Circulation Journal
Online ISSN : 1347-4820
Print ISSN : 1346-9843
Experimental Investigation
Effectiveness of Statin-Eluting Stent on Early Inflammatory Response and Neointimal Thickness in a Porcine Coronary Model
Katsumi MiyauchiTakatoshi KasaiTakayuki YokayamaKouichiro AiharaTakeshi KurataKan KajimotoShinya OkazakiHaruo IshiyamaHiroyuki Daida
Author information

2008 Volume 72 Issue 5 Pages 832-838


Background Drug-eluting stent (DES) implantation is routine during coronary revascularization because DES significantly reduce rates of restenosis and target lesion revascularization compared with bare metal stent (BMS). However, available DES have limitations, such as late thrombosis because of delayed healing with poorer endothelialization and persistent local inflammation. Statins can inhibit cell proliferation, inflammation, and restore endothelial function. The present study evaluated the ability of stent-based cerivastatin delivery to reduce stent-induced inflammatory responses and adverse effects on endothelial function, and to inhibit neointimal hyperplasia in a porcine coronary model. Methods and Results Pigs were randomized into groups in which the coronary arteries (9 pigs, 18 coronaries in each group) had either a cerivastatin-eluting stent (CES) or a BMS. All animals survived without any adverse effects. Inflammatory cell infiltration evaluated using scanning electron microscopy on day 3 after stenting was significantly decreased in the treated vessels (inflammation score: 1.15±0.12 vs 2.43±0.34, p<0.0001). At day 28, endothelial function with intracoronary infusion of bradykinin was preserved in both the CES and BMS groups. Volumetric intravascular ultrasound images revealed decreased intimal volume in the CES group (28.3±5.4 vs 75.9±4.2 mm3, p<0.0001). Histomorphometric analysis showed reduced neointimal area (1.74±0.45 vs 3.83±0.51 mm2, p<0.0001) in the CES group despite similar injury scores (1.77±0.30 vs 1.77±0.22, p=0.97). Conclusion In porcine coronary arteries CES significantly decreased neointimal hyperplasia with a decreased early inflammatory response and without endothelial dysfunction. (Circ J 2008; 72: 832 -838)

Information related to the author
Previous article Next article