Why the study?
Does platelet glycoprotein IIIa mAb-eluting stent reduce intimal hyperplasia and thrombosis in New Zealand white rabbit arteries compared to stainless steel stents?
Does platelet glycoprotein IIIa mAb-eluting stent reduce intimal hyperplasia and thrombosis in New Zealand white rabbit arteries compared to stainless steel stents?
Platelet glycoprotein IIIa mAb-eluting stents promote rapid endothelialization and may prevent thrombosis while inhibiting neointima proliferation in a preclinical rabbit model.
May accelerate endothelialization and curb hyperplasia in rabbits; leaves open translation to human stent outcomes.
Since the percutaneous coronary intervention (PCI) was first introduced into China in 1984, this procedure has become widely accepted as an important step in coronary revascularization. This study aims to evaluate intimal hyperplasia and thrombosis after implantation of platelet glycoprotein IIIa monoclonal antibody (mAb)-eluting stent in the New Zealand white rabbit abdominal aorta or iliac artery by comparing CT angiography and pathological experiments. The antibody-eluting stents were prepared by the passive absorption method. Arterial intima in the stented segment and 0.5 cm adjacent to the stented site were observed and analyzed by scanning electron microscopy (SEM) and cross-sectional staining. Endothelialization and thrombosis on the stent surface were visualized by CT angiography and three-dimensional (3D) reconstruction technique in animals surviving from 1 to 12 weeks. Compared to stainless steel stents, the surface of antibody-eluting stents was covered with a complete endothelial layer after four weeks. Both CT angiography and pathological results showed intimal hyperplasia (p < 0.05) after 12 weeks. Therefore, pathological methods are the goldern standard for evaluation of intimal hyperplasia while CT angiography has a higher specificity in demonstrating the intimal changes after stent implantation for 12 weeks. The mAb-eluting stent has the potential to prevent thrombosis formation due to the interaction of stent with blood, and decreases the stenosis ratio by inhibiting neointima proliferation.
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Zhang et al. (2015) studied this question.
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