Coronary stents: in these days of climate change should all stents wear coats?

T he most significant advancement in percutaneous coronary intervention (PCI) since the introduction of angioplasty in 1978 has been the routine coronary stenting of de novo lesions. The resultant improvement in short term procedural outcome and reduced restenosis 2 has made PCI the treatment of choice for single vessel coronary artery disease and launched it into more complex anatomy. Restenosis has, however, not been eliminated and angiographically occurs in 20–30% of cases where bare metal stents are used, with the clinical recurrence rate approximately half of that. Restenosis following balloon angioplasty was largely as a result of immediate elastic recoil and/or the subsequent phenomenon of maladaptive vessel shrinkage in response to injury or negative remodelling. In the era of routine coronary stenting these have been usurped by neointimal hyperplasia as the cause of restenosis within stented segments or in-stent restenosis (ISR). Histologically, this is in part a giant cell mediated foreign body reaction and partly a vascular response to injury. A higher frequency of further restenosis limits the long term clinical outcome following treatment of ISR, and preventing or limiting the initial restenotic process seems a more plausible way of reducing the problem and hence the need for target lesion revascularisation (TLR). The most promising options for this are, however, not without potential problems. Adjunctive intravascular brachytherapy leads to grossly delayed endothelialisation and the need for long term antiplatelet treatment to prevent stent thrombosis. In addition the long term phenomena of ‘‘restenotic catch-up’’ and changes in vascular wall architecture are still being evaluated. Drug eluting stents offer the possibility of delivering therapeutic levels of active metabolite locally (assuming stents are well opposed) while systemic levels are negligible. There are potential concerns regarding long term arterial thinning and, as with brachytherapy, delayed endothelialisation with thrombosis and late restenosis have been reported although there may be differences between the various active agents. Incomplete coverage of the stent struts by endothelial cells or a delay in the speed of endothelialisation necessarily leads to an increased risk of subacute stent thrombosis (SAT); the clinical consequences of which are typically abrupt, unpredictable, and severe (myocardial infarction) unlike the situation with ISR, which is usually a gradual resumption of pre-existing symptoms. The frequency of SAT is low (, 2% for elective and 5% for bailout stenting) and as with any low frequency event, statistical evaluation requires a large population to evaluate potential treatment effects. Reducing restenosis and thrombogenicity by improved biocompatibility has previously been the focus of attention, but latterly interest has shifted more toward producing inert delivery platforms for drug elution or gene transfer. Stent coatings and alterations in the metallic composition of stents are therefore central to these issues and for the purpose of this discussion have been divided into alternate metal alloys, mechanical surface changes, and the addition of other biologically ‘‘active or inert’’ compounds.