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High-sensitivity cardiac troponin serving as a useful marker for the early recognition of relapse of isolated cardiac sarcoidosis: a case report

BACKGROUND: Isolated cardiac sarcoidosis is a relatively rare disease that is difficult to manage because of challenges in determining the progression and flare-up of cardiac lesions. Routine reduction of glucocorticoid doses may lead to treatment failure and disease relapse, which are associated wi...

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Detalles Bibliográficos
Autores principales: Tashiro, Akira, Tanaka, Yasuaki, Hikita, Hiroyuki, Takahashi, Atsushi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9007436/
https://www.ncbi.nlm.nih.gov/pubmed/35434504
http://dx.doi.org/10.1093/ehjcr/ytac116
Descripción
Sumario:BACKGROUND: Isolated cardiac sarcoidosis is a relatively rare disease that is difficult to manage because of challenges in determining the progression and flare-up of cardiac lesions. Routine reduction of glucocorticoid doses may lead to treatment failure and disease relapse, which are associated with increased mortality. CASE SUMMARY: Herein, we present the case of a 49-year-old woman with isolated cardiac sarcoidosis in whom high-sensitivity cardiac troponin served as a biomarker for tailoring immunosuppressive therapy. She presented with progressive dyspnoea on exertion for 2 months and had elevated levels of high-sensitivity cardiac troponin I (hs-cTnI) at presentation. A diagnosis of isolated cardiac sarcoidosis was made based on the finding of electrocardiography, echocardiography, cardiac magnetic resonance imaging, and 18F-fluorodeoxyglucose (FDG) positron emission tomography. After the introduction of glucocorticoids, the hs-cTnI concentration immediately decreased, followed by the disappearance of FDG uptake in the heart. However, 2 months after oral prednisolone was reduced to the maintenance dose, the hs-cTnI concentration began to increase gradually, and 2 months later, worsening heart failure, progression of impaired left ventricular function, and de novo accumulation of FDG in the heart were observed, confirming the relapse of cardiac sarcoidosis. Intensified glucocorticoid therapy resulted in another immediate decrease in hs-cTnI concentration and improved heart failure management. DISCUSSION: This case highlights the potential of hs-cTnI to serve as a serum biomarker for monitoring disease activity and response to immunosuppressive therapy in patients with cardiac sarcoidosis. The hs-cTnI could be a highly sensitive and cost-effective biomarker reflecting the inflammatory status of cardiac sarcoidosis.