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Circulation. 1997;95:1098-1100

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(Circulation. 1997;95:1098-1100.)
© 1997 American Heart Association, Inc.


Articles

Stent Thrombosis

Closing in on the Best Preventive Treatment

Donald S. Baim, MD; Joseph P. Carrozza, Jr, MD

the Interventional Cardiology Section, Beth Israel–Deaconess Medical Center (East Campus), Boston, Mass.

Correspondence to Donald S. Baim, MD, Chief, Interventional Cardiology Section, Beth Israel–Deaconess Medical Center (East Campus), 330 Brookline Ave, Boston, MA 02215.


Key Words: Editorials • platelets • thrombosis • stent • angioplasty


*    Introduction
 
Amazing progress has been made in the use of metallic endoprostheses (stents) in the human coronary circulation since the pioneering work of Sigwart 10 years ago. Of the three initial designs (the self-expanding mesh [Wallstent, Schneider], the coil stent [Gianturco-Roubin, Cook], and the slotted-tube stent [Palmaz-Schatz, Johnson & Johnson]), only the latter two designs are currently available in the United States (the Gianturco-Roubin since mid-1993 and the Palmaz-Schatz since mid-1994). Yet in that short time, coronary stenting has revolutionized catheter intervention. Stents (alone or in combination with other devices such as rotational atherectomy) are now used in >30% of interventions nationally and >50% of interventions in many laboratories, including our own. While their approval was based on abrupt or threatened abrupt closure (Gianturco-Roubin) and reduction of restenosis in focal de novo native lesions (Palmaz-Schatz), the majority of current use falls outside those narrow categories (and includes restenotic lesions, vein grafts, longer lesions, etc), for which registry data suggest clinical benefit over conventional angioplasty, although definitive trials to document benefit over conventional balloon angioplasty are still incomplete.

From the beginning of stent implantation, acute (<24 hour) and subacute (1- to 14-day) thrombosis of the stented segment has been one of the most feared complications. Despite use of heparin, aspirin, dipyridamole, and low-molecular-weight dextran, the incidence of this event was 24% in the early Wallstent experience1 and 16% in the early Palmaz-Schatz experience.2 The first response was to add further pharmacological barriers to thrombosis. Addition of oral warfarin (with an uninterrupted switch . . . [Full Text of this Article]




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