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An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis
Published on: February 8, 2019
Acute stent thrombosis in a patient with giant cell arteritis
Jason Andrade1, Abdullah Al Ali, Jacqueline Saw
1Division of Cardiology, University of British Columbia, Vancouver General Hospital, Vancouver.
Insights
Giant cell arteritis can cause acute stent thrombosis in patients with myocardial infarction, even with dual antiplatelet therapy. This case suggests prolonged, aggressive antiplatelet therapy may be needed for acute coronary syndromes in inflammatory conditions.
Area of Science:
- Cardiology
- Rheumatology
- Pharmacology
Background:
- Giant cell arteritis (GCA) is a systemic vasculitis primarily affecting large and medium-sized arteries.
- Non-ST elevation myocardial infarction (NSTEMI) requires prompt revascularization and antiplatelet therapy.
Observation:
- A 70-year-old man with NSTEMI and suspected GCA developed acute stent thrombosis 70 hours post-percutaneous coronary intervention (PCI) despite dual antiplatelet therapy.
- Platelet aggregometry revealed reduced responsiveness to clopidogrel, which improved as GCA symptoms resolved with prednisone treatment.
Findings:
- This is the first reported case of acute stent thrombosis associated with GCA.
- The pro-inflammatory state in GCA may impair the efficacy of standard antiplatelet agents like clopidogrel.
Implications:
- Patients with acute coronary syndromes and concurrent inflammatory conditions like GCA may require more aggressive or prolonged antiplatelet strategies.
- Further research is warranted to explore the interaction between systemic inflammation and antiplatelet therapy response in cardiovascular patients.
Abstract:
A 70-year-old man presented with a non-ST elevation myocardial infarction attributable to a 99% occlusion of his mid-left anterior descending artery and concomitant symptoms suggestive of giant cell arteritis. He underwent bare metal stenting, with an excellent angiographic result, and was placed on dual antiplatelet therapy, as well as oral prednisone 30 mg twice daily, while awaiting confirmatory temporal artery biopsy. Unfortunately, 70 h after percutaneous coronary intervention, he developed acute stent thrombosis. Platelet aggregometry demonstrated that he was responsive to acetylsalicylic acid, but marginally responsive to clopidogrel. Over the next 30 days, he had a marked clinical improvement, with an improvement in platelet response to clopidogrel that paralleled the clinical resolution of his vasculitis. The present case reports the first incidence of acute stent thrombosis associated with giant cell arteritis, and suggests that the proinflammatory milieu of acute inflammatory arthritides may warrant prolonged, aggressive antiplatelet therapy in the setting of an acute coronary syndrome.
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