Influence of Stent Length and Heparin Coating on Platelet Activation

Beythien, C.; Gutensohn, K.; Bau, J.; Hamm, Christian W.; Kühnl, P.; Meinertz, Thomas; Terres, Wolfram

doi:10.1016/s0049-3848(98)00198-4

Cited by 35 publications

(23 citation statements)

References 24 publications

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“…In accordance with our findings, Beythien et al have demonstrated that a heparin coating may not influence the detectable platelet activation, but it can prolong the time until stent thrombosis. 39 Fibrinogen adheres to stainless steel after contact with blood, 40 and as a result it is converted to fibrin by the activation of the coagulation cascade. In our experiment, fibrinogen levels remained similar to control values under all study conditions, and in this respect all materials behaved similarly.…”

Section: -33mentioning

confidence: 99%

Platelet responses and coagulation activation on polylactide and heparin–polycaprolactone‐L‐lactide ‐coated polylactide stent struts

Hietala

Maasilta

Välimaa

et al. 2003

J Biomedical Materials Res

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Despite modern stent technology and effective antiplatelet therapy, metallic stents carry the risk of (sub)acute thrombosis. Our aim was to examine short-term differences in platelet deposition and coagulation activation between biodegradable polylactide (PLA), heparin-polycaprolactone-L-lactide-coated polylactide (hepa-P(CL95/L-LA5)-PLA), and stainless steel (SS) stent struts. Gel-filtered platelets (GFP) and platelet-rich plasma (PRP) were labeled with 10 nM (3)H-serotonin. Platelet deposition was measured after incubation of the stent struts in human serum albumin-coated wells at 37 degrees C in either GFP or PRP. Platelet morphology was studied by scanning electron microscopy (SEM). For coagulation activation, the stent struts were incubated in either PRP or platelet-poor plasma (PPP), anticoagulated with D-phenylalanyl-L-prolyl-L-arginine chloromethyl ketone (PPACK), followed by measurement of fibrinogen, thrombin time (TT), prothrombin fragment 1+2 (F1+2), and thrombin-antithrombin complex (TAT). SS showed adherence of larger amounts of GFPs than did PLA at a platelet density of 300 x 10(6)/mL (p < 0.05). Furthermore, representative SEM studies showed more platelet spreading on SS than on PLA stent struts. Between PLA and SS, coagulation activity did not differ at any assessment. Based on prolonged TT values in plasma, the heparin coating strongly inhibited coagulation (p < 0.05). The values of soluble TAT and F1+2 for PLA were similar to those of controls, i.e., to incubated suspensions without a stent strut. In conclusion, when compared with stainless steel, both PLA and hepa-P(CL95/L-LA5)-PLA appear hemocompatible as intravascular stent materials.

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Section: -33mentioning

confidence: 99%

Platelet responses and coagulation activation on polylactide and heparin–polycaprolactone‐L‐lactide ‐coated polylactide stent struts

Hietala

Maasilta

Välimaa

et al. 2003

J Biomedical Materials Res

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“…Heparin coating has no significant influence on platelet activation in an in vitro model [9]. In a model of canine coronary arteries thrombosis and neointima formation no differences were found between coated and uncoated stents [19].…”

Section: Heparin Coatingmentioning

confidence: 92%

“…Stent design may define blood flow properties and so activate blood particles by strut-induced turbulence. Long stents lead to more platelet activation than short stents [9]. High positive current density of stent surfaces can attract negatively charged platelets with the consequence of adhesion, aggregation, and jeopardy of clot formation.…”

Section: Materials and Designmentioning

confidence: 99%

Biocompatibility to Reduce Thrombogenicity of Intracoronary Stents

Beythien¹,

Brockmann²,

Meinertz³

et al. 1999

Transfus Med Hemother

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In interventional cardiology major technical advances have been accomplished in the last 20 years. Especially, the introduction of endovascular prostheses (stents) was an important step forward. With the implantation of stents in coronary arteries by Sigwart and colleagues over 10 years ago to manage acute occlusion and restenosis after PTCA, the problems of thrombogenicity and biocompatibility were evident. Strict anticoagulation had reduced the risk of in-stent thrombus formation. The problem of late neointimal proliferation with development of restenosis is still not resolved. Many different designs, materials, and coatings were proposed to reduce thrombogenicity and optimize biocompatibility. Stent structure can influence flow conditions, surface charge can attract platelets or coagulation factors, and corrosion with diffusing ions may induce proliferation of surrounding tissues. Stent surface treatment, several metal alloys, and drug-eluting or drug-stable coatings are under investigation to improve the short-term and long-term results. In the mid 1990s the introduction of an extended antiplatelet therapy and a new implantation technique with high-pressure stent deployment have improved the results. However, the optimal stent still does not exist. This article describes possible reasons and some new promising versions.

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“…Flow cytometry may also be used to elucidate patients with different GP IIIa phenotypes, such as the GP IIIa-Pro33 phenotype, who have more fibrinogen binding after stimulation with ADP and may possibly have a greater risk of thrombotic events [33]. Flow cytometry has been used in the development of less thrombotic endovascular stents [34, 35]. Platelet-bound P-selectin in congestive heart failure patients, as determined by flow cytometry, was increased more than twofold when compared with normal controls [36].…”

Section: Flow Cytometrymentioning

confidence: 99%

Clinical Utility of Available Methods for Determining Platelet Function

et al. 1999

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Determination of platelet function has become increasingly important as new antiplatelet drugs are being developed. Objective means to monitor the pharmacological effects of these agents, in order to maximize efficacy and minimize toxicity, is needed. The available methods for determination of platelet function at the current time are reviewed, including platelet aggregometry, the PFA-100, flow cytometry, platelet contractile force, the rapid platelet function assay, the clot signature analyzer, Sonoclot, and thromboelastography. The principle, advantages, disadvantages, and clinical utility of each method is presented. The uses of the various methods of determining platelet function reported in the literature are summarized, in an effort to provide information regarding the applicability of those different methods.

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Influence of Stent Length and Heparin Coating on Platelet Activation

Cited by 35 publications

References 24 publications

Platelet responses and coagulation activation on polylactide and heparin–polycaprolactone‐L‐lactide ‐coated polylactide stent struts

Platelet responses and coagulation activation on polylactide and heparin–polycaprolactone‐L‐lactide ‐coated polylactide stent struts

Biocompatibility to Reduce Thrombogenicity of Intracoronary Stents

Clinical Utility of Available Methods for Determining Platelet Function

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