抄録
Drug-eluting stents (DES) have been proven to reduce the rate of restenosis by marked inhibition of neointimal hyperplasia, but unusual vessel responses to DES, such as substantially impaired arterial healing characterized by incomplete endothelialization and persistent inflammatory response, have been recognized. The culprit sites in acute coronary syndrome (ACS), especially acute myocardial infarction, have large necrotic cores with a paucity of smooth muscle cells. In these lesions, penetration of the stent struts into the necrotic core is frequently observed after stent implantation. Pathologic observations have revealed that the lesions stented with DES frequently show greater delay in arterial healing than those treated with bare-metal stents. Thus, ACS culprit sites could be at persistent risk for thrombosis after DES implantation.
