title: Thrombotic and Hemorrhagic Complications of Stenting Coronary Arteries: Incidence, Management, and Prevention.
abstract: Stents are intravascular prostheses which provide endoluminal scaffolding, effectively reducing elastic recoil and sealing local dissections. Stents have become the treatment of choice for acute vessel closure following percutaneous coronary intervention. In addition, by providing a large, smooth lumen, stenting increases procedural success and decreases late restenosis compared with conventional balloon angioplasty. All stents evaluated clinically are constructed of non-corrosive metallic alloys which are inherently thrombogenic.The incidence of stent thrombosis ranges from 0.4-18%. While acute thrombosis is uncommon, subacute thrombosis may occur from 5 to 21 days (mean 7 days) after placement. Predictors of stent thrombosis include stenting for bailout indication, angiographically visible thrombus after implantation, stenting of smaller vessels, presence of residual dissection after stenting, poor distal runoff, incomplete stent expansion and stenting in the setting of acute myocardial infarction. Stent thrombosis is associated with high incidence of Q-wave myocardial infarction (70-90%) and mortality (7-20%), and is best treated with emergency catheterization and balloon angioplasty.To prevent stent thrombosis, aggressive procedural and postprocedural pharmacological regimens employing antiplatelet agents (aspirin, dipyridamole and dextran) and anticoagulation (heparin followed by warfarin) have been used. While these regimens have reduced the incidence of stent thrombosis to <5%, they are associated with a high incidence of vascular and hemorrhagic complications, increased length of hospitalization and total cost. To decrease the incidence of stent thrombosis and obviate the need for anticoagulation, strategies such as intravascular ultrasound guided "optimal stenting" and addition of the antiplatelet agent ticlopidine, are being evaluated. In the future coating of stents with agents such as heparin, may further reduce the risk of thrombosis and the requirement for long-term anticoagulation.
authors.affiliation: Charles A. Dana Research Institute and Harvard-Thorndike Laboratory, Cardiovascular Division, Beth Israel Hospital, Boston, Massachusetts.
authors.initials: JP
authors.lastname: Carrozza
authors.initials: DS
authors.lastname: Baim