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- ANTARES, Aspirin alone antiplatelet regimen after intracoronary placement of the carbostent
- COAST, heparin-coated stent placement for the treatment of stenoses in small coronary arteries of symptomatic patients
- DISTINCT, BiodivYsio stent in controlled trial
- EASI, European antiplatelet stent investigation
- ISR, in-stent restenosis
- PC, phosphorylcholine
- PCI, percutaneous coronary intervention
- QCA, quantitative coronary angiography
- SAT, subacute stent thrombosis
- SiC, silicon carbide
- SOPHOS, study of phosphorylcholine coating on stents
- STRIDE, study of anti-restenosis with the BiodivYsio dexamethasone-eluting stent
- TLR, target lesion revascularisation
- TRUST, Tenax for the prevention of restenosis and acute thrombotic complications
The 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 restenosis1,2 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).3
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 thrombosis4 and late restenosis5 …