354results about How to "Prevent restenosis" patented technology

Post-interventional neointimal hyperplasia in arteries is treated by the application of ultrasonic energy. Usually, an intravascular catheter having an interface surface is positioned at a target site in the artery which has previously been treated. The interface surface is vibrationally excited to apply energy to the arterial wall in a manner which inhibits smooth muscle cell proliferation in the neointimal layer.

An intravascular stent and method for inhibiting restenosis, following vascular injury, is disclosed. The stent has an expandable, linked-filament body and a drug-release coating formed on the stent-body filaments, for contacting the vessel injury site when the stent is placed in-situ in an expanded condition. The coating releases, for a period of at least 4 weeks, a restenosis-inhibiting amount of a monocyclic triene immunosuppressive compound having an alkyl group substituent at carbon position 40 in the compound. The stent, when used to treat a vascular injury, gives good protection against clinical restenosis, even when the extent of vascular injury involves vessel overstretching by more than 30% diameter. Also disclosed is a stent having a drug-release coating composed of (i) 10 and 60 weight percent poly-d/-lactide polymer substrate and (ii) 40-90 weight percent of an anti-restenosis compound, and a polymer undercoat having a thickness of between 1-5 microns.

The present invention provides improved stents and other prostheses for delivering substances to vascular and other luminal and intracorporeal environments. In particular, the present invention provides for therapeutic capable agent eluting stents with minimized undesirable loss of the therapeutic capable agent during expansion of the stent.

Disclosed are methods, compounds and compositions useful for treatment of a patient with valvular dysfunction. The invention relates to using stem cells, modified stem cells, derivatives thereof, and agents stimulatory to stem cells in order to substantially ameliorate, and in some cases induce a therapeutic benefit, to a patient suffering from a dysfunction of the mitral, aortic, tricuspid, or pulmonary valve. In some embodiments the invention treats the valve dysfunction itself, whereas in other embodiments treatment of associated cardiac structures is performed. Furthermore, in other embodiments the invention permits physiological compensation for the valve dysfunction, prolonging the time until surgical intervention is needed.

A method for the provision of a coating on an implantable medical device results in a medical device having a bio-absorbable coating. The coating includes a bio-absorbable carrier component. In addition to the bio-absorbable carrier component, a dissolved therapeutic agent component can also be provided. The coated medical device is implantable in a patient to effect controlled delivery of the coating, including the dissolved therapeutic agent, to the patient.

This invention provides compositions and methods for producing a medical device coated with a matrix and an antibody which reacts with an endothelial cell antigen. The matrix coating the medical device may be composed of synthetic material, such as polyurethane, poly-L-lactic acid, cellulose ester or polyethylene glycol. In another embodiment, the matrix is composed of naturally occurring materials, such as collagen, fibrin, elastin, amorphous carbon. In a third embodiment, the matrix may be composed of fullerenes. The fullerenes range from about C60 to about C100. The medical device may be a stent or a synthetic graft. The antibodies promote adherence of endothelial cells on the medical device. The antibodies may be mixed with the matrix or covalently tethered through a linker molecule to the matrix. Following adherence to the medical device, the endothelial cells differentiate and proliferate on the medical device. The antibodies may be different types of monoclonal antibodies. Methods of preparing such composition and methods of treating a mammal with atherosclerosis or other types of vessel obstruction are disclosed. By facilitating adherence of endothelial cells to the surface of the medical device, the methods and compositions of this invention will decrease the incidence of restenosis as well as other thromboembolic complications resulting from implantation of medical devices.

PCT No. PCT/CA93/00388 Sec. 371 Date Mar. 24, 1995 Sec. 102(e) Date Mar. 24, 1995 PCT Filed Sep. 22, 1993 PCT Pub. No. WO94/07505 PCT Pub. Date Apr. 14, 1994A method is provided of inhibiting the narrowing of the vascular tubular walls of an animal by the proliferation of endothelial cells in the area of trauma after the vascular tubular walls have been traumatized, the method comprising the administration of a therapeutically effective non-toxic amount of a form of hyaluronic acid selected from the group consisting of hyaluronic acid and pharmaceutically acceptable salts thereof to the animal to inhibit the narrowing of the vascular tubular walls by the proliferation of endothelial cells into the area of trauma.

A stent is provided in combination with a growth factor, specifically pleiotrophin or an analog or derivative thereof, which promotes endothelialization of the stent and re-endothelialization of the stented region of an injured site in a body lumen. In particular applications, the stent is an endolumenal stent and the growth factor promotes healing via endothelialization and substantially prevents restenosis. The growth factor is delivered from the stent formulated as a protein or peptide, or as a gene transfer vector. Methods for the treatment of vascular injury using pleiotrophin are also disclosed.

Restenosis is inhibited through local delivery of anti-restenotic agents including angiotensin converting enzyme inhibitors; nicotine receptor agonists, agents that increase concentrations of nitric oxide, anti-angiogenic agents, agonists of the TGF-beta receptor; death domain receptor ligands; and thrombin inhibitors. In one embodiment of the invention, the localized delivery is effected through the use of a stent modified for delivery of the agent at the site of injury from balloon angioplasty.

The present invention provides improved stents and other prostheses for delivering substances to vascular and other luminal and intracorporeal environments. In particular, the present invention provides for therapeutic capable agent eluting stents with minimized undesirable loss of the therapeutic capable agent during expansion of the stent.

Extremely hydrophobic nitric oxide (NO) releasing polymers are disclosed. The extremely hydrophobic NO-releasing polymers provided are extensively cross-linked polyamine-derivatized divinylbenzene diazeniumdiolates. These polymers can be loaded with extremely high NO levels and designed to release NO in manners than mimic natural biological systems. The NO-releasing extremely hydrophobic polymers provided can maintain a sustained NO release for periods exceeding nine months. Also provided are related medical devices made using these NO-releasing extremely hydrophobic polymers.

The invention provides a medicine eluting balloon catheter, which comprises a balloon catheter body and a medicine coating, wherein the balloon catheter body comprises a balloon; the outside surface of the balloon has a plurality of grooves; and the medicine coating is coated on the grooved part and flat part of the outside surface of the balloon. The medicine eluting balloon catheter is characterized in that grooves protrude in a reversed direction when the balloon is fully expanded. The medicine eluting balloon catheter disclosed by the invention can carry more medicines and reduce loss of the medicines in a conveying process; and the medicine eluting balloon catheter directly pour and cast medicines remaining in the grooves into blood through reversed protrusion to accelerate the release of the medicines and to increase the medicine concentration at a target position, so that the medicines can quickly concentrate and act on the target position to well prevent the blood vessel tissue at the target position from regeneration and restenosis.

Medical devices and related methods for making and using same suitable for treating or inhibiting restenosis are proved. Specifically, compositions and methods for I kappa B alpha (IkBα)nuclear factor kβ (NFkβ) complex breakdown inhibition are provided. One embodiment includes a CRM-1 protein binding composition such as leptomycin B. Another embodiment includes a combination of a CRM-1 protein binding composition and a nucleic acid encoding for mammalian IkBα. Medical devices disclosed include catheters and vascular stents.