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Letters
April 11, 2012

CYP2C19 Genotype and Cardiovascular Events—Reply

Author Affiliations

Author Affiliation: Division of Cardiovascular Medicine, Cleveland Clinic Foundation, Cleveland, Ohio (nissens@ccf.org).

JAMA. 2012;307(14):1482-1485. doi:10.1001/jama.2012.447

In Reply: Dr Shuldiner and colleagues criticize my assertion that physicians should require a prospective randomized trial before using CYP2C19 pharmacogenomics in clinical practice. Specifically, they state that such a conservative approach “may be denying patients access to potentially life-saving individualized alternative therapies.”

I could not more strongly disagree. For decades, women were treated with hormone therapy to prevent heart disease based on observational studies, only to find out that such treatments increase, rather than decrease, morbidity and mortality.1,2 Similarly, inappropriate use of surrogate end points has repeatedly promoted adoption of therapies that later proved ineffective or harmful. Examples include drugs to increase high-density lipoprotein cholesterol or reduce blood glucose such as rosiglitazone.3,4 Platelet reactivity testing represents another unvalidated surrogate end point and cannot be a substitute for studies that measure morbidity and mortality, which are the outcomes of importance to patients and physicians.

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