PharmaSonics Inc announced the issuance of a key method patent, U.S. Patent No. 6,210,393, covering the use of intravascular Sonotherapy treatment to inhibit intimal hyperplasia, the accumulation of scar-type of tissue within a stent. Intimal hyperplasia is the main cause of restenosis or re-narrowing of a stented blood vessel. PharmaSonics has also applied for an international patent (PCT) to cover the same vascular treatment method.
Pharmasonics has developed the intravascular Sonotherapy system, a device-based anti-restenosis therapy, adjunctive to stenting and complementary to drug coated-stent technologies.
Restenosis rates for patients undergoing stent implantation remain high, reaching up to 50 per cent for certain high-risk patients. Stents eliminate vessel closure following angioplasty, but since they are metal implants, they encourage intimal hyperplasia, which may lead to restenosis within the stent.
Restenosis caused by intimal hyperplasia occurs when smooth muscle cells within the vessel wall migrate to the inner surface of the wall and proliferate through the stent struts, eventually causing re-occlusion. Intravascular Sonotherapy treatment uses non-ionizing, non-ablative therapeutic ultrasound energy to reduce the proliferation of smooth muscle cells, thereby reducing vessel renarrowing.
Menahem Nassi, PharmaSonics president and CEO stated, "PharmaSonics has established intellectual property ownership for the application of therapeutic ultrasound to reduce the incidence of vascular restenosis due to smooth muscle cell proliferation. Additional Sonotherapy treatment patents are pending U.S. patent office review. The objective of these patents is to broaden the intellectual property protection for PharmaSonics' Sonotherapy treatment beyond stent-induced hyperplasia and to include the reduction of hyperplasia resulting from vascular injury such as surgery, graft implantation and balloon angioplasty."
Currently intravascular Sonotherapy treatment is undergoing intense clinical investigation to determine its efficacy at reducing the rate of restenosis induced by stent implantation in both coronary de novo stents and patients already suffering from in-stent restenosis.'