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(Circulation. 2003;108:2.)
© 2003 American Heart Association, Inc.

Editorials

Stent Thrombosis

An Issue Revisited in a Changing World

Yasuhiro Honda, MD; Peter J. Fitzgerald, MD, PhD

From the Center for Research in Cardiovascular Interventions, Stanford University, Stanford, Calif.

Correspondence to Peter J. Fitzgerald, MD, PhD, Center for Research in Cardiovascular Interventions, Stanford University, 300 Pasteur Dr, Room H3554, Stanford, CA 94305-5637. E-mail ivus@crci.stanford.edu

Key Words: Editorials • stents • thrombosis • ultrasonics

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The concept of stenting—intravascular mechanical support by transluminally placed endoprostheses—was first proposed by Charles Dotter >30 years ago.¹ As an intrinsic property of the metallic endoprostheses, early thrombotic occlusion of freshly deployed stents has been a concern since their introduction to human coronary circulation in 1986.² The unacceptably high rates (up to 24%) of thrombotic events seen in early clinical experience were first approached pharmacologically by aggressive anticoagulation with low-molecular-weight dextran, dipyridamole, and warfarin. Although this strategy helped reduce the incidence of stent thrombosis into a single-digit range, the benefit was obtained at a cost of significantly longer hospitalization and increased hemorrhagic/vascular complications. As intravascular ultrasound (IVUS) began to have widespread use in the clinical environment in the early 1990s, the importance of mechanical optimization at stent deployment for the prevention of stent thrombosis was underscored. The collaborative work of J.M. Tobis and A. Colombo demonstrated an unexpectedly high percentage of IVUS-detected stent deployment issues, including incomplete stent expansion, incomplete apposition, and asymmetric expansion, even after angiographically successful results.^3,4 These observations led to the concept of high-pressure stent deployment with IVUS guidance, achieving lower rates of subacute thrombosis with antiplatelet therapy alone (aspirin and ticlopidine).⁵ The superiority of this antiplatelet therapy after "optimal" stent expansion with routine high pressure post-dilatation was subsequently confirmed by several randomized trials when compared with other antithrombotic regimens.^6,7

See p 43

Nevertheless, stent thrombosis has not been eliminated; in this modern stent era, the incidence is reported to be 1% overall and can be more . . . [Full Text of this Article]

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