Pharmacogenomics and Clopidogrel, December 28, 2011, Nissen 306 (24): 2727 — JAMA

Pharmacogenomics and Clopidogrel

Irrational Exuberance?

1. Steven E. Nissen, MD

[+] Author Affiliations

1. Author Affiliation: Department of Cardiovascular Medicine, Cleveland Clinic Foundation, Cleveland, Ohio.

Since this article does not have an abstract, we have provided the first 150 words of the full text.

KEYWORDS:
• CARDIOVASCULAR DISEASES,
• CLOPIDOGREL,
• CYP2C19 PROTEIN, HUMAN,
• DRUG REACTION, ADVERSE,
• GENETIC SCREENING,
• GENOTYPE,
• METABOLIC PHENOMENA,
• PATIENT SAFETY,
• PHARMACOKINETICS,
• PLATELET AGGREGATION INHIBITORS,
• PLATELET FUNCTION TESTS,
• STENTS,
• THROMBOSIS.

On March 12, 2010, the US Food and Drug Administration (FDA) announced that clopidogrel would receive a “boxed warning,” the agency's highest level of alert (Box).¹ The background for this warning originated from the observation that clopidogrel is a prodrug that requires metabolic conversion to its active moiety by cytochrome P450 subclass 2C19 (CYP2C19). Specifically, the boxed warning cautioned that slow metabolism of clopidogrel was associated with higher cardiovascular event rates and suggested that genetic testing could identify individuals who were slow metabolizers, thereby allowing physicians to implement “alternative treatment strategies.” This FDA announcement was instantly controversial. In a highly unusual move, the American Heart Association (AHA) and American College of Cardiology (ACC) rapidly issued a consensus document stating that “The evidence base is insufficient to recommend either routine genetic or platelet function testing at the present time.”² This scientific controversy has continued unabated for nearly 2 …

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Pharmacogenomics and Clopidogrel, December 28, 2011, Nissen 306 (24): 2727 — JAMA



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