Circulation Journal Official Journal of the Japanese Circulation Society http://www. j-circ.or.jp rug-eluting stents (DES) have dramatically reduced angiographic restenosis and the clinical need for repeat revascularization procedures. 1,2 Currently, DES are being used "off-label" in higher-risk patients and in more complex lesions such as the culprit lesions of acute coronary syndrome (ACS), and concerns have arisen about the appropriateness of the routine use of DES in the "real world". 3,4 Furthermore, even in patients with acute myocardial infarction (AMI), it has been reported that DES reduces the rate of restenosis compared with that with bare-metal stents (BMS). 5,6 However, randomized studies comparing DES with BMS in patients with AMI have been relatively small and have had limited periods of follow-up. Furthermore, late (LST) and/or very late stent thrombosis (VLST) has emerged as a distinct entity overshadowing the use of DES, and concerns persist as to whether this phenomenon might jeopardize the long-term outcome after DES implantation. 7,8 Observational studies comparing DES and BMS in patients with AMI also have conflicting results. 9,10 I describe here the safety issues of DES implantation for ACS cases, especially AMI, from a pathological standpoint.
Possibility of Increased Risk of Stent ThrombosisAfter DES Implantation at Culprit Sites of AMIThe structure of plaques may affect the relationship of the stent struts to underlying tissue and therefore affect arterial responses to stent implantation, especially with regard to vessel healing. Vulnerable plaque (characterized by a necrotic core with an overlying thin-ruptured cap infiltrated by macrophages and with a paucity of smooth muscle cells) is the most common underlying substrate in AMI. 11 In highly necrotic plaques, stent struts penetrate deeply into the lipid core and are not in direct contact with the vessel wall (either arterial media or fibrocellular plaque) (Figure 1). Neointimal growth and reendothelialization occur via the migration and proliferation of vascular smooth muscle and endothelial cells from the uninjured arterial edges, adjoining arterial branches, and vasa vasorum. A stent placed in an artery with significant plaque prolapse with a large lipid core could produce delayed development of a compact endothelialized neointima as a result of the relative paucity of migrating and proliferating smooth muscle cells in close proximity to the struts. Thus, even in cases of BMS implantation, the AMI culprit lesion is one of the most important underlying mechanisms of LST identified by pathological study. 12 It has been reported that DES implantation generally results in delayed arterial healing compared with BMS under similar duration (Figures 2,3). 13,14 Therefore, vessel healing at the culprit lesion in AMI cases treated with DES is substantially delayed compared with that in cases receiving DES for stable angina. 15 A clinical study using optical coherence tomography also demonstrated a markedly high frequency of inadequately appo...