doi: 10.1161/01.ATV.0000142444.02057.e7
© 2004 American Heart Association, Inc.
Letters to the Editor |
Aortic Stiffness Does Not Mediate the Relation Between Pulse Pressure and CRP
Hopital Rangueil, INSERM 558, Toulouse, France
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
To the Editor:
Dr Yasmin et al1 have described a positive correlation between C reactive protein level and arterial stiffness in individuals selected at random from local general practice lists. From these data the authors suggest that inflammation may be involved in arterial stiffening. As quoted by Yasmin et al, we have reported2 in population based sample (891 subjects randomly selected from the electoral rolls whom 13% with treated hypertension), a positive correlation between pulse pressure and c reactive protein independent of carotid-femoral pulse wave velocity. This correlation remained after exclusion of patients with treated risk factors. Also, we showed in a post hoc analysis3 of a randomized trial (the REASON project) that the greater the decrease in pulse pressure, the greater the decrease in the proportion of patients with high C reactive protein levels. These results suggest that pulse pressure per se may modulate CRP secretion. There are several plausible mechanisms by which pulse pressure could increase inflammation levels, and in particular CRP levels, which provides a downstream integration of overall cytokines activation. Indeed, it has been demonstrated that shear stress was associated with increased production of reactive oxygen species4,5 and of cytokines such as tumor necrosis alpha or interleukin 6.6 Therefore, in addition to the hypothesis raised by Yasmin et al,1 our findings argue a causal relationship leading from pulse pressure to inflammation.
1. Yasmin, McEniery CM, Wallace S, Mackenzie IS, Cockcroft JR, Wilkinson IB. C-reactive protein is associated with arterial stiffness in apparently healthy individuals. Arterioscler Thromb Vasc Biol. 2004; 24: 969–974.
2. Amar J, Ruidavets JB, Sollier CB, Bongard V, Boccalon H, Chamontin B, Drouet L, Ferrieres J. Relationship between C reactive protein and pulse pressure is not mediated by atherosclerosis or aortic stiffness. J Hypertens. 2004; 22: 349–355.[Medline] [Order article via Infotrieve]
3. Amar J, Ruidavets JB, Peyrieux JC, Mallion JM, Ferrieres J, Safar M, Chamontin B. Relationship between C reactive protein and pulse pressure. Comparison between low dose preindopril/indapamide first line combination and atenolol on changes in c reactive protein: a link with pulse pressure? XIV European meeting on hypertension, Paris, France. Abstract book S276.
4. Ryan SM, Waack BJ, Weno BL, Heistad DD. Increases in pulse pressure impair acetylcholine-induced vascular relaxation. Am J Physiol. 1995; 268: H359–H363.
5. Lacy F, Kailasam MT, O’Connor DT, Schmid-Schonbein GW, Parmer RJ. Plasma hydrogen peroxide production in human essential hypertension: role of heredity, gender, and ethnicity. Hypertension. 2000; 36: 878–884.
6. Nomura S, Tandon NN, Nakamura T, Cone J, Fukuhara S, Kambayashi J. High-shear-stress-induced activation of platelets and microparticles enhances expression of cell adhesion molecules in THP-1 and endothelial cells. Atherosclerosis. 2001; 158: 277–287.[CrossRef][Medline] [Order article via Infotrieve]
Pulse Pressure and CRP: An Inflammatory Issue
Wales Heart Research Institute, University Hospital, Cardiff, UK
Clinical Pharmacology Unit, University of Cambridge, Addenbrooke’s Hospital, Cambridge, UK
In response:
We thank Amar et al for their interest in our recent article demonstrating, for the first time, a relationship between inflammation and arterial