Abstract

Stents are now used in 40–80% of percutaneous coronary interventional procedures. This popularity is based upon extrapolation from available data, which discloses a better immediate angiographic appearance than after PTCA, an ability to ‘bail out’ poor PTCA results and superior late clinical and angiographic results compared with PTCA in certain lesion subsets. The enthusiasm for stents has translated into an outpouring of stent designs, each with competing claims for superiority. Meanwhile in-stent restenosis, although occurring in a smaller proportion of patients than restenosis after PTCA (in highly selected subsets), is the most important limiting factor of stenting. There are a number of reasons for this. First, it is frequent; though we are, as yet, not experiencing the epidemic that was first feared. The steadily increasing number of percutaneous procedures brings with it a concomitant number of stenting procedures. About half of these patients will experience a cardiac event in the 3 years after stenting. Second, more challenging lesions are being treated, so that the majority are ‘non-Benestent’, and may be expected to have a higher rate of in-stent restenosis than seen in the early trials. Third, in-stent restenosis is technically challenging to treat, especially when diffuse, in the setting of long stented segments and in bifurcations. Fourth, in-stent restenosis is preventing the use of stent implantation in a large number of patients and lesions, notably in small vessels and in the setting of diffuse disease. And yet there is very limited clinical evidence that one stent design is associated with a lower rate of in-stent restenosis than any other.

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