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San Francisco, CA—Data presented Thursday at TCT 2013 demonstrated that platelet function testing only modestly improves therapeutic adjustment of antiplatelet therapy, whereas another study showed that genotype testing may aid clinicians in optimizing antiplatelet therapy.
Tracy Y. Wang, MD, of the Duke Clinical Research Institute, Durham, N.C., presented findings from the TRANSLATE-POPS Study, which was embedded within the TRANSLATE-ACS observational study. The researchers investigated platelet function testing with the VerifyNow P2Y12 test (Accumetrics) in patients with STEMI and non-STEMI treated with PCI and adenosine diphosphate receptor inhibitors.
Incidence of therapy adjustment before hospital discharge in the arm that received routine platelet function testing (device group; n=2,013) vs. the usual care group, which did not receive routine platelet function testing (n=1,853) served as the primary endpoint.
Wang reported that the device group was associated with a small increase in therapy adjustment (see Figure).
“Routine platelet function testing had only a modest impact on antiplatelet therapy adjustment,” Wang concluded.
Further analysis indicated the drug was switched in 10.6% of usual care patients and 14.5% in the device group (P=.02). “The majority of adjustments manifested as switches, rather than adjustments in dose,” Wang said. These switches were primarily from clopidogrel to prasugrel (Effient, Daiichi Sankyo/Eli Lily) or ticagrelor (Brilinta, AstraZeneca).
Secondary endpoint results at 30 days indicated that MACE rates were 4.5% in the device group and 5.1% in the usual care group (OR 0.93; 95% CI 0.66-1.31; P=.69).
Results of the GIANT study presented by Bernard R. Chevalier, MD, of the Institut Cardiovasculaire Paris Sud in Massy, France, offered a slightly stronger recommendation for the clinical impact of CYP2C19 genotype testing within 48 hours in patients with acute MI treated with primary PCI.
The primary endpoint was death, MI and stent thrombosis at 1 year in slow responders to appropriate antiplatelet therapy after genotyping compared with non-slow responders, who also received genotyping.
Among 272 very slow/slow responders who were adjusted to optimal therapy, the primary endpoint rate was 3.3% compared with 3.04% of 1,118 normal or high responders (P=.83 for superiority; P<.0001 for non-inferiority).
“There is no significant difference between these two groups,” Chevalier said. “This genotype information obtained before discharge allowed treatment optimization in 86% of patients. This is a significant impact in terms of adjustment of treatment. We should seriously consider genotyping.”
Among very low/low responders who did not receive adjusted treatment (dose adjustment or drug switching) after genotyping, the primary endpoint rate was higher when compared with patients who did receive treatment adjustment (15.6% vs. 3.3%; P=.04).
At 1 year, MACCE rates were 8.6% for the normal or high response group and 10.2% in the low response group with adjusted therapy (P=NS). Chevalier added that there was no difference between the two groups in terms of major bleeding at 1 year.
Chevalier reports conflicts of interest with several device and pharmaceutical manufacturers.
Wang reports conflicts of interest with several pharmaceutical manufacturers.