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Published on: October 15, 2010
Direct association between C-reactive protein serum levels and endothelial dysfunction in patients with claudication
J De Haro1, F Acin, A Lopez-Quintana
1Angiology and Vascular Surgery Service, Hospital Universitario Getafe, Madrid, Spain. deharojoaquin@yahoo.es
High-sensitivity C-reactive protein (hsCRP), an inflammation marker, is elevated in patients with endothelial dysfunction and intermittent claudication. This suggests hsCRP may play a role in peripheral arterial disease development.
Area of Science:
- Cardiovascular Research
- Inflammation Biology
- Vascular Medicine
Background:
- Endothelial dysfunction is a key factor in peripheral arterial disease (PAD) pathogenesis.
- Inflammation plays a significant role in the development and progression of atherosclerosis.
- High-sensitivity C-reactive protein (hsCRP) is a widely recognized marker of systemic inflammation.
Purpose of the Study:
- To investigate the association between hsCRP levels and endothelial dysfunction in patients with intermittent claudication.
- To determine if hsCRP is related to impaired flow-mediated arterial dilation (FMAD) in this patient group.
Main Methods:
- A cross-sectional study involving 156 patients with intermittent claudication was conducted.
- Patients were selected using stratified sampling based on various risk factors.
- Flow-mediated arterial dilation (FMAD) and plasma hsCRP levels were measured to assess endothelial function and inflammation.
Main Results:
- Patients with reduced FMAD (<3%) exhibited significantly higher plasma hsCRP levels compared to those with normal FMAD (>3%).
- A significant negative correlation was observed between hsCRP levels and FMAD (r=-0.465, p<0.05).
- Elevated fibrinogen levels were also associated with impaired endothelial function.
Conclusions:
- Impaired endothelial function in intermittent claudication is linked to increased plasma concentrations of inflammatory markers like hsCRP.
- These findings suggest that inflammation, indicated by hsCRP, may contribute to the underlying mechanisms of peripheral arterial disease.
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