Background: Coronary artery stents can induce platelet activation by shear forces and contact to the biomaterial. This activation is one important trigger for thrombosis. Coating of stents is a possible approach to prevent this side effect. The purpose of this study was to evaluate in vitro the biocompatibility of stents coated with diamond-like carbon (DLC). Materials and Methods: For in vitro testing, DLC-coated stents were compared with noncoated 316L stainless steel stents. For this purpose, cell culture assays, videomorphometric, electron microscopic and flow-cytometric techniques were applied. Results: Growth assays with smooth muscle cells and endothelial cells revealed that DLC did not affect proliferation rates and did not have cytotoxic effects. Video-based morphometry and scanning electron microscopy showed an ultrasmooth surface and homogenous expansion patterns of the DLC stents. For analysis of platelet antigens in a circulating loop model, flow cytometry was applied. Our experiments showed no significant changes in mean channel fluorescence intensity for the structural antigens CD41a (p = 0.6) and CD42b (p = 0.1). In contrast, the expression of the activation-dependent antigens CD62p and CD63 increased significantly in noncoated stents compared to DLC-coated stents (p < 0.05). Conclusion: Coating of intracoronary stents with DLC significantly reduces platelet activation. Hereby, biocompatibility is improved.
Acute occlusion of stented coronary vessels still occurs in up to 3%. Activated platelets have been found to play a major role in the pathogenesis of these complications. We therefore analyzed the efficacy of a heparin coating of coronary stents and investigated the ex vivo efficacy of different antiplatelet drugs. Each of seven healthy volunteers was treated with each of the following medications for 7 days: ASA 100 mg/day, ASA 300 mg/day, ticlopidine 250 mg/day, and ticlopidine 500 mg/day. Three standardized in vitro silicon tubing models, one of them containing an uncoated stent, one a heparin-coated stent, and one without a stent (control) were filled with PRP and circulation was started. TOS in systems with heparin-coated stents was 2.4-times longer compared to systems with uncoated stents (P<0.001), and 1.5-times longer compared to the control (P<0.01). The increase of CD62p expression within the first 5 min was 2.5-times higher in systems with uncoated stents and 1.7-times higher in the control than in systems with heparin-coated stents (P<0.05). Aggregometry revealed significant medication- and dose-dependent inhibition of platelet aggregability for all medications. Heparin-coating of coronary stents reduces their thrombogenicity significantly. ASA and ticlopidine effectively reduce platelet activation ex vivo. The used in vitro system facilitates a reproducible method to estimate the thrombogenicity of coronary stents prior to in vivo trials.
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