Prosthesis (i.e. – artificial body members) – parts thereof – or ai – Arterial prosthesis – Stent combined with surgical delivery system
Reexamination Certificate
2001-01-12
2004-03-23
Prebilic, Paul B. (Department: 3738)
Prosthesis (i.e., artificial body members), parts thereof, or ai
Arterial prosthesis
Stent combined with surgical delivery system
C137S012000, C015S104030
Reexamination Certificate
active
06709449
ABSTRACT:
TECHNICAL FIELD
The invention relates generally to the field of angioplasty and more specifically to stent implantation after angioplasty. More specifically, the invention relates to methods and means of reducing coronary restenosis.
BACKGROUND
Coronary restenosis after angioplasty and stent implantation placement remains a substantial problem, as outlined by Willerson, J. T., 1997
, Circulation
, 96:383-385. While recent randomized studies show that stent implantation reduces restenosis significantly compared to balloon angioplasty (see Rankin, J. M., et al., 1999
, N Engl J Med
, 341:2005-6), stents have not eliminated restenosis, especially in complex lesion subsets such as diffuse disease and small vessels. The observation that in-stent restenosis may be diffuse suggests that a generalized reaction to the stent may be a possible etiology. Such a reaction might be to the metal, or alternatively from residual contaminants on the stent from the manufacturing process, as described by Shih, C. C. et al., 2000
, J Biomed Mater Res
, 52:395-403.
Previous animal studies established a significant correlation between the degree of arterial injury caused by metallic wire coils and the resultant neointimal thickness and lumen stenosis at the stent site. See Schwartz, R. S. et al., 1992
, J Am Coll Cadiol
, 19:267-74, and Karas, S. P. et al., 1992
, J Am Coll Cardiol
, 20:467-74.
More recently, the inflammatory reaction induced by stent struts after stent manipulation was found positively associated with neointimal hyperplasia. See Kornowski, R. et al., 1998
, J Am Coll Cardiol
, 31:224-30. Chronic inflammatory cells around stent struts have also been seen in a recent pathology report of coronary stenting in humans (Farb, A. et al., 1992
, Circulation
, 99:44-52).
In light of these findings, a reduction of the stent-induced inflammatory response has the potential to prevent excessive neointimal formation within stents. Measures directed at inhibiting adhesion molecules (Barron, M. K. et al., 1997
, Circulation
, 96:3587-3592), tissue proteinases (Lucas, A. et al., 1996
, Circulation
, 94:2890-900) and macrophage activation (Rogers, C. et al., 1998
, Proc. Natl. Acad. Sci. USA
, 95:10134-10139) have been tested to suppress the inflammatory reaction after vascular injury, but further experimentation is required to better understand their clinical relevance.
Several reports indicate that manual stent manipulation before implantation may cause foreign body contamination (Whelan, D. M. et al., 1997
, Cathet Cardiovasc Diagn
, 40:328-332; Kornowski, R. et al., 1999
, Coronary Artery Dis
, 10:9-14) and increased neointimal hyperplasia (Kornowski, R., et al., 1998
, J Am Coll Cardiol
, 31:224-30).
Restenosis remains an important limitation of percutaneous interventions for coronary artery disease, despite major procedural advances over the past decade. Experimental studies and pathology reports suggest important relationships among inflammation, vascular injury, and neointimal growth. Monocytes contribute to neointimal thickening with bulk within the intima (see Moreno, P. R., et al., 1996
, Circulation
, 94:3098-3102) by generating injurious reactive oxygen intermediates, as noted by Peri, G. et al, 1990
, J. Immunol
, 144:1444-1448, and through elaboration of growth and chemotactic factors (see Assoian, et al., 1987
, Proc. Natl. Acad. Sci. USA
, 84:6020-6024), as well as by matrix metalloproteinase production capable of degrading extracellular constituents, thereby facilitating cell migration (Sukhova, G. K., et al., 1998
, J. Clin. Invest
, 102:576-583).
SUMMARY
We have determined that exposing sterile stents to a high pressure wash immediately before implantation can eliminate residual surface stent contaminants and reduce the inflammatory response elicited by the stent.
Accordingly, the invention is found in a stent treatment apparatus that includes a stent washing chamber that is configured to accept a stent, a fluid inflow port, and a fluid outflow port. The fluid inflow port and the fluid outflow port are in fluid communication with the stent washing chamber.
The invention is also found in a stent treatment apparatus that includes stent washing means for pressure washing a stent preloaded on a balloon catheter, as well as fluid inflow means for providing a washing fluid to the stent washing means and fluid outflow means for removing the washing fluid from the stent washing means. The apparatus also includes receiving means for receiving a catheter within the stent washing apparatus.
The invention is also found in a stent delivery system that includes a stent and a stent washing apparatus, where the apparatus includes a stent washing chamber that has an inlet, an outlet, and a central region configured to accept a stent. The apparatus also has a fluid inflow port and a fluid outflow port, with the fluid inflow port and the fluid outflow port in fluid communication with the stent washing chamber.
The invention is also found in a method of delivering a stent. The method includes steps of placing a preloaded stent into a stent washing apparatus, contacting the preloaded stent with a washing fluid under pressure, removing the washing fluid, and extending the preloaded stent beyond the stent washing apparatus into a touhy.
The invention is also found in a method of loading a stent with a drug. The method includes steps of placing a preloaded stent into a stent washing apparatus, contacting the preloaded stent with a solution comprising a drug, providing sufficient residence time to permit transfer of the drug into and onto the stent, removing the drug solution, and extending the preloaded stent beyond the stent washing apparatus into a touhy.
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Kornowski, R. et al., “In-Stent Restenosis: Contributions of Inflammatory responses and Arterial Injury to Neointimal Hyperplasia”,J. Am. Coll. Cardiol., vol. 31, No. 1, pp. 224-230 (Jan. 1998).
Kornowski, R. et al., “Granulomatous ‘foreign body reactions’ contribute to exaggerated in-stent restenosis”,Coronary Artery Dis., vol. 10, No. 1, pp. 9-14 (1999).
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Bayes-Genis Atoni
Camrud Allan R.
Schwartz Robert S.
Mayo Foundation for Medical Education and Research
Merchant & Gould P.C.
Prebilic Paul B.
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