Author Affiliations: Zena and Michael Wiener Cardiovascular Institute, and the Marie-Josee and Henry R. Kravis Cardiovascular Health Center, The Mount Sinai School of Medicine, New York, New York, and the Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain (Dr Fuster); and Mount Sinai Heart, Mount Sinai Medical Center, New York, New York (Dr Sweeny).
Effective platelet inhibition has become a cornerstone in the management of patients with acute coronary syndrome (ACS). The addition of clopidogrel to aspirin has provided significant reductions in major cardiovascular events in patients with ACS in general, and particularly among those treated invasively by percutaneous coronary intervention (PCI).1 Yet studies have demonstrated that the therapeutic response of clopidogrel is variable among patients,2 and low or incomplete platelet inhibition has been associated with increased risk for major adverse cardiovascular events.3
Fuster V, Sweeny JM. Clopidogrel and the Reduced-Function CYP2C19 Genetic Variant: A Limited Piece of the Overall Therapeutic Puzzle. JAMA. 2010;304(16):1839–1840. doi:10.1001/jama.2010.1566
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