Abizaid Figure 3 In higher risk cohorts, differences in late loss are more strongly associated with risk of restenosis. Abbreviations: TLR, target lesion revascularization. incidence of stent thrombosis, a review of the literature suggests that the incidence of late stent thrombosis with SES is compa- rable with that of bare metal stents (Bavry et al 2005; Iakovou et al 2005; Moreno et al 2005; Kereiakes et al 2006; Weisz et al 2006; Park et al 2006; Schampaert et al 2006; Urban et al 2006). The individual trials/analyses are shown in Table 1. It has been suggested that treatment with a drug-eluting stent results in delayed arterial healing when compared with bare metal stents of similar implant duration. It has also been postulated that the cause of late stent thrombosis associated with DES is multifactorial, with delayed healing in combina- tion with other clinical and procedural risk factors playing a role (Joner et al 2006). The available evidence indicates that the predictors of stent thrombosis are premature anti-platelet therapy interruption, primary stenting in acute MI, and total stent length. However, if we are to gain a better understand- ing of the problems of DES thrombosis it would appear that an extended period of follow-up in a randomized, controlled trial or a large registry such as e-SELECT will be necessary. Thankfully, the incidence of late stent thrombosis appears to be very rare. Nevertheless, its impact can be tragic. Closed cell design The distribution of an eluted drug in the tissue of a vessel wall is not at all homogenous, and this might reﬂect the pattern of the stent struts. While the dose distribution may be sub-therapeutic in one spot, it may be toxic in the direct vicinity of the struts. Homogenous drug distribution would also require a symmetric deployment of a stent, which does not necessarily happen in the real world. Overlapping stents may lead to doubling of the intended dose, and longitudinally the drug tissue levels may vary considerably from proximal to distal end. An open cell versus a closed cell stent design has different characteristic patterns of apposition to the cell wall, leading again to a difference in the delivered dose, with a closed cell design appearing to offer better drug distribution. The CYPHER stent’s closed-cell design results in uni- form vessel coverage, making it an optimal platform for drug delivery. With a closed-cell design, when the stent is deployed in a tortuous site, cell size is minimally affected either on the outer aspect or inner aspect of the bend, and uniform vessel coverage and dosing are maintained. In con- trast, with open-cell design, tortuosity can cause dramatic changes in cell sizes. This may result in both excessively large cells on the outer side of the bend and small cell sizes on the inner surface of the bend. Consequently, there is non-uniform coverage of the vessel wall and non-uniform dosing, both with potential under dosing and over dosing. Closed-cell design results in optimal drug delivery to tortuous anatomy, for example, in lesions of the right coronary artery and in eccentric lesions, as encountered in highly asymmetric proximal left anterior descending plaque. 198 Vascular Health and Risk Management 2007:3(2)