Coronary stent thrombosis

Stent thrombosis (ST) is a serious complication of percutaneous coronary interventions (PCI) with high mortality rates of up to 45%. Bare metal stents (BMS) and drug-eluting stents (DES) present similar rates of early (0.6%-1.2%) and late (0.3%-0.4%) ST. Very late ST is a specific entity after implantation of first-generation DES (sirolimus and paclitaxel) with an observed rate at 0.6% events/year. Strong predictors for early and late ST include: inadequate platelet inhibition, acute coronary syndromes (ACS), procedure-related factors such as stent underexpansion or dissection and patient-related factors such as diabetes, renal failure or a low left ventricular ejection fraction. Very late ST has been associated with delayed endothelial healing and drug-induced hypersensitivity reaction with exaggerated positive vessel remodeling, secondary incomplete stent apposition and paradoxical vasoconstriction. Dual antiplatelet therapy plays a key role in the prevention of ST. Premature dual antiplatelet therapy interruption (< 6 months after PCI) and clopidogrel resistance (25% of patients) are strongly associated with ST. Finally, promising new pharmacologic agents such as prasugrel and ticagrelor have been introduced, permitting more predictable inhibition of platelet aggregation and enabling a further reduction in ST risk.