Beta-particle-emitting stents radiate enthusiasm in the search for effective prevention of restenosis.

Renarrowing of a coronary artery (restenosis) at the site of earlier balloon angioplasty is in 1996 still a clinical problem, with an incidence of 30% to 50%. Despite 20 years of experimental and clinical research, the biology of restenosis is still not fully understood. These studies have, however, greatly enhanced our insight into the restenosis process. The most widely accepted concept is that restenosis is the result of the vascular healing response to the injurious treatment. This response includes several phases: elastic recoil, thrombosis, inflammation, proliferation, and organization (or remodeling). Application of therapies aimed at reducing restenosis according to this paradigm has been partially successful. One approach involves the limitation of the thrombotic phase by effectively blocking the platelet glycoprotein IIb/ IIIa receptor1 (preliminary results from the CAPTURE and EPILOG studies support this approach). In these studies, the need for repeated coronary revascularization was substantially reduced but not eliminated. A second approach is the use of coronary stents. By limiting the residual lesion, elastic recoil, and late remodeling, stents reduce the need for both revascularization and angiographic restenosis2 3 compared with balloon angioplasty.

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