Stent thrombosis

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 the risk for ST. Genetic and phenotypic variability in the platelet inhibitory response to clopidogrel may be associated with high on-treatment residual platelet reactivity and a consequent risk for ST. Inter-individual variability in response to clopidogrel may 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, fastidious procedural stent deployment and periprocedural adjunctive pharmacotherapy, and concludes with education and adherence to antiplatelet therapy. The optimal duration of dual antiplatelet therapy (DAPT) has evolved and more recently, strategies of short duration DAPT followed by single agent antiplatelet therapy (SAPT) or DAPT de-escalation from a high intensity P2Y12 inhibitor (ticagrelor or prasugrel) to clopidogrel have supplanted longer DAPT durations by reducing the risk for bleeding, with a similar or reduced risk of ischemic events when compared with longer durations of...