Platelet volume has been reported to be increased in vascular disease. Therefore, we studied the relationship of mean platelet volume and platelet count as well as flow cytometrically measured platelet size and platelet function in 50 patients with peripheral arterial disease and 50 healthy volunteers. Platelet activation was measured by P-selectin expression analysis on resting and on stimulated platelets, and the determination of platelet aggregates and platelet-derived microparticles using flow cytometry. P-Selectin expression on platelets was significantly elevated in patients suffering from peripheral arterial disease (all P<0.0001). Platelet aggregates (P<0.0001) and platelet-derived microparticles (P<0.0001) were significantly higher in the patient group compared with controls, whereas mean platelet volume and platelet count showed no significant differences. Platelet count was inversely related to mean platelet volume in patients and controls (r = -0.43, P<0.001). The present study supports the hypothesis of platelet hyperreactivity and circulating activated platelets in peripheral arterial disease. Mean platelet volume, and platelet count cannot be used as predictive markers for platelet activation in peripheral arterial disease patients.
these findings support the concept of ongoing thrombogenesis in the subclinical progression of PVD and demonstrate the high diagnostic sensitivity of flow cytometric analysis of platelet activation.
Aim of this study was the development of a flow cyiometric assay to detect platelet activation using in vitro stimulation with physiological agonists. Therefore, in healthy subjects and insulin-dependent diabetics with and without microangiopathy (retinopathy and/or nephropathy) the surface expression density of fibrinogen receptor complex gpIIb/IIIa (CD41), von Willebrand factor complex gpIb/IX (CD42b), ctgranule protein GMP-140 (CD62P), and of lysosomal protein gp53 (CD63) were measured ex vivo and after in vitro stimulation using ADP and thrombin receptor activator peptide 6 (TRAP-6). Best discrimination (p<0.05) between diabetics and controls were observed in the surface expression density of GMP-140 after maximum stimulation with the weak agonist ADP (20 μπιοΐ/ΐ) and sub-maximal stimulation with the strong agonist TRAP-6 (5 μπιοΐ/ΐ). Induced platelet aggregometry using collagen, ristocetin, ADP, and TRAP-6 and plasma concentrations of platelet factor 4 and -thromboglobulin failed to show any differences between the groups. GMP-140 levels were analyzed in a dual-color whole blood assay (CD41-PE and CD62P-F1TC) in 50 healthy controls and 60 patients suffering from peripheral arterial occlusive disease. Highly significant differences (p<0.005) were found between the two groups in the ex vivo as well as in the in vitro stimulated samples (mean fluorescence ±SEM ex vivo: 0.43 ±0.02 vs. 0.50 ±0.02; 5 μπιοΐ/ΐ ADP 0.93 ±0.03 vs. 1.30 ±0.04; 10 μιηοΐ/ΐ TRAP-6 3.30 ±0.17 vs. 3.91 ±0.16; all p<0.005). In conclusion, the in vitro platelet stimulation assay is an easy, fast, and sensitive tool for the detection of platelet hyperreactivity.Schl sselw rter: Thrombozytenaktivierung; Durchflu zytometrie; Diabetische Angiopathien/Blut. P latelets play an essential role in primary hemostasis. After damage of the vascular endothelium platelets are activated by contact to subendothelial structures, e.g. collagen fibrils, von Willebrand factor, fibronectin. A whole cascade of changes in platelet morphology and function follows the primary adherence.of platelets via specific receptors. Circulating dis-20 J Lab Med 1999; 23 (1): 020-026
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