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CRP in non-dippers: new perspectives and old queries

Journal of Human Hypertension volume 22, pages 447–449 (2008)Cite this article

C-reactive protein (CRP), a very sensitive biomarker of systemic inflammation, is an acute phase reactant that was discovered over 70 years ago to be a blood protein that binds to the C-polysaccharide of pneumococci. CRP is the most reliable and accessible biomarker for clinical use. In recent years, it has attracted much attention, with numerous articles pointing out its role not only in the prediction of cardiovascular risk and in the progression of atheromatous disease in patients with pre-existing cardiovascular disease, but also in apparently healthy individuals.1, 2 Many clinicians went so far as to consider CRP as a preclinical marker for cardiovascular disease, and clinical guidelines suggested CRP measurement as an adjunct to traditional cardiovascular risk factors with a view to improving the prediction of the absolute risk of coronary artery disease. On the other hand, subsequent meta-analyses and studies with larger populations were also published, which showed that the epidemiological relation between CRP levels and coronary artery disease incidence was less strong than reported previously, and indicated that CRP is a relatively modest predictor of coronary events.3, 4

C-reactive protein is frequently elevated in hypertensive patients as well;5 basic data have attributed to hypertension a link with low-grade inflammation. In particular, it is postulated that blood pressure elevation is accompanied by vascular inflammation and that the magnitude of blood pressure and CRP levels have an additive effect in the prognosis of cardiovascular risk. Notably, cross-sectional independent associations between high blood pressure and CRP levels have also been reported.6 However, there are studies that call into question the strength of the link between CRP and hypertension. Bautista et al.7did not manage to reveal a significant association between essential hypertension and CRP when they examined the latter independently of other markers. This may imply that in a non-homogeneous patient population, many other clinical factors might affect the relationship of CRP with essential hypertension. These factors may instantaneously modify vascular inflammatory status.

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References

  1. Ridker PM . Clinical application of C-reactive protein for cardiovascular disease detection and prevention. Circulation 2003; 107: 363–369.

    Article  Google Scholar 

  2. Ridker PM, Buring JE, Shih J, Matias M, Hennekens CH . Prospective study of C-reactive protein and the risk of future cardiovascular events among apparently healthy women. Circulation 1998; 98: 731–733.

    Article  CAS  Google Scholar 

  3. Danesh J, Whincup P, Walker M, Lennon L, Thomson A, Appleby P et al. Low grade inflammation and coronary heart disease: prospective study and updated meta-analyses. BMJ 2000; 321: 199–204.

    Article  CAS  Google Scholar 

  4. Danesh J, Wheeler JG, Hirschfield GM, Eda S, Eiriksdottir G, Rumley A et al. C-reactive protein and other circulating markers of inflammation in the prediction of coronary heart disease. N Engl J Med 2004; 350: 1387–1397.

    Article  CAS  Google Scholar 

  5. Kakar P, Lip GYH . Towards understanding the aetiology and pathophysiology of human hypertension: where are we now? J Hum Hypertens 2006; 20: 833–836.

    Article  CAS  Google Scholar 

  6. Bautista LE . Inflammation, endothelial dysfunction, and the risk of high blood pressure: epidemiologic and biological evidence. J Hum Hypertens 2003; 17: 223–230.

    Article  CAS  Google Scholar 

  7. Bautista LE, Vera LM, Arenas IA, Gamarra G . Independent association between inflammatory markers (C-reactive protein, interleukin-6, TNF-α) and essential hypertension. J Hum Hypertens 2005; 19: 149–154.

    Article  CAS  Google Scholar 

  8. Pedrinelli R, Dell’Omo G, Di Bello V, Pellegrini G, Pucci L, Del Prato S et al. Low-grade inflammation and microalbuminuria in hypertension. Arterioscler Thromb Vasc Biol 2004; 24: 2414–2419.

    Article  CAS  Google Scholar 

  9. Nakhai-Pour HR, Grobbe DE, Bots ML, Muller M, van der Schouw YT . C-reactive protein and aortic stiffness and wave reflection in middle-aged and elderly men from the community. J Hum Hypertens 2007; 21: 949–955.

    Article  CAS  Google Scholar 

  10. Tsioufis C, Syrseloudis D, Dimitriadis K, Thomopoulos K, Tsiachris D, Pavlidis P et al. Disturbed circadian blood pressure rhythm and C-reactive protein in essential hypertension. J Hum Hypertens 2008. e-pub ahead print.

  11. Larrousse M, Bragulat E, Segarra M, Sierra C, Coca A, de La Sierra A . Increased levels of atherosclerosis markers in salt-sensitive hypertension. Am J Hypertens 2006; 19: 87–93.

    Article  CAS  Google Scholar 

  12. Daskalopoulou SS, Mikhailidis DP . How low should we go with cholesterol lowering? Hellenic J Cardiol 2004; 45: 136–139.

    Google Scholar 

  13. Marnell L, Mold C, Du Clos TW . C-reactive protein: ligands, receptors and role in inflammation. Clin Immunol 2005; 117: 104–111.

    Article  CAS  Google Scholar 

  14. Kovacs A, Tornvall P, Nilsson R, Tegner J, Hamsten A, Bjorkegren J . Human C-reactive protein slows atherosclerosis development in a mouse model with human-like hypercholesterolemia. Proc Natl Acad Sci USA 2007; 104: 13768–13773.

    Article  CAS  Google Scholar 

  15. Panagiotakos DB, Chrysochoou C, Pitsavos C, Skoumas J, Zeibekis A, Papaioannou I et al. The prevalence of clinical and biochemical markers related to cardiovascular disease: design and preliminary results from the ATTICA study. Hellenic J Cardiol 2003; 44: 308–316.

    Google Scholar 

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  1. Cardiology Department, Heraklion University Hospital, Crete, Greece

    P E Vardas & M E Marketou

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  1. P E Vardas
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  2. M E Marketou
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Correspondence to P E Vardas.

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Vardas, P., Marketou, M. CRP in non-dippers: new perspectives and old queries. J Hum Hypertens 22, 447–449 (2008). https://doi.org/10.1038/jhh.2008.33

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