Treatment of in-stent restenosis using cytotoxic radiation

Surgery – Instruments – Light application

Reexamination Certificate

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Details

C606S015000, C606S191000, C606S194000

Reexamination Certificate

active

06200307

ABSTRACT:

BACKGROUND OF THE INVENTION
The present invention concerns methods and systems for treatment of restenosis in body lumens such as blood vessels and, in particular, the treatment of in-stent restenosis.
Endoluminal stents are commonly used to treat obstructed or weakened body lumens, such as blood vessels and other vascular lumens. Numerous stents exist for this purpose, including those made of metals, fibers and other biocompatible materials. In general, the stent is either formed outside the body and then guided into place (e.g., adjacent to an obstruction) through a body lumen, or is positioned into place prior to formation and is then expanded and/or formed in situ within the body lumen. Once deployed, the stent can remain in the body lumen where it will maintain the patency of the lumen and/or support the walls of the lumen which surround it.
One factor impeding the success of stent technology in endoluminal treatments is the frequent occurrence of in-stent restenosis, characterized by proliferation and migration of smooth muscle cells within and/or adjacent to the implanted stent, causing reclosure or blockage of the body lumen. While the reasons for such smooth muscle cell proliferation following stent implantation are not entirely clear, it is believed that positioning of the stent within the body lumen may somehow irritate or damage the surrounding lumen walls and activate medial smooth muscle cells lining the walls.
Current methods for treating endoluminal restenosis, such as that which occur within or around a stent, generally consist of invasive procedures which physically remove atherosclerotic plaque by, for example, shaving or ablating the plaque, or by implanting a second stent. However, these procedures can cause further damage to the area of treatment and/or initiate further smooth muscle cell proliferation.
Accordingly, it is an object of the present invention to provide a substantially non-invasive method of treating in-stent restenosis by applying radiation to the smooth muscle cells which have grown within or around a stent implant in a manner that does not substantially damage the surrounding lumen wall or the stent itself, while resulting in a reduction of smooth muscle cell mass.
SUMMARY OF THE INVENTION
Methods and systems are disclosed for treating in-stent restenosis using radiation having a wavelength sufficient to kill or promote cellular death (e.g., through programmed cell death), or otherwise remove smooth muscle cells which have proliferated, or which might otherwise proliferate, in the proximity of (i.e., within, around or adjacent to) a stent within a body lumen, causing (or potentially causing) at least partial blockage of the lumen. Devices are disclosed for providing such therapeutic radiation at the stent with or without concurrent mechanical (e.g. balloon dilation) angioplasty. Treatment methods are also disclosed which include irradiating smooth muscle cells in the region of the stenosis with non-ablative, cytotoxic radiation, such as UV radiation. A cytotoxic, photoactivatable chromophore may also be delivered to the treatment site prior to irradiation. The methods and systems can be used prophylactically or to treat in-stent restenosis after blockage has occurred without further damage to surrounding tissue.
In-stent restenosis can be treated effectively and with minimal tissue damage using cytotoxic, nonablative radiation, such as UV radiation. The radiation kills or otherwise inactivates smooth muscle cells which have proliferated or are susceptible to proliferation within and/or adjacent to a stent in a body lumen, causing the cells to retract from the stenosed region. The radiation is preferably delivered to the area around (e.g., within or adjacent to) the stent via an optical fiber or other waveguide incorporated, for example, into a percutaneous catheter.
The term “in-stent restenosis,” as used herein, includes partial or complete blockage of a body lumen in an area of stent implantation due in whole or in part to proliferation of medial smooth muscle cells within or around (e.g., adjacent to) the stent. The term “cell overgrowth” as used herein is intended to describe any condition involving the proliferation of cells in proximity to a stent. The term “body lumen,” as used herein, includes any body lumen capable of containing a tent, such as vascular, urological, biliary, esophageal, reproductive, endobronchial, gastrointestinal, and prostatic lumens. The term “non-ablative, cytotoxic radiation,” as used herein, means radiation which directly or indirectly (e.g., by apoptosis) kills or otherwise causes the removal of smooth muscle cells in a stenosed region, resulting in a reduction in tissue mass and/or an increase in the diameter of the lumen, without the use of heat ablation.
In one embodiment of the invention, the cytotoxic, non-ablative radiation is ultraviolet (UV) radiation having a wavelength of less than about 280 nanometers, down to about 240 nanometers (due to the limited transmission efficiency of glass optical fibers at lower wavelengths). The effect of UV radiation having this wavelength range, commonly known as UV “C” radiation, at the doses necessary to penetrate the build up of smooth muscle cell mass, causes direct cellular death of most cells and can cause programmed cell death in other cells, resulting in a reduction in cell mass without heating or damaging the surrounding tissue.
In another embodiment of the invention, the cytotoxic, non-ablative radiation has a longer wavelength, such as UV “A” or “B” radiation in the wavelength range of about 280 nanometers to 400 nanometers, or visible radiation having a wavelength of about 400 to 700 nanometers, or infrared radiation from about 700 nanometers to 2.6 micrometers, and is used in conjunction with a photoactivatable, cytotoxic chromophore which is activated upon exposure to light at some or more of these wavelengths. The term “photoactivatable, cytotoxic chromophore,” as used herein, encompasses chromophores capable of being absorbed by mammalian tissues and being activated upon exposure to light so cells of the tissue die or cease to proliferate. In the present invention, the photoactivatable chromophore is delivered to tissue which has increased in mass (e.g., due to smooth muscle cell proliferation) within or around a stent and is causing restenosis of the lumen supported by the stent. The tissue is then exposed to radiation of a sufficient wavelength to activate the chromophore. Once activated by the light, the chromophore causes direct programmed death (apoptosis) thereby decreasing the number of cells and the mass of the tissue.
Suitable chromophores for use in the invention are generally selected for absorption of light that is deliverable from common radiation sources (e.g. UV light ranging from 240-400 nanometers, or visible light having wavelengths of 400 nanometers or longer). For example, photoactivatable psoralens and hematoporphyrins can be administered systemically or locally to the stenosed region prior to irradiation, thereby rendering smooth muscle cells in the region more susceptible to radiation. Other suitable chromophores are well known in the art and include those which are photoactivated upon irradiation with either long-wave UV light (PUVA) (See, e.g., U.S. Pat. No. 5,116,864 (Mar. et al.) or with visible light (see, e.g., U.S. Pat. No. 5,514,707 (Deckelbaum et al.), the disclosures of which are incorporated herein by reference.)
Various radiation sources can be use in accordance with the present invention to deliver non-ablative, cytotoxic radiation to a stenosed region within or around a stent. Generally, the radiation is delivered via a laser catheter carrying a fiber optic waveguide. Either pulsed or continuous wave (“CW”) lasers can be used in the present invention, and the lasant medium can be gaseous, liquid or solid state. The laser can be a pulsed excimer laser, such as a KrF laser. Alternatively, rare earth-doped solid state lasers, ruby lasers and Nd:YAG lasers can be operated directly or in conjunction with frequency m

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