Inflammation and platelet activation in peripheral arterial occlusive disease

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.

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) B(2) by immunoassay and circulating platelet-monocyte aggregates (PMAs) by flow cytometry.

Plasma PMAs and urinary 11-dehydro-TXB(2) were significantly increased in PAOD patients compared with controls (P<0.01 for all). A positive correlation between 11-dehydro-TXB(2) and CRP was found in the study population (r(s)=0.63, P<0.001). Using logistic regression analysis, CRP was the only independent correlate of 11-dehydro-TXB(2) (β(CRP)=11.9, P<0.01), whereas only the presence of PAOD was an independent predictor of high PMA levels (β(PAOD)=13.7, P=0.001). Chronic administration of acetylsalicylic acid reduced 11-dehydro-TXB(2), but not PMA and CRP.

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