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Paradoxical association of C-reactive protein with endothelial function in rheumatoid arthritis

Michael V Holmes1, Benyu Jiang, Karen McNeill

  • 1King's College London, British Heart Foundation Centre, Department of Clinical Pharmacology, St. Thomas' Hospital, London, UK.

Plos One
|May 4, 2010
PubMed

Insights

C-reactive protein (CRP) may protect blood vessels, not cause atherosclerosis. In rheumatoid arthritis patients, higher CRP correlated with better endothelial function, suggesting a protective role for nitric oxide.

Area of Science:

  • Cardiovascular Science
  • Rheumatology
  • Biochemistry

Background:

  • C-reactive protein (CRP) is linked to cardiovascular disease (CVD), but its causal role is debated.
  • A potential protective effect of CRP on endothelium-derived nitric oxide (EDNO) has been proposed.

Purpose of the Study:

  • To investigate the association between CRP levels and EDNO-dependent vasomotor function.
  • To assess the relationship between CRP and subclinical atherosclerosis and arteriosclerosis in rheumatoid arthritis (RA) patients.

Main Methods:

  • Compared high-sensitivity CRP, flow-mediated dilation (FMD), intima-media thickness (IMT), and aortic pulse wave velocity (PWV) in RA patients (n=59) and controls (n=123).
  • Analyzed correlations between CRP and vascular measures within the RA cohort.

Main Results:

  • Patients with RA had elevated IMT and PWV compared to controls, but similar FMD.
  • In RA patients, FMD showed a positive independent correlation with CRP (P<0.01).
  • No significant correlation was found between CRP and IMT or PWV in RA patients.

Conclusions:

  • Findings suggest CRP does not causally contribute to atherogenesis.
  • Results support a protective role for CRP in maintaining EDNO bioavailability.
Abstract

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