-brain natriuretic peptide, which is emerging as a strong risk factor²) and have used more sensitive statistical approaches to adjustment. In most studies, after full adjustment the odds ratios between extreme quantiles have been too modest (generally under 2, but sometimes under 1.5) to be clinically useful or justify the additional expense of measuring CRP. In this respect, the study by Bos et al³ is unique because it addresses different subtypes of stroke, including subtypes of ischemic strokes such as large-artery hemispheric strokes, small-vessel lacunar stroke, and hemorrhagic strokes. There was no independent association between CRP concentration and incident stroke or its subtypes. The limitations of CRP as a predictor with incremental value (either using the methods of area under the curve or statistics) have been discussed by Lloyd-Jones⁴ et al and have been demonstrated elegantly by Danesh et al.⁵ Despite their reservations, inflammation (of which CRP may be a generalized marker) may . . . [Full Text of this Article]