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Pathological assessment of very late bare metal stent thrombosis in the left main coronary artery: a case report
BACKGROUND: Late catch-up phenomenon following stent implantation is a well-known complication. However, no report has evaluated thrombosis after 9 years with multi-modality and pathological evaluation. CASE SUMMARY: A 71-year-old man with stable angina underwent elective percutaneous intervention o...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7954259/ https://www.ncbi.nlm.nih.gov/pubmed/33738424 http://dx.doi.org/10.1093/ehjcr/ytaa572 |
Sumario: | BACKGROUND: Late catch-up phenomenon following stent implantation is a well-known complication. However, no report has evaluated thrombosis after 9 years with multi-modality and pathological evaluation. CASE SUMMARY: A 71-year-old man with stable angina underwent elective percutaneous intervention of the left main coronary artery with implantation of a bare metal stent (BMS) 9 years ago. At the 9-year follow-up, coronary computed tomography (CCT) and coronary angiography (CAG) findings revealed a thrombus-like structure in the BMS slightly protruding into the sinus of Valsalva. Therefore, the previously prescribed double-antiplatelet therapy was replaced with an anticoagulant and clopidogrel, and a potent statin treatment was initiated. After the changes in drug treatment, follow-up examinations with CCT at 1 and 3 months suggested a decrease in the size of the thrombus; however, it appeared to increase after 6 months. Subsequently, the patient underwent surgical intervention. Pathological assessment of the explanted stent showed a proteoglycan-dominated extracellular matrix with few smooth muscle cells suggesting an organized thrombus. DISCUSSION: It should be emphasized that multiple factors might be responsible for very late stent thrombosis, such as peri-stent strut chronic inflammation involving proteoglycans, stent protrusion, and poorly controlled type 2 diabetes mellitus, possibly further inducing inflammatory cells. |
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