The following are 10 points to remember about the duration of dual antiplatelet therapy (DAPT) after coronary artery stenting:

1. Platelet activation and aggregation on the stent surface is the main mechanism leading to stent thrombosis (ST). DAPT has become a cornerstone of post–percutaneous coronary intervention (PCI) management and effectively reduces the risk of ST.
2. Pharmacological inactivation of the enzyme cyclooxygenase by its acetylation by acetylsalicylic acid and concomitant blockade of the P2Y12 receptor on the platelet surface by reversible or irreversible receptor antagonists (e.g., clopidogrel, ticagrelor, or prasugrel) effectively reduces platelet aggregation.
3. DAPT after coronary stent implantation effectively reduces blood clotting, and is mandatory during and after PCI.
4. DAPT appears to benefit in two distinct ways; first the prevention of ST, and second the reduction of coronary syndromes unrelated to previous PCIs.
5. The disadvantage of prolonged DAPT is an increased bleeding risk. While prolonged DAPT reduces ischemic events, the rate of bleeding increases with prolonged DAPT.
6. Although the evidence is preliminary, the mandatory duration of DAPT for the prevention of ST after stent implantation may be as low as 6, 3, or even 1 month depending, on stent generation and procedural factors.
7. On the other hand, prolonged DAPT beyond 1 year may be beneficial in patients at increased risk for disease progression or very late ST.
8. Current evidence encourages DAPT duration to be individualized based on overall risk assessment and careful clinical management.
9. Since all relevant information about individual bleeding and ischemic risk may not be available during PCI, it may be more prudent to take the decision of DAPT duration during follow-up when the mandatory first phase of DAPT is completed.
10. The role of long-term DAPT as well as aspirin monotherapy will be further evaluated in the ongoing GLOBAL LEADERS trial, and will provide additional insight.

Keywords: Acetylation, Adenosine, Aspirin, Blood Coagulation, Blood Platelets, Coronary Vessels, Cyclooxygenase Inhibitors, Disease Progression, Ischemia, Percutaneous Coronary Intervention, Platelet Aggregation, Platelet Activation, Prostaglandin-Endoperoxide Synthases, Risk Assessment, Stents, Thrombosis, Thiophenes, Ticlopidine

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