Published May 30, 2011 | Version v1
Journal article Open

Prasugrel resistance may be linked to the sticky platelet syndrome. Report of one case

  • 1. Grupo Genética Intervencionista. Departamento de Hemodinámica, Departamento de Biología Molecular, Instituto Nacional de Cardiología Ignacio Chávez, México, DF.; Departamento de Farmacología, Facultad de Medicina, Universidad Nacional Autónoma de México, México, DF.
  • 2. Grupo Genética Intervencionista. Departamento de Hemodinámica, Departamento de Biología Molecular, Instituto Nacional de Cardiología Ignacio Chávez, México, DF.
  • 3. Departamento de Farmacología, Facultad de Medicina, Universidad Nacional Autónoma de México, México, DF.

Description

Background: Prasugrel is the most potent antiplatelet agent, even more than clopidogrel and is an alternative for the treatment and prevention of acute coronary syndromes. Despite the effectiveness of these drugs, it could be an inadequate response to reduce the hyperactivity of platelets measured by platelet aggregation test.

Patients and Methods: We studied six consecutive patients undergoing percutaneous coronary intervention which received a 60mg loading dose of prasugrel. Platelet aggregation was performed using as agonists ADP and epinephrine, were identified gene polymorphisms ABCB1, CYP2C19, CYP3A5 and P2RY12 and tissue factor was measured by ELISA.
Results: One of the six patients showed platelet hyperactivity even after treatment with prasugrel and clopidogrel, and 3.6 fold tissue factor in plasma compared with patients studied without platelet hyperactivity. No patient had the polymorphisms studied.
Conclusion: We report the case of a patient showing decreased response to prasugrel and clopidogrel manifesting with platelet hyperactivity.

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