Stent thrombosis (ST) is a rare but potentially life-threatening event that can occur following percutaneous coronary intervention (PCI) with stent implantation. Several factors related to the procedure or patient features can favor thrombus formation and development of ST. Dual Antiplatelet Therapy (DAPT) with aspirin and P2Y12 inhibitors is the cornerstone of strategy for reducing incidence of ST. Two main causes of DAPT failure have been identified: the inappropriately premature antiplatelet therapy discontinuation and hyporesponsiveness to antiplatelet drugs. There is growing evidence that a residual high on treatment platelet reactivity (HPR) is associated with increased risk of thrombotic complications after PCI, including ST. In recent years numerous platelet function tests were developed and some of these have been extensively used in clinical studies to evaluate residual platelet reactivity, after antiplatelet drugs administration. The identification of patients with HPR is fundamental for optimization of antiplatelet treatment. Nevertheless first studies suggested that achieving a more intense platelet inhibition, switching from standard to an intensified treatment regimen on the basis of platelet reactivity, has failed to show any benefit in terms of clinical events. Certainly individualized pharmacological treatment of patients undergoing PCI remains one of the most important objectives in order to prevent serious PCI complications, such us ST.

Department of Cardiovascular Sciences Campus Bio Medico University of Rome Italy