Stents

Stents are primarily a treatment for restenosis. Each year in the United States, more than 500,000 people with coronary artery disease are treated with PTCA, or percutaneous transluminal coronary angioplasty. Unfortunately, restenosis—the re-narrowing of the coronary artery—occurs within three to six months in 40% to 50% of patients who undergo PTCA. Restenosis is the formation of a new blockage at the site of the PTCA.

There are two major mechanisms for restenosis. The first is by thrombosis, or blood clotting, at the site of the treatment. The second mechanism of stenting.

Stents are stainless steel, nitinol, titanium or cobalt mesh-like devices (some coated with gold) that appear similar to the spring in a ballpoint pen. Stents are delivered into the coronary artery on a catheter during a PTCA procedure. They are then deployed in the artery either by expansion of a balloon or by a unique selfexpanding delivery design. The stent serves as a scaffold to prop open the inside of the artery (the lumen), which increases blood flow to the heart muscle. Ultimately, the stent becomes covered with cells and, over time, part of the artery. Stents are currently used in approximately most percutaneous interventions (PCIs) for coronary artery disease.

The concept of attaching drugs to stents in order to reduce the risk of restenosis is not a new one. As mentioned above, thrombosis-related restenosis has been one of the most common problems associated with PTCA and stent intervention, although it has been successfully dealt with using anti-platelet drugs. The key to successful drug-eluting stents for the prevention of restenosis, however, is the very long-term delivery of drugs that prevent restenosis caused by cellular proliferation—scar tissue growth.