Abstract
BackgroundWithin the general population, levels of C-reactive protein (CRP) are positively associated with atherosclerotic cardiovascular disease (CVD). Whether CRP is causally implicated in atherogenesis or is the results of atherosclerosis is disputed. A role of CRP to protect endothelium-derived nitric oxide (EDNO) has been suggested. We examined the association of CRP with EDNO-dependent vasomotor function and subclinical measures of atherosclerosis and arteriosclerosis in patients with raised CRP resulting from rheumatoid arthritis (RA).Methodology/Principal FindingsPatients with RA (n = 59) and healthy control subjects (n = 123), underwent measures of high sensitivity CRP, flow-mediated dilation (FMD, dependent on EDNO), intima-media thickness (IMT, a measure of subclinical atherosclerosis) and aortic pulse wave velocity (PWV, a measure of arteriosclerosis). IMT and PWV were elevated in patients with RA compared to controls but FMD was similar in the two groups. In patients with RA, IMT and PWV were not correlated with CRP but FMD was positively independently correlated with CRP (P<0.01).Conclusions/SignificanceThese findings argue against a causal role of CRP in atherogenesis and are consistent with a protective effect of CRP on EDNO bioavailability.
Highlights
C-reactive protein (CRP), a biomarker of systemic inflammation, independently associates with endothelial dysfunction, subclinical atherosclerosis and arteriosclerosis[1,2] and clinical manifestations of atherosclerosis in the general population[3,4]
Conclusions/Significance: These findings argue against a causal role of CRP in atherogenesis and are consistent with a protective effect of CRP on endothelium-derived nitric oxide (EDNO) bioavailability
It is important to clarify, whether when raised levels of CRP arise from a non-vascular cause, CRP retains its association with cardiovascular disease (CVD)
Summary
C-reactive protein (CRP), a biomarker of systemic inflammation, independently associates with endothelial dysfunction, subclinical atherosclerosis and arteriosclerosis[1,2] and clinical manifestations of atherosclerosis in the general population[3,4]. It is important to clarify, whether when raised levels of CRP arise from a non-vascular cause (i.e. a stimulus for CRP other than atherosclerosis), CRP retains its association with CVD This would validate the potential use of CRP for risk assessment irrespective of co-morbidity and/or the cause of raised CRP, and would add weight to the putative causal role of CRP in CVD. Levels of C-reactive protein (CRP) are positively associated with atherosclerotic cardiovascular disease (CVD). We examined the association of CRP with EDNO-dependent vasomotor function and subclinical measures of atherosclerosis and arteriosclerosis in patients with raised CRP resulting from rheumatoid arthritis (RA)
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