P. Maga1, M. Sanak2, J. Jawien3, B. Rewerska4, M. Maga4, A. Wachsmann4, M. Koziej4, I. Gregorczyk-maga4, R. Nizankowski1 11-dehydro Thromboxane B2 Levels after Percutaneous Transluminal Angioplasty in Patients with Peripheral Arterial Occlusive Disease during a One Year Follow-up Period

Atherosclerosis is an inflammatory vascular disease of the arteries (1), and its prevalence is increasing in developed countries. Among the many inflammatory cells and their mediators, there is a specific class of lipids that act as mediators of inflammation. Thromboxane A2 (TXA2) is a member of the family of lipids known as eicosanoids (2). TXA2 is a vasoconstrictor and a potent hypertensive agent. It also directly activates platelet aggregation (3, 4). The major TXA2 metabolites are thromboxane B2 (TXB2) and 11-dehydro-TXB2, the latter of which is an inactivation product of TXA2 that forms in the plasma from its parental compound by hydrolysis within a matter of several seconds. Typically, 11-dehydro-TXB2 is almost completely cleared through the urine; however, its levels may increase due to the activation of platelets during blood sampling or intravascular procedures. Thus, 11-dehydro-TXB2, which has a half-life of approximately 45 minutes, has been proposed as a tool to monitor the systemic production of thromboxanes in cardiovascular disorders (5). We wanted to know if thromboxane levels in patients with peripheral arterial occlusive disease (PAOD) were changed following percutaneous transluminal angioplasty (PTA). In PAOD, the treatment of patients with aspirin plays an important role. Thromboxane metabolism in platelets is inhibited by aspirin, which irreversibly blocks the enzyme cyclooxygenase-1 in platelets (5).