Coagulation, Fibrinolysis and Platelet P-selectin Expression in Peripheral Vascular Disease

Koksch, Mario; Zeiger, F; Wittig, Klaus; Siegemund, A.; Reininger, Cornelia; Pfeiffer, Doris; Ruehlmann, C

doi:10.1053/ejvs.2000.1294

Cited by 38 publications

(32 citation statements)

References 30 publications

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“…The most intensely investigated receptor is P-selectin; we and many others have found an increased expression of P-selectin in a wide variety of disease states with increased thromboembolic risk. [11][12][13][14][15][16][17][18][19] Similar results have been found for CD 63 and PAC 1 expression and for thrombospondin binding. 11,16,17 Much less is known about platelet activation in response to haemorrhagic events.…”

Section: Introductionsupporting

confidence: 69%

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Absence of compensatory platelet activation in patients with severe haemophilia, but evidence for a platelet collagen-activation defect

et al. 2002

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Severe haemophilia is a serious, haemorrhagic disorder of the plasmatic coagulation system. In this study we investigated, whether 'compensatory' activation of the platelet coagulation system occurs in this situation. Platelet function was investigated with aggregation, adhesion and flow cytometric assays. In addition, we performed clot and platelet plug formation tests and determined endogenous thrombin potentials in patients with severe haemophilia A or B; results were compared to those of healthy controls. Platelet aggregation in response to stimulation with ADP, ristocetin and epinephrine was similar in patients and controls; aggregation in response to collagen was reduced significantly in haemophiliacs. Flow cytometric analysis of P-selectin (CD 62P) and CD 63, of the conformationally changed GP IIb/IIIa with PAC 1 and of thrombospondin bound to CD 36 (GP IV) was performed at baseline and post stimulation. Baseline expression of all markers was similar in haemophiliacs and controls. After stimulation of the platelet thrombin receptors with the thrombin receptor activating peptide (TRAP) 6, the surface expression of all markers increased significantly; again, the expression was similar in haemophiliacs and controls. With thrombelastography and PFA 100 analysis, clot formation under low shear and platelet plug formation under high shear is measured. Both test results revealed a significantly reduced clot and platelet plug formation capacity in severe haemophiliacs. Our results did not reveal signs of enhanced platelet preactivation in haemophiliacs, indicating that baseline platelet reactivity in severe haemophilia remains in a neutral state, despite the severely haemorrhagic condition. As expected, both thrombin and clot formation capacities were impaired significantly in severe haemophilia. The reduced response to collagen-based platelet stimulation tests is indicative of a concomitant platelet function defect. This defect probably contributes to the intensity of bleeding events in patients with severe haemophilia.

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Section: Introductionsupporting

confidence: 69%

“…[11][12][13][14][15][16][17][18][19] In animal models, raised P-selectin expression was seen following experimental haemorrhage. 20,21 Thus, these receptors seem to play an important role for effective haemostasis.…”

Section: Discussionmentioning

confidence: 99%

Absence of compensatory platelet activation in patients with severe haemophilia, but evidence for a platelet collagen-activation defect

et al. 2002

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“…Although suggestive that the prosthetic graft itself is capable of inducing a prothrombotic derangement, other factors, including widespread atherosclerotic disease, may contribute to the ongoing hemostatic derangement. [80][81][82] High levels of cytokines have been found in stored RBC concentrates, including IL-1, IL-6, and tumor necrosis factor alpha. 83 Cytokines may be potent coagulation stimulators and thus the volume of blood transfusion may contribute to the perioperative coagulation derangement witnessed after aneurysm repair.…”

Section: Discussionmentioning

confidence: 99%

Coagulation, fibrinolysis, and platelet activation in patients undergoing open and endovascular repair of abdominal aortic aneurysm

Davies

Abdelhamid

Wall

et al. 2011

Journal of Vascular Surgery

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“…18 Aspirin resistance involves, besides thromboxane formation, an impaired inhibition of platelet aggregation and an increased expression of P-selectin, a marker of ␣-granule secretion associated with the progression of atherosclerosis. 19 We have previously proposed to classify aspirin resistance into three major categories, 20 of which one (type 1) includes the inhibition of platelet thromboxane formation in vitro but not in vivo (pharmacokinetic type). Type 2 is characterized by the inability of aspirin to inhibit platelet thromboxane formation in vivo and in vitro (pharmacodynamic type).…”

Section: Discussionmentioning

confidence: 99%

Functional and Biochemical Evaluation of Platelet Aspirin Resistance After Coronary Artery Bypass Surgery

et al. 2003

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Background-Aspirin inhibits platelet activation and reduces atherothrombotic complications in patients at risk of myocardial infarction and stroke. However, a sufficient inhibition of platelet function by aspirin is not always achieved. The causes of this aspirin resistance are unknown. Methods and Results-Patients undergoing coronary artery bypass grafting (CABG) have a high incidence of aspirin resistance. To evaluate functional and biochemical responses to aspirin, platelet-rich plasma was obtained before and at days 1, 5, and 10 after CABG. Thromboxane formation, aggregation, and ␣-granule secretion were effectively inhibited by 30 or 100 mol/L aspirin in vitro before CABG, but this inhibition was prevented or attenuated after CABG. Whereas the inhibition of thromboxane formation and aggregation by aspirin in vitro partly recovered at day 10 after CABG, oral aspirin (100 mg/d) remained ineffective. The inducible isoform of cyclooxygenase in platelets, COX-2, has been suggested to confer aspirin resistance. In fact, immunoreactive COX-2 was increased 16-fold in platelets at day 5 after CABG, but the COX-2 selective inhibitor celecoxib did not alter aspirin-resistant thromboxane formation. By contrast, the combined inhibitor of thromboxane synthase and thromboxane receptor antagonist terbogrel equally prevented thromboxane formation of platelets obtained before (control) and after CABG. Conclusions-Platelet aspirin resistance involves an impairment of both in vivo and in vitro inhibition of platelet functions and is probably due to a disturbed inhibition of platelet COX-1 by aspirin. (Circulation. 2003;108:542-547.)

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Coagulation, Fibrinolysis and Platelet P-selectin Expression in Peripheral Vascular Disease

Abstract: 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.

Cited by 38 publications

References 30 publications

Absence of compensatory platelet activation in patients with severe haemophilia, but evidence for a platelet collagen-activation defect

Absence of compensatory platelet activation in patients with severe haemophilia, but evidence for a platelet collagen-activation defect

Coagulation, fibrinolysis, and platelet activation in patients undergoing open and endovascular repair of abdominal aortic aneurysm

Functional and Biochemical Evaluation of Platelet Aspirin Resistance After Coronary Artery Bypass Surgery

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