Optimal Duration of Antiplatelet Therapy in Recipients of Coronary Drug-Eluting Stents (original) (raw)
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The American Journal of Cardiology, 2009
It remains unclear whether dual antiplatelet therapy >12 months might carry a better prognosis after percutaneous coronary intervention (PCI) with drug-eluting stents (DESs). To address the hypothesis that in the real world the risk of very late thrombosis after PCI with DESs can be decreased by an extended use of clopidogrel, we set up the Two-Year ClOpidOgrel Need (TYCOON) registry and prospectively investigated the impact on very late thrombosis of 12-versus 24-month dual antiplatelet regimens in an unselected population. The registry enrolled 897 consecutive patients who underwent PCI with stenting from January 1, 2003, to December 31, 2004, and had dual antiplatelet therapy. All patients had a 4-year clinical follow-up. In the 447 patients with DES implantation, the dual antiplatelet regimen after PCI was given for 12 months in the 173 patients treated in 2003 (12-month group) and for 24 months in the 274 patients treated in 2004 (24-month group). Comparison between groups did not reveal any significant difference in baseline clinical characteristics, angiographic and procedural features, and major adverse cardiac events. During follow-up, there were 5 cases of stent thrombosis after PCI in the 12-month DES group and 1 case in the 24-month DES group (p ؍ 0.02). Specifically, there were 2 cases of subacute thrombosis (1 in each group), no case of late thrombosis, and 4 cases of very late thrombosis occurring at 13, 15, 17, and 23 months after DES implantation in the 12-month group only. In conclusion, a 2-year dual antiplatelet regimen with aspirin and clopidogrel can prevent the occurrence of very late stent thrombosis after PCI with DESs.
Thrombosis Research, 2009
Background: Increased doses of antiplatelet therapy have been proposed to overcome the variability of response. However, the chronic dose of aspirin after DES remains controversial. Methods and results: We assessed in a prospective and randomized study the benefit of higher dose of aspirin, in association with clopidogrel, on aspirin response and non COX-specific platelet testing in patients receiving Drug Eluting Stent (DES) for stable angina pectoris. 50 consecutive patients receiving DES for stable angina pectoris were prospectively included. They received loading dose of 250 mg aspirin and 600 mg clopidogrel and antiplatelet response was assessed with Arachidonic Acid-induced aggregation (AA-Ag) and ADP-induced aggregation (ADP-Ag) for aspirin and clopidogrel response respectively. Patients were randomized to either 75 or 160 mg of aspirin with 150 mg clopidogrel and platelet testing were repeated one month after hospital discharge. The two groups (aspirin "75 mg" or "160 mg") had no difference for aspirin response: AA-Ag (5.2 ± 1.7% vs 6 ± 2%, p = 0.75) and non COX-specific pathway testing: ADP-Ag (47 ± 3% vs 49 ± 4%, p = 0.61). Conclusion: The present study did not show any benefit of higher dose of aspirin neither on aspirin responsiveness, nor on inhibition of non COX-specific pathway. These data does not support use of higher dose than 75 mg of aspirin in association with clopidogrel in patients receiving DES, especially while higher doses have been associated with increased bleeding risk.
European heart journal, 2015
This open-label, randomized, and multicentre trial tested the hypothesis that, on a background of aspirin, continuing clopidogrel would be superior to stopping clopidogrel at 12 months following drug-eluting stent (DES) implantation. Patients (N = 1799) who had undergone placement of ≥1 DES for stable coronary artery disease or acute coronary syndrome were included in 58 French sites (January 2009-January 2013). Patients (N = 1385) free of major cardiovascular/cerebrovascular events or major bleeding and on aspirin and clopidogrel 12 months after stenting were eligible for randomization (1:1) between continuing clopidogrel 75 mg daily (extended-dual antiplatelet therapy, DAPT, group) or discontinuing clopidogrel (aspirin group). The primary outcome was net adverse clinical events defined as the composite of death, myocardial infarction, stroke, or major bleeding. Follow-up was planned from a minimum of 6 to a maximum of 36 months after randomization. Owing to slow recruitment, the s...
Aspirin and Clopidogrel: Lessons from PCI-CLARITY, COMMIT & CHARISMA
Platelet activation plays a critical role both in spontaneous coronary artery thrombosis due to atherosclerotic plaque rupture and in thrombotic complications following percutaneous coronary intervention (PCI) with coronary artery stenting. Aspirin use has been shown to safely reduce ischemic events throughout the spectrum of clinical conditions of coronary artery disease (CAD). Therefore, aspirin is part of the standard treatment given to patients with CAD, including those undergoing PCI. Despite the inhibition of cyclooxygenase by aspirin, however, platelet activation can still occur through thromboxane-independent pathways, leading to the aggregation of platelets and the formation of thrombin. For that reason, a more potent antiplatelet effect was sought by using other agents -thienopyridines (ticlopidine, clopidogrel) and glycoprotein IIb/IIIa (GpIIb/IIIa) inhibitors, usually in combination with aspirin. Indeed, depending on the clinical scenario and the concomitant anticoagulants used, regimens combining 2 or more of these antiplatelet agents have resulted in fewer ischemic events and sometimes more bleeding events compared with aspirin alone.
International Journal of Cardiology, 2011
Indications for percutaneous coronary intervention with stent placement are increasing; some candidates already require oral anticoagulation. Safety of triple antithrombotic therapyaspirin (ASA), clopidogrel and oral anticoagulation (OAC)remains largely unknown. In order to study hemorrhagic complications in those patients, we identified thirty-three patients from our anticoagulation clinic registry who were prescribed triple antithrombotic therapy. All hemorrhagic events were collected and classified as non-severe (NSH) or severe (SH). The same population provided a control to determine increased risk from addition of a second antiplatelet drug. Overall, patients were followed for 53 patient-months while on triple therapy (TT) and 869 patient-months on double therapy. Patients in TT group had more hemorrhages (90.6% patient-years vs 8.29% patient-years, p b 0.01) due to an increase in NSH (90.6% patient-years vs 5.52% patient-years, p b 0.01), without changes in SH. Mean international normalized ratio (INR) was similar in both groups and INR at bleeding time was not uniformly increased. We conclude that in patients with an AAS and OAC based regimen, addition of clopidogrel because of a stent placement results in a significant increase in NSH but no increase in SH.