Antiplatelet therapy for Reduction of MYocardial Damage during Angioplasty 4 - ARMYDA-4 - Presented at TCT 2007
The goal of the trial was to compare the efficacy and safety of a 600 mg clopidogrel loading dose with placebo among patients undergoing percutaneous coronary intervention (PCI) who were on chronic clopidogrel therapy.
Patients Screened: 464
Patients Enrolled: 360
Mean Follow Up: 1 month
Mean Patient Age: Mean age 65 years
Chronic therapy with clopidogrel (> 10 days) with stable angina or non-STE ACS undergoing PCI.
Primary PCI; platelet count <70x103/ml; high risk of bleeding; coronary bypass graft surgery in the previous 3 months
Death, MI, or target vessel revascularization (TVR) at 30 days
Any postprocedural increase of markers of myocardial injury >UNL (CK-MB, troponin I, myoglobin); mean peak values of CK-MB, troponin I and myoglobin after intervention; occurrence of any vascular/hemorragic complications; platelet function testing
Following diagnostic angiography, patients on chronic clopidogrel therapy undergoing PCI were randomized in a double-blind manner to a clopidogrel load of 600 mg (n = 180) or placebo (n= 180). Platelet function, CKMB, troponin-I, myoglobin, and CRP were measured prior to PCI and at 8 and 24 hours post-PCI.
Indication for PCI was non-ST elevation ACS in 38% of patients. Approximately one-third of patients had diabetes and 30% had a prior MI. Statins were used by 94% of patients. Multivessel disease was present in 40% of patients, although only 16% underwent multivessel PCI. The vessel treated was the left anterior descending artery in 40% of patients, and 60% had a type B2/C lesion. Drug-eluting stents were used in 42% of cases.
There was no difference in the primary endpoint of death, MI or TVR at 30 days between the clopidogrel re-load and placebo group (8% vs. 7%, p = 0.96), all of which were MIs; there were no deaths or TVR in the trial. Among the secondary endpoints, there was no difference in the frequency of CKMB elevation (27% vs. 30%, p = 0.58) or in peak CKMB (mean 5.3 ng/ml vs. 5.6 ng/ml, p = 0.90) for clopidogrel re-load vs. placebo. Likewise, troponin-I elevation did not differ between groups (45% vs. 46%, p = 0.98), nor did peak troponin-I (mean 0.52 ng/ml vs. 0.39 ng/ml, p = 0.55). Bleeding rates were identical in the treatment groups, with no major bleeds in either arm and 4% of patients having minor bleed in each group. Platelet reactivity was similar between groups at all timepoints.
Among patients undergoing PCI who were on chronic clopidogrel therapy, use of an additional loading dose of clopidogrel was not associated with a difference in the primary endpoint of death, MI or TVR at 30 days compared with placebo.
While there was no excess of bleeding with an additional clopidogrel load in this small trial, there was also no clinical benefit of re-loading patients, whether evaluated using clinical endpoints or biomarker measures of necrosis. Even platelet function measures showed no difference at the time of PCI or through 24 hours post-PCI. These data suggest that re-loading patients who are on chronic clopidogrel therapy is not needed for PCI.
Presented by Dr. Germano Di Sciascio, at TCT 2007, Washington, DC.
Keywords: Platelet Aggregation Inhibitors, Angina, Stable, Drug-Eluting Stents, Troponin I, Myoglobin, Coronary Disease, Ticlopidine, Hemorrhage, Diabetes Mellitus, Percutaneous Coronary Intervention
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