Drug-specific thienopyridine resistance in patient with recurrent coronary stent thrombosis.
Davor Miličić, Boško Škorić, Daniel Lovrić
Abstract
Davor Miličić, Boško Škorić, Daniel Lovrić
Abstract
A 56-year-old male was admitted for elective percutaneous coronary intervention. Four days later he developed subacute stent thrombosis in the proximal stent in his right coronary artery. Using the Multiplate(R) ASPI and ADP test, we detected combined aspirin and clopidogrel resistance. The doses of aspirin and clopidogrel were increased to 300 mg and 150 mg, respectively. This resulted with optimization of aspirin response, but clopidogrel resistance was doseindependent. Three days later, the patient developed a new episode of ST-elevation myocardial infarction due to recurrent subacute thrombosis in the proximal stent. Consequently, clopidogrel was switched to ticlopidine 250 mg twice daily with resultant optimal platelet inhibition in the ADP test and the patient became clinically stable. This case indicates the clinical benefit from routine assessment of platelet responsiveness to antiaggregation therapy in patients with stent thrombosis. Also, clopidogrel resistance is drug-specific and not necessarily a class-effect phenomenon. By modifying drugs' doses, type of thienopyridine, or both, we can optimize antiplatelet therapy and the clinical course.
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A 56-year-old male was admitted for elective percutaneous coronary intervention. Four days later he developed subacute stent thrombosis in the proximal stent in his right coronary artery. Using the Multiplate(R) ASPI and ADP test, we detected combined aspirin and clopidogrel resistance. The doses of aspirin and clopidogrel were increased to 300 mg and 150 mg, respectively. This resulted with optimization of aspirin response, but clopidogrel resistance was doseindependent. Three days later, the patient developed a new episode of ST-elevation myocardial infarction due to recurrent subacute thrombosis in the proximal stent. Consequently, clopidogrel was switched to ticlopidine 250 mg twice daily with resultant optimal platelet inhibition in the ADP test and the patient became clinically stable. This case indicates the clinical benefit from routine assessment of platelet responsiveness to antiaggregation therapy in patients with stent thrombosis. Also, clopidogrel resistance is drug-specific and not necessarily a class-effect phenomenon. By modifying drugs' doses, type of thienopyridine, or both, we can optimize antiplatelet therapy and the clinical course.
Key concepts: Thienopyridine, Medicine, Clopidogrel, Ticlopidine, Percutaneous coronary intervention, Aspirin, Antiplatelet drug, Cardiology