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ARCTIC: Antiplatelet therapy not improved by monitoring platelet function
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LOS ANGELES — New data from the ARCTIC study suggest that adjusting antiplatelet therapy based on platelet-function monitoring did not lead to better clinical outcomes in patients undergoing coronary stenting.
“Personalized medicine is an important goal for both patients and physicians, but it appears that it is a difficult goal to reach for antiplatelet therapy,” Gilles Montalescot, MD, PhD, of the Centre Hospitalier Universitaire Pitié-Salpêtrière in Paris, said during a presentation at the American Heart Association Scientific Sessions 2012.
For the trial, Montalescot and colleagues randomly assigned 2,440 patients scheduled for PCI with drug-eluting stents at 38 centers to one of two strategies: drug adjustment based on platelet-function monitoring using the VerifyNow P2Y12 and aspirin point-of-care assays (n=1,213) or conventional care (n=1,227). Monitoring occurred in the cath lab before stent implantation and in the outpatient clinic at 2 to 4 weeks after the procedure.
Before the procedure, 7.6% of patients taking aspirin and 34.5% of those taking clopidogrel (Plavix, Sanofi-Aventis) in the monitoring group had high platelet reactivity. Of those who responded poorly to clopidogrel, 80% were reloaded with a high dose of clopidogrel on the table before the start of the procedure, and 3% received a loading dose of prasugrel (Effient, Daiichi Sankyo/Eli Lilly). Administration of glycoprotein IIb/IIIa inhibitors was also five times greater in the monitoring group vs. the conventional care group (P<.001).
At 2 to 4 weeks after implantation, fewer patients had high platelet reactivity. Patients in the monitoring group, however, were more likely to be taking a high dose of aspirin (>100 mg) or a high dose of clopidogrel (≥150 mg) or prasugrel, Montalescot said.
Results indicated that the primary endpoint — a composite of death, MI, stent thrombosis, stroke or urgent revascularization at 1 year after implantation — did not differ significantly between groups, with 34.6% of patients assigned to monitoring and 31.1% of those assigned conventional care experiencing an event (HR=1.13; 95% CI, 0.98-1.29).
Similarly, there was no difference in the main secondary endpoint of stent thrombosis or any urgent revascularization, which occurred in 4.9% of those in the monitoring group and 4.6% of the conventional care group (HR=1.06; 95% CI, 0.74-1.52), Montalescot said.
The rate of major bleeding events also did not differ significantly between treatment arms (monitoring, 2.3% vs. conventional care, 3.3%; P=.15).
Analyses did not reveal a trend toward benefit for monitoring for either the primary or secondary endpoints across all prespecified subgroups, according to Montalescot.
“Platelet-function testing with antiplatelet therapy adjustment before and after coronary stenting does not improve clinical outcome as compared with conventional treatment without platelet-function testing,” Montalescot said. “Our results do not support the routine use of platelet-function testing in patients undergoing stenting.” – by Melissa Foster
For more information:
Collet JP. N Engl J Med. 2012;doi:10.1056/NEJMoa1209979.
Montalescot G. Late-breaking clinical trials: Practice implications for CAD and VTE. Presented at: the American Heart Association Scientific Sessions 2012; Nov. 3-7, 2012; Los Angeles.
Disclosure: See the study for a full list of disclosures.
Perspective
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Eric R. Bates, MD
Based on this study, I would make several conclusions. At a population level, it has been consistently demonstrated that clopidogrel hyporesponsiveness predicts ischemic risk, but optimization of platelet-function test results by adjusting therapy is not associated with a better clinical outcome. At the patient level, platelet-function testing is neither sensitive nor specific enough to guide tailored antiplatelet therapy. Perhaps we would get different results with a different platelet-function analyzer, but I doubt it. Maybe we need to evaluate a specific subgroup; maybe we need a different cutpoint to more accurately determine which group is at risk; or maybe we are measuring at the wrong time point to identify the patients who are truly at risk and might benefit from further therapy. However, I would conclude at this time, as others before me have, that platelet reactivity appears to be a risk marker, which is very useful for research studies, but it does not appear to be a modifiable risk factor that will impact the decision on whether or not to adjust individual antiplatelet therapy.
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