Inflammation and platelet activation in peripheral arterial occlusive disease
| Autor: | Maurizio Degan, Clara Santonastaso, Alessandro Lechi, Gian Cesare Guidi, Cristiano Fava, Pietro Minuz, Rosa Maria Tommasoli, Sergio De Marchi, Martina Montagnana, Pietro Delva, Roberta Spadaro, Enrico Arosio |
|---|---|
| Rok vydání: | 2007 |
| Předmět: |
medicine.medical_specialty
11-dehydro-thromboxane Thromboxane Population Ischemia and circulating platelet monocyte aggregates Inflammation peripheral arterial obliterative disease Internal medicine medicine Platelet Platelet activation Thrombus education platelet education.field_of_study inflammation business.industry medicine.disease Pathophysiology Immunology Cardiology Original Article medicine.symptom Cardiology and Cardiovascular Medicine business |
| Zdroj: | International Journal of Angiology. 16:84-88 |
| ISSN: | 1615-5939 1061-1711 |
| Popis: | Peripheral arterial occlusive disease (PAOD) of the lower limbs is a prototypical atherosclerosis-determined disease. This local reduction in arterial lumen diameter leads to chronic ischemia in a limited number of subjects while diffuse atherosclerosis, as well as coexisting cardiovascular risk factors, are determinants of major cardio- and cerebrovascular events (1). Platelet activation is a requirement for atherothrombosis and a predictor of its occurrence (2,3). Increased platelet activation was observed in patients with effort-induced leg pain (stage II of the Leriche-Fontaine classification of PAOD) and was found to be related to coexisting cardiovascular risk factors, rather than atherosclerosis per se (4). There is evidence that the progression of PAOD is also related to inflammation (5,6). Alterations in inflammatory markers correlate independently with walking distance and other clinical indexes of functional impairment in patients with PAOD, and predict the clinical outcome of the disease (7–9). Plasma C-reactive protein (CRP), as well as other markers of inflammation, are predictors of future cardiovascular events in the general population and in subjects with cardiovascular risk factors, suggesting a causal relationship between inflammation and the progression of atherosclerosis (6,10,11). Inflammation has a central role in the pathophysiology and clinical progression of atherosclerosis, from the initial accumulation of T lymphocytes and monocytes in the subendothelium, to plaque instability and thrombotic complication (12,13). Activated platelets participate in the development of atherosclerosis by promoting inflammation in the vessel wall and forming the thrombus (14–16). Therefore, a close relationship between inflammation and platelet activation may be hypothesized in PAOD at any stage of the disease. The aim of the present study was to explore the relationships among the presence of overt atherosclerosis, inflammation and platelet activation in patients with mild to severe PAOD and appropriate controls. In vivo platelet activation was quantified by measuring the urinary excretion of a major thromboxane (TX) A2 metabolite, 11-dehydro-TXB2, and circulating platelet-monocyte aggregates (PMAs). While urinary 11-dehydro-TXB2 is mostly generated by the activity of prostaglandin H synthase (cyclo-oxygenase)-1 in platelets, PMAs derive from the interaction of activated platelets with circulating leukocytes mediated by adhesion molecules. |
| Databáze: | OpenAIRE |
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