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- FR, fast release
- IL, interleukin
- IVUS, intravascular ultrasound
- mTOR, mammalian target of rapamycin
- PBMA, polybutylmethacrylate
- PCNA, proliferating cell nuclear antigen
- PEVA, polyethylenevinylacetate
- RAVEL, randomised study with sirolimus coated BX Velocity balloon expandable stent in the treatment of patients with de novo native coronary lesions
- SR, slow release
- VEGF, vascular endothelial growth factor
Drug eluting stents represent one of the fastest growing fields in interventional cardiology today.
At the congress of the European Society of Cardiology in Amsterdam in 2000, I (PWS) was asked to give the Andreas Gruentzig Lecture. In the week preceding the lecture, we re-angiographied patients 32 and 33 of the initial cohort of patients who had received a rapamycin eluting stent in Sao Paulo and in Rotterdam. Scrutinising the 4–6 month angiographic and ultrasonic results of these patients, I became overwhelmingly convinced that we were the privileged witnesses of a new phenomenon: the almost complete abolition of intra-stent neointimal proliferation. Colleagues, invasive and non-invasive cardiologists, old friends, and financial analysts were surprised by the unusual “excess of enthusiasm” coming from somebody who has built over the years a reputation as a critical assessor, never one to be carried away by the hype of a new wave in interventional cardiology. In the history of this field I have recognised (and “got excited” by, as my American colleagues used to put it) only two revolutionary developments: the introduction of the moveable and steerable guidewire by John Simpson, and the advent of the stent (Palmaz-Schatz, Wallstent). The drug eluting stent is the third such development, and almost one year later I would like to restate the fact that we are entering a new era in interventional cardiology. Why? Because the principle of an eluting stent is sound, and because the three major technical challenges have been mastered—the controlled release of an efficient drug from a stable coating.
Drug administration for the prevention of restenosis has been tested in the past—with disappointing results throughout. A proposed explanation for the repeated failure of clinical drug studies has been that agents given systematically cannot reach sufficient concentrations in injured arteries, which has a signficant impact …