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Updated: Jul 13, 2026

Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction
Published on: May 28, 2019
[Suspected clopidogrel resistance associated with recurrent coronary stent thrombosis--a case report]
Anna Tomaszuk-Kazberuk1, Bozena Sobkowicz, Monika Usowicz-Szaryńska
1Klinika Kardiologii, Akademia Medyczna, ul. Skłodowskiej-Curie 24 A, 15- 276 Białystok. walkaz@poczta.fm
Insights
This case study highlights a patient with recurrent stent thrombosis despite standard antiplatelet therapy, suggesting potential combined resistance to clopidogrel and aspirin.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Acute ST-elevation myocardial infarction (STEMI) requires prompt revascularization.
- Dual antiplatelet therapy with aspirin (ASA) and clopidogrel is standard post-percutaneous coronary intervention.
Observation:
- An 81-year-old man experienced recurrent STEMI due to in-stent thrombosis despite initial loading doses and subsequent dose adjustments of clopidogrel and ASA.
- The patient underwent multiple stent implantations and experienced further thrombotic events.
Findings:
- Suspected clopidogrel resistance was addressed by switching to ticlopidine, increasing ASA dosage, and adding low-molecular heparin.
- The patient stabilized after the medication change, indicating a potential combined resistance to clopidogrel and ASA in a specific patient subgroup.
Implications:
- This case suggests a need to consider antiplatelet resistance in patients with recurrent stent thrombosis.
- Further research is warranted to identify and manage patients with combined clopidogrel and ASA resistance.
Abstract:
We describe a case of an 81-year-old man with acute ST-elevation myocardial infarction (STEMI), who received a loading dose of clopidogrel (300 mg) and aspirin (ASA) (300 mg) prior to primary coronary intervention of critical left anterior descending coronary artery stenosis. Three days later he developed recurrent acute STEMI due to the in-stent thrombosis and a second stent implantation was performed. The dose of clopidogrel (75 mg) remained unchanged, while the dose of ASA was increased from 75 mg to 150 mg. Three days later the patient had an other STEMI due to the in-stent thrombosis and additional stent implantation with IIb/IIIa blocker was performed. Clopidogrel resistance was suspected. Therefore, clopidogrel was replaced by ticlopidine, the dose of ASA was increased and low-molecular heparin was administered. Since then, the patient has been clinically stable. Our case indicates the existence of a subgroup of patients with combined clopidogrel and ASA resistance.
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