Coronary arteries provide blood and nutrients to the heart muscle. The arteries are subject to atherosclerosis or hardening of the arteries. Vascular regions have plaques formed within, resulting in stenosed regions having reduced cross-sectional area. The reduced area causes a reduction in transport of blood, oxygen, and nutrients which can result in angina, myocardial infarction and death.
A commonly used method for treating atherosclerosis is Percutaneous Transluminal Coronary Angioplasty (PTCA). PTCA includes insertion of a balloon catheter through an insertion in the femoral artery near the groin, advancement of the balloon over the aortic arch, advancement within the selected coronary artery, continuing until the balloon portion is placed across the stenosed region. The balloon is inflated, widening the narrowed vessel region.
After catheter withdrawal, significant vessel reclosure may develop. The reclosure may occur within hours or days of dilation, an "abrupt reclosure." When reclosure does occur, it more commonly occurs progressively, within six months of the angioplasty. The gradual reclosure is referred to as "restenosis", and largely negates the dilatation treatment. More highly stenosed vessel regions have a greater chance of becoming restenosed.
One approach to dealing with restenosis utilizes stents, short tubular sections, placed across the recently dilatated vessel region. Stents can be either self-expanding or balloon-expandable. Stents are normally left in place indefinitely. As the stent is forever pushing radially outward against the vessel wall, the wall can be undesirably irritated over long time periods. Stent ends, which push radially outward, are adjacent to soft tissue which can be irritated by the stent end. Stents commonly have wire mesh or spring structures, with openings in the stent walls. "Intimal hyperplasia", rapid tissue growth through stent openings has also been reported. While the exact mechanism of restenosis is not understood, it is believed that the vessel narrowing is due more to cellular growth and/or a response to vessel injury than to an elastic rebound mechanism.
Thus, to prevent restenosis, use of a stent, or a stent without additional therapy, may not be a solution for all patients. An alternative to stents or an additional treatment associated with the use of stents may be desirably for some patients.
Once therapy for reducing restenosis which has been suggested is heated balloon angioplasty. Some attempts were directed to making the tissues "flow", by heating vessel tissue at 60 and 80 degrees C. Other attempts utilized high temperatures for the stated purpose of sealing the splitting of the intimal layers of the blood vessel walls, fusing tissue and coagulating. However, such attempts led to increased rather than decreased restenosis.
What is desirable and has not heretofore been provided is a method for inhibiting restenosis after a stent has been put in place. What would be more desirable is a method for inhibiting restenosis not requiring any stent placement.