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Nonculprit Lesion MI After PCI in ACS Patients
Study Questions:
What is the effect of more potent antiplatelet therapy on the basis of the timing and etiology of recurrent myocardial infarction (MI) or cardiovascular (CV) death following percutaneous coronary intervention (PCI) for acute coronary syndrome (ACS)?
Methods:
The investigators further divided events in the TRITON-TIMI 38 study (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasugrel–Thrombolysis In Myocardial Infarction 38) into three distinct categories. Procedure-related events were CV deaths or MI directly related to PCI (MI type 4a). Stent-related deaths or MI were events that were classified as an Academic Research Consortium definite or probable stent thrombosis (MI type 4b). Spontaneous CV deaths or MI were events that were not related to a procedure or stent and/or were classified as type 1 or 3 MI. Thrombolysis In Myocardial Infarction (TIMI) major non–coronary artery bypass grafting-associated bleeding was defined as in the main trial. The time to first event in the two treatment groups was analyzed using Kaplan-Meier curves and compared using the log-rank test. Sequential landmark analyses were performed starting from randomization, day 30, day 90, and day 180.
Results:
Among the first events occurring within 30 days, 584 (69.0%) were procedural, 126 (14.9%) stent thrombosis related, and 136 (16.1%) spontaneous. After 30 days, 22 (4.7%) were procedural, 63 (13.5%) were stent thrombosis related, and 383 (81.8%) spontaneous. Prasugrel significantly reduced the incidence of MI or CV death for stent thrombosis related (1.0% vs. 2.1%; p < 0.001) and spontaneous events (3.9% vs. 4.8%; p = 0.012), with a directionally consistent numerical reduction for procedural events (4.4% vs. 5.1%; p = 0.078). Prasugrel increased spontaneous, but not procedural, major bleeding.
Conclusions:
The authors concluded that long-term potent antithrombotic therapy reduces de novo (spontaneous) atherothrombotic events in addition to preventing complications associated with stenting of the culprit lesion following ACS.
Perspective:
This post hoc study reports that among patients with ACS who received PCI, over 80% of ischemic events occurring after 30 days were spontaneous, or de novo, events. Furthermore, potent dual platelet inhibition for ≥1 year after ACS showed similar efficacy for late stent thrombosis and de novo atherothrombosis. Such protection, however, needs to be balanced against ongoing risks of bleeding with intensive therapy. While these data suggest that extended dual antiplatelet therapy improves CV outcomes in patients after ACS, predominately by reducing de novo atherothrombotic ischemic events, additional studies are needed to identify patients treated with PCI likely to derive the greatest benefit of extended-duration dual antiplatelet therapy following ACS.
Clinical Topics: Acute Coronary Syndromes, Invasive Cardiovascular Angiography and Intervention, Prevention, Interventions and ACS
Keywords: Acute Coronary Syndrome, Blood Platelets, Fibrinolytic Agents, Hemorrhage, Myocardial Infarction, Myocardial Ischemia, Percutaneous Coronary Intervention, Platelet Aggregation Inhibitors, Secondary Prevention, Stents, Thrombolytic Therapy, Thrombosis, Treatment Outcome
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