Abstract
Obstructive lesions in small coronary vessels are frequent, but the percutaneous coronary intervention (PCI) of these lesions remains a challenge in contemporary practice. Failure of revascularization after PCI is principally related to restenosis of the treated vessel [1]. After PCI, vessel caliber is inversely proportional to the antirestenotic efficacy of the treatment [2,3]. Consequently, the drawbacks intrinsic to PCI, such as mechanical vessel recoil and constrictive remodeling (after plain old balloon angioplasty), as well as neointimal hyperplasia (after stent implantation), become deleterious in this setting, principally due to the vessel’s reduced ability to accommodate a given degree of late lumen loss necessitating repeat revascularization procedures. The introduction of bare-metal stents (BMS) has represented a monumental leap in interventional cardiology; however, their use in small vessels did not provide the benefits demonstrated in other types of lesions. A noteworthy trial, ISAR-SMART, comparing balloon angioplasty with BMS in vessels with a caliber between 2.0 and 2.8 mm, showed no significant differences between the two groups in angiographic or clinical restenosis at follow-up [4]. The limitations of BMS for preventing restenosis are explained by the fact that the absolute magnitude of extra acute gain achievable by stenting over balloon angioplasty in small-vessel disease is relatively small and does not compensate for the reduced capacity of these small-caliber vessels to accommodate for increased neointimal hyperplasia seen after stent implantation. The pathophysiological mechanisms underlying BMS failure in this setting have led to the search for pharmaceutical methods and biological modalities to prevent restenosis. Therefore, by targeting the biological mechanisms that underlie neointimal hyperplasia and by providing an effective delivery system that results in adequate local tissue–drug
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