Int J Angiol 2007; 16(3): 84-88
DOI: 10.1055/s-0031-1278255
Original Articles

© Georg Thieme Verlag KG Stuttgart · New York

Inflammation and platelet activation in peripheral arterial occlusive disease

Martina Montagnana1 3 , Cristiano Fava2 3 , Enrico Arosio2 , Maurizio Degan2 , Rosa Maria Tommasoli1 , Sergio De Marchi2 , Pietro Delva2 , Roberta Spadaro2 , Gian Cesare Guidi1 , Alessandro Lechi2 , Clara Lechi Santonastaso1 , Pietro Minuz2
  • 1Department of Biomedical and Morphological Sciences;
  • 2Department of Biomedical and Surgical Sciences, University of Verona, Verona, Italy
  • 3These authors contributed equally to this work
Further Information

Publication History

Publication Date:
27 April 2011 (online)


OBJECTIVES: Epidemiological evidence indicates that inflammation accompanies the progression of atherosclerosis. The aim of the present cross-sectional study was to define relationships between platelet activation and inflammation in patients with mild to severe (stages II to IV) peripheral arterial occlusive disease (PAOD) and matched controls. The effect of chronic administration of low-dose acetylsalicylic acid was investigated.

METHODS: Subjects were studied on a single occasion. C-reactive protein (CRP) and two indexes of in vivo platelet activation were measured — the urinary excretion of 11-dehydrothromboxane (TX) B2 by immunoassay and circulating platelet-monocyte aggregates (PMAs) by flow cytometry.

RESULTS: Plasma PMAs and urinary 11-dehydro-TXB2 were significantly increased in PAOD patients compared with controls (P<0.01 for all). A positive correlation between 11-dehydro-TXB2 and CRP was found in the study population (rs=0.63, P<0.001). Using logistic regression analysis, CRP was the only independent correlate of 11-dehydro-TXB2crp=11.9, P<0.01), whereas only the presence of PAOD was an independent predictor of high PMA levels (βpaod=13.7, P=0.001). Chronic administration of acetylsalicylic acid reduced 11-dehydro-TXB2, but not PMA and CRP.

CONCLUSIONS: There is evidence that platelet activation in patients with PAOD is related to the vascular disease and is dependent on the severity of inflammation.