Current status of stents

Abstract

T he use of intraarterial stents was first described by Dotter’ in 1969. Coronary stenting was introduced by S&wart et al2 using the Medivent Wallstent. Initial and long-term results of this stent have been described.3p4 Other stents tested in human coronaries include the Palmaz-Schatz5 and GianturcoRoubin6 stents. In this issue of The American Journal of Cardiology, de Jaegere et al7 describe the initial European experience with the Wiktor stent. Phase I U.S. clinical trials of this device were recently completed at the Ochsner Clinic in New Orleans. Table I summarizes design, material, complications and percentage of success of the different stents most frequently ~sed.~-iO It is not easy to decide which device should be considered best. Whereas the Wiktor stent (with better visibility) presents a high technical success and ease of implantation, the Palmaz-Schatz is currently the most widely used in the U.S. Although intensive anticoagulation is necessary, the subacute occlusion rate appears to be less for this device. The ideal stent should be visible, but have the minimal amount of material. The stent with the greatest amount of metal (the Wallstent) appears to have the highest rate of thrombosis. Reducing the amount of stent material also appears to decrease recurrence rates.’ l Complications of stenting: Acute or subacute thrombosis is a major complication of stenting.7 It is most likely responsible for sudden death that can occur during the first days after implantation or even several months later. Several factors play an important role in the development of thrombosis: material of the stent, percentage of the area covered by the device, lack of coating with anticoagulants, lack of aggressive systemic anticoagulation, and perhaps hemodynamics that may affect the blood flow. The stents differ in inherent thrombogenicity because of surface chemistry, amount of stent material present, and electrical charge of the metal used. Significant hemorrhagic complications (secondary to anticoagulant therapy) have been reported in all studies of stent implantation. This can vary from groin site hematomas to gastrointestinal and genitourinary hemorrhages needing blood transfusion, and unfortunately, death due to cerebral hemorrhage.5 Stenting probably does not reduce neointimal hyperplasia. This is logical, because stent placement does not modify the basic healing process after arterial injury.12,13 Ellis et all4 are correct in postulating that any effect on recurrent stenosis is related to the initial effect