In vitro model to test the thrombogenicity of coronary stents

Beythien, C.; Terres, Wolfram; Hamm, Christian W.

doi:10.1016/0049-3848(94)90170-8

Cited by 35 publications

(13 citation statements)

References 19 publications

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“…To achieve the high radial stability, the total mass, weigh t, and profile have been in· creased, exceeding that of a Palmaz medium stent by 35% (0.061 glcm compared to 0.045 glcm; P < .05). A disadvantage of more endovascular stent material is a higher rigidity, thus increasing the profile during insertion of the stent and, possibly, a greater thrombogenicity (27). Also, the concept of compliance mis· match has been applied to stented arteries (28).…”

Section: • Weightmentioning

confidence: 99%

Physical Properties of Endovascular Stents: An Experimental Comparison

Duda

Wiskirchen

Tepe

et al. 2000

Journal of Vascular and Interventional Radiology

186

116

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Section: • Weightmentioning

confidence: 99%

Physical Properties of Endovascular Stents: An Experimental Comparison

Duda

Wiskirchen

Tepe

et al. 2000

Journal of Vascular and Interventional Radiology

186

116

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“…A previously described and modified ex vivo thrombosis model 15 was used to examine platelet and platelet-leukocyte aggregation under more physiological conditions. An 80-cm silicon tubing with an inner diameter of 3 mm was carefully filled with 6 mL citrated whole blood via a 3-way faucet and placed in a water bath at 37°C.…”

Section: Measurement Of Platelet Aggregation and Platelet-leukocyte Cmentioning

confidence: 99%

Sulfatides Activate Platelets Through P-Selectin and Enhance Platelet and Platelet–Leukocyte Aggregation

Merten

Beythien

Gutensohn

et al. 2005

ATVB

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Objective-Sulfatides are sulfated glycosphingolipids present on the surface of a variety of cells; however, their exact physiological function is not known. Recently, we have shown that the inhibition of sulfatide-P-selectin interactions leads to disaggregation of platelet aggregates. Methods and Results-In this study, we show that sulfatides activated platelets as they increased activation of GPIIb/IIIa (PAC-1 epitope) and expression of P-selectin on the platelet surface. Furthermore, sulfatides aggregated washed platelets in a dose-dependent manner and enhanced platelet aggregation in platelet-rich plasma. Previous activation of platelets was necessary for this effect. Monoclonal anti-P-selectin antibodies inhibited not only sulfatide-induced PAC-1 binding to platelets but also sulfatide-induced platelet aggregation, suggesting that sulfatides activate platelet GPIIb/IIIa via signaling through P-selectin. The proaggegatory effect of sulfatides was also observed in an ex vivo thrombosis model using whole blood and pulsatile flow at 37°C. In this model, sulfatides significantly enhanced platelet aggregation and the formation of platelet-leukocyte aggregates. Conclusions-We show that sulfatide-P-selectin interactions lead to subsequent platelet activation and P-selectin expression, forming a positive feedback loop that can potentiate formation of stable platelet aggregates. In addition, sulfatides enhance the aggregation of platelet-leukocyte aggregates. These mechanisms may play a significant role in hemostasis and thrombosis.

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“…PRP (6 ml) was filled into the tubing system. After recalcification to a final concentration of 10 mmol/l, the plasma was moved with a roller pump at a flow rate of 8 ml/min (2 cm/s) at 37°C [4]. In each test, two systems were used in parallel, one with a Strecker stent (Boston Scientific, Watertown, USA), and one control without a stent.…”

Section: Methodsmentioning

confidence: 99%

Biocompatibility of Tantalum Coronary Stents: Investigations by Flow Cytometry

Gutensohn¹,

Beythien²,

Bau³

et al. 1997

26. Hämophilie-Symposion 1995

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In our study, we applied fluorescence-activated flow cytometry to examine activation-dependent alterations of platelet antigens caused by contact with coronary tantalum stents. In an in vitro model, tantalum wire stents (n = 1O) were placed in a silicon tubing and platelet-rich plasma (PRP) was filled into the system. After recalcification, PRP was gently moved by a roller pump. Over the course of 10 min, aliquots were drawn at fixed time intervals. The sampIes were immediately prepared for flow cytometry and labeled with monoclonal antibodies against CD62p, CD63, CD41a and CD42b. The mean channel fluorescence intensity (MCFI) of GMP140 and gP53 increased within the first minutes and continued to rise over the whole time course. There was a significant difference in MCFI between the tube with a stent and the control tube without a stent (CD62p, P < 0.05; CD63, P < 0.005)· The increase in CD62p and CD63 expression can be explained by the contact of platelets with the artificial surface of the stent and the shear forces of the metallic mesh. Platelets expressing activation-dependent neoantigens on their surface, especially P-selectin, are known to be associated with a higher predisposition for thrombosis. Therefore, additional medical precaution may help to prevent restenosis in these patients.

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In vitro model to test the thrombogenicity of coronary stents

Cited by 35 publications

References 19 publications

Physical Properties of Endovascular Stents: An Experimental Comparison

Physical Properties of Endovascular Stents: An Experimental Comparison

Sulfatides Activate Platelets Through P-Selectin and Enhance Platelet and Platelet–Leukocyte Aggregation

Biocompatibility of Tantalum Coronary Stents: Investigations by Flow Cytometry

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