American Journal of Cardiology
Volume 78, Issue 3, Supplement 1 , Pages 13-17, 14 August 1996

Subacute Stent Thrombosis and the Anticoagulation Controversy: Changes in Drug Therapy, Operator Technique, and the Impact of Intravascular Ultrasound

Centro Cuore Columbus, Milan, Italy

Cardiology Division, Lenox Hill Hospital, New York, New York 10021, USA

Abstract 

Clinical trials have shown that stents are superior to other catheter-based coronary interventions in terms of reduced complications and improved long-term efficacy. With utilization of high-pressure balloon inflation and intravascular ultrasound (IVUS) guidance, stent implantation can now be performed safely without anticoagulation (i.e., with lower rates of stent thrombosis and vascular complications). In 2 recent prospective clinical trials, stent thrombosis occurred in 3.5% of cases despite anticoagulant therapy, which resulted in an average of 7% vascular and bleeding complications. Initial use of IVUS during traditional stent deployment showed that 80% of stents were underexpanded and led to the hypothesis that stent thrombosis might be decreased as a result of optimal stent placement under IVUS guidance without the need for anticoagulation. In a prospective clinical trial to test this hypothesis, three factors were found to reduce stent thrombosis: full stent expansion, complete apposition to the vessel wall, and full lesion coverage. Predictors of thrombotic risk in this era of high-pressure stent deployment without anticoagulation include low ejection fraction, residual dissections, slow flow, multiple stents per lesion, and smaller postprocedure stent luminal diameter. To optimize stent expansion, stent dilation should be performed using a mean inflation pressure of 18 atm with a noncompliant or minimally compliant balloon sized to the vessel being treated (B/V ratio = 1.1). Controversy still remains about the best poststent antiplatelet regimen, and results of a recent trial should indicate whether heparin coating provides additional protection from stent thrombosis. (AM J Cardiol 1996;78(suppl 3A): 13–17)

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PII: S0002-9149(96)00486-9

American Journal of Cardiology
Volume 78, Issue 3, Supplement 1 , Pages 13-17, 14 August 1996