Nicotine addiction and an elevated cholesterol level exhibit negative effects on platelet activation in patients with chronic Buerger’s disease

Introduction: Buerger’s disease, or thromboangitis obliterans (TAO), is a vascoocclusive disorder of unknown etiology. Cigarette smoking is considered to be a main risk factor for the development of TAO. The aim of the study: The aim of this study was to assess the activation of platelets in patients with Buerger’s disease compared to the control group. Materials and methods: Thirty patients (24 men and 6 women, median age 51.4 years) with TAO were included in the study. In the control group there were twenty healthy adults (16 men and 4 women, median age 44.0 years). Platelets’ activation was measured by light aggregometry and flow cytometry methods with, and without, platelet activators, such as thrombin receptor agonist peptide-TRAP-6 and adenosinodiphosphate-ADP. Results: The velocity and intensity of aggregation increased in patients with TAO (p<0.05). MFI (mean fluorescence intensity) of P-selectine, CD63 (GP53-component of lysosomal membrane) and PAC-1 (platelet activation complex-1) on platelets increased in patients (p<0,05). Significantly higher aggregation velocities were noted in smoking patients in response to collagen (Coll) and to arachidonic acid (AA). Aggregation velocity in response to AA and epinephrine (EPI) was higher in smokersIn patients with an increased cholesterol level platelet aggregation and the MFI of plateletswas also higher.. Conclusion: P-selectin (CD62P), an active form of the receptor for fibrinogen (PAC-1), and the lysosomal protein (CD63) on platelets can parcipate in pathogenesis of TAO. Also smoking and lipid disturbances increases platelet activation in this group of patients.