ABSTRACT
Restenosis in general, especially in-stent restenosis, is still the major limitation of percutaneous coronary interventions (PCI) and predominantly responsible for major adverse cardiac events (MACE) in follow-up studies and registries [Hoffmann and Mintz 2000]. Since in-stent restenosis is due to cell proliferation, stents coated with antiproliferative drugs promise to be the next revolution in the field of interventional cardiology [Gunn and Cumberland 1999]. The hope is that these drug-coated stents will overcome the problem of restenosis by providing lesion-directed intravascular delivery of drugs that interrupt the molecular cascade leading to in-stent restenosis. These drugcoated stents provide a perfect opportunity for local vascular drug delivery without prolonging the procedure. Potential advantages of drug-coated stents include:
a) targeted drug delivery to precise area requiring treatment b) delivery at the time of implant injury c) ongoing delivery through phases of healing d) no additional materials or procedures required
Four interactive parameters may contribute to the success of a drug-coated stent in reducing restenosis: stent platform, selected drug(s), drug delivery vehicle or carrier, and the underlying vascular tissue. Stent implantation is associated with endovascular injury followed by a healing response. High degrees of injury appear to translate into more restenosis in the long term presumably because of more robust fibrotic healing responses. Ideally, the selected drug should interrupt multiple steps in the pathway that leads to restenosis, providing an effective anti-restenotic activity. For drug-eluting stents, the delivery vehicle must release the drug into the vessel in a manner that is consistent with the drug’s mode of action. The drug and carrier must be compatible and together control drug release kinetics. Finally, the carrier and the drug individually or together have the potential to alter the tissue characteristics in the vessel. The cumulative effects of all these drug-coated
stent parameters should interrupt the cascade associated with the healing response that culminates in restenosis.
