Providers intensified antiplatelet therapy in only one of five patients who were poor metabolizers of clopidogrel, despite an FDA boxed warning. Results from the real-world analysis were published online Nov. 5 in Circulation: Cardiovascular Quality and Outcomes.
In 2010, the FDA added a boxed warning to the label for clopidogrel (Plavix, Bristol-Myers Squibb/Sanofi Aventis), focusing on patients who do not effectively metabolize the drug because of impaired CYP2C19 function. The agency informed physicians that genetic tests were available and advised them to consider use of other antiplatelet medications or alternative dosing strategies for these patients.
“Although the role of genetic testing to guide antiplatelet prescribing is currently debated, it is important to understand whether and how CYP2C19 testing influences physician prescribing patterns for secondary preventive antiplatelet therapy and, more generally, how willing physicians are to order this type of testing,” wrote lead author Nihar R. Desai, of the Yale New Haven Health System in New Haven, Conn., and colleagues.
Desai et al conducted a real-world analysis using claims data from a genetic test manager, Generation Health, and a pharmacy benefits manager, CVS Caremark. The two groups had designed a program that allowed patients prescribed clopidogrel who had acute coronary syndrome or PCI to undergo elective CYP2C19 genotype and phenotype testing. CVS Caremark funded the study.
Researchers evaluated data from 2010 to 2012, including changes in prescribing 120 days or less after reporting of test results. They found that of the 6,032 potential eligible participants, 499 patients completed testing. Of those, 31 percent were carriers of one or more reduced function allele.
Intensification of antiplatelet therapy occurred more frequently in carriers vs. noncarriers (20.5 percent vs. 1.7 percent). Carriers were more likely to have their medication switched from clopidogrel to prasugrel (Effient, Eli Lilly/Daiichi Sankyo; 17.8 percent vs. 1.7 percent). But only 20 percent of poor metabolizers had their antiplatelet therapy intensified.
“These findings may have resulted from the providers’ lack of understanding about how to interpret genetic test results or a belief that genetic testing has not been definitively established as a reliable approach to tailoring antiplatelet therapy,” they wrote. “In addition, providers may have been reluctant to switch to one of the novel antiplatelet agents because of their relative lack of clinical experience with them.”
Desai et al reported that about half of providers didn’t respond to the prescriber outreach and of those who indicated their patients were clinically eligible, about a quarter declined the test.
They cautioned that their study sample was relatively small.