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In-Stent Restenosis Exacerbated by Drug-Induced Severe Eosinophilia after Second-Generation Drug-Eluting Stent Implantation

Patient: Male, 83 Final Diagnosis: In-stent restenosis Symptoms: Chest discomfort Medication: — Clinical Procedure: Cardiac catheterization Specialty: Cardiology OBJECTIVE: Unusual clinical course BACKGROUND: In-stent restenosis (ISR) is still a recognized clinical problem in the era of drug-eluting...

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Detalles Bibliográficos
Autores principales: Yagi, Hiroki, Amiya, Eisuke, Ando, Jiro, Watanabe, Masafumi, Yanaba, Koichi, Ikemura, Masako, Fukayama, Masashi, Komuro, Issei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: International Scientific Literature, Inc. 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4168766/
https://www.ncbi.nlm.nih.gov/pubmed/25227966
http://dx.doi.org/10.12659/AJCR.891106
Descripción
Sumario:Patient: Male, 83 Final Diagnosis: In-stent restenosis Symptoms: Chest discomfort Medication: — Clinical Procedure: Cardiac catheterization Specialty: Cardiology OBJECTIVE: Unusual clinical course BACKGROUND: In-stent restenosis (ISR) is still a recognized clinical problem in the era of drug-eluting stent (DES). Some previous studies have suggested that circulating eosinophils play an important role in both restenosis and thrombosis after DES implantation. However, the contribution of eosinophils to the pathogenesis of ISR has not yet been concisely clarified. CASE REPORT: We present the case of an 83-year-old male Japanese patient with ISR exacerbated by drug-induced severe eosinophilia. He had previous histories of coronary stent implantations by DES and was referred to our hospital because of erythema with severe eosinophilia (maximum was 6500/μl [48% of total white blood cell count]). Around the same time, the patient developed ISR, for which a stent was deployed 2 years earlier. Arterial wall injury due to the increase in circulating eosinophils was verified in several findings, such as the increase of D-dimer and brain natriuretic peptide. In addition, the histology of the resected tissue from erythema demonstrated that the nuclei of endothelial cells were swollen where eosinophils and lymphocytes heavily infiltrated into the extravascular space, suggesting the presence of vascular injury. This injury due to the increase in circulating eosinophils may have a marked impact on the pathologic process of ISR in DES implantation. CONCLUSIONS: Just a few anecdotal reports are available of ISR occurring in the setting of hypereosinophilia. The clarification of the mechanism in this patient provides a new effective therapeutic strategy against ISR in the setting of DES implantation.