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ACS), showed reduced ischaemic events, but increased BARC 3 and 5 major bleeding, during ticagrelor monotherapy compared with aspirin monotherapy from 1 to 2 years after PCI.572 The double-blind, non-inferiority TWILIGHT trial, conducted in 7119 patients [35% CCS, 65% NSTE (non-ST-segment elevation)-ACS] undergoing high-risk PCI (defined as multivessel, stenting of >30 mm, thrombotic, two-stent bifurcation, left main, proximal LAD, or atherectomy-treated calcified lesions) and uneventfully receiving 3 months of ticagrelor-based DAPT after PCI, showed that ticagrelor monotherapy 90 mg b.i.d. (twice daily) compared with ticagrelorbased DAPT for an additional 12 months significantly reduced the primary endpoint of clinically relevant bleeds (BARC 2, 3, and 5, or BARC 3 and 5), with no significant increase in the composite of any death, MI, or stroke (3.9% in both groups).573 P P Clopidogrel Aspirin Vorapaxar Ticagrelor Prasugrel Cangrelor Rivaroxaban Apixaban Edoxaban UFH Enoxaparin Eptifibatide Tirofiban Dabigatran VKA Bivalirudin Argatroban Fondaparinux GP IIb/IIIa GP IIb/IIIa PAR I PAR 4 TxA2 P2Y12 receptor Thromboxane receptor ADP Plaque rupture or plaque erosion TF:FVIIa coagulation Platelet rolling and adhesion Platelet activation Platelet aggregation Fibrinogen Fibrinogen Fibrin FXa Thrombin Thrombin Fibrin network Platelet fibrin thrombus Figure 10 Antithrombotic drugs for chronic coronary syndromes: pharmacological targets. ADP, adenosine diphosphate; FVIIa, activated factor VII; FXa, activated factor X; GP, glycoprotein; PAR, protease-activated receptor; TF, tissue factor; TxA2, thromboxane A2; UFH, unfractionated heparin; VKA, vitamin K antagonist. Orally administered drugs are shown on a blue background, parenterally administered ones on red. Aspirin prevents TxA2 formation by acetylating platelet cyclooxygenase-1. ESC Guidelines 3461 Downloaded from academic.oup.com/eurheartj/article/45/36/3415/7743115 by guest on 07 October 2026