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Hypertension. 2009;53:e39
Published online before print May 4, 2009, doi: 10.1161/HYPERTENSIONAHA.109.129361
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(Hypertension. 2009;53:e39.)
© 2009 American Heart Association, Inc.


Letters to the Editor

Polymorphisms of Inflammatory Markers/Mediators and Arterial Stiffness

Charalambos Vlachopoulos; Dimitrios Terentes-Printzios; Ioanna Dima; Konstantinos Aznaouridis; Christodoulos Stefanadis

Peripheral Vessels Unit, 1st Department of Cardiology, Hippokration Hospital, Athens Medical School, Athens, Greece


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

To the Editor:

We read with interest the article by Schumacher et al,1 which sheds new light into the still-controversial issue of the contribution of C-reactive protein (CRP) in the pathogenesis of cardiovascular disease. To this end, the authors tested the causality of CRP in arterial stiffness using genetically elevated CRP levels. However, such a causal relationship, through the mendelian randomization assumption, could not be established. Although CRP levels were associated with CRP genes and aortic pulse wave velocity (aPWV), none of the CRP genetic variants were associated individually or in combination with aPWV.

These findings are supported by our previous study that has established a causal relationship between acute inflammation and arterial stiffness.2 Although there was an overall positive correlation between CRP and aPWV, we showed that there was time dissociation in their response. CRP was elevated after 8 hours but reached its peak at 32 hours (increase by 1.77 mg/L), whereas aPWV reached its peak at 8 hours (increased by 0.43 m/s) and returned to baseline levels after 32 hours. Also, bearing in mind that arterial stiffness is determined by endothelial function, further corroboration to the noncausal association between CRP increase and arterial stiffening is provided by the study of Clapp et al,3 which showed normalization of endothelial dysfunction several hours after typhoid vaccination in spite of increased CRP levels. However, it should be noted that the CRP gene is highly polymorphic, and, accordingly, it would be interesting to investigate additional polymorphisms of CRP and their relation with . . . [Full Text of this Article]




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J. R. Cockcroft, C. M. McEniery, I. B. Wilkinson, and Y. Ben-Shlomo
Response to Polymorphisms of Inflammatory Markers/Mediators and Arterial Stiffness
Hypertension, June 1, 2009; 53(6): e40 - e40.
[Full Text] [PDF]