Stent thrombosis (old)

Summary

Although stent thrombosis (ST) is less frequent following the introduction of new generation drug-eluting stents (DES) and the evolution in adjunctive pharmacotherapies, it remains the most dreaded and deadly consequence of coronary stent deployment. Specific patient, target lesion, and procedural related factors have been identified which increase risk for ST. Genetic and phenotypic variability in the platelet inhibitory response to clopidogrel may be associated in high on-treatment residual platelet reactivity and/or consequent risk for ST. Inter-individual variability in response to clopidogrel may, at times, be overcome by increasing clopidogrel dose but most often requires switching from clopidogrel to a novel platelet P2Y12 receptor inhibitor. Prevention of ST requires a multifaceted approach which begins with patient risk stratification and choice of stent platform, includes fastidious procedural stent deployment and periprocedural adjunctive pharmacotherapy, and concludes with education and adherence to longer-term dual antiplatelet therapy (DAPT). The optimal duration of DAPT therapy to reduce ST has been investigated in a recent large-scale randomised, placebo controlled clinical trial which compared 30 versus 12 months of DAPT in subjects who had tolerated one year of therapy. Longer duration (30 months) therapy was associated with a significant reduction in both ST and myocardial infarction (MI) not...