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

Abstract

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.

Keywords: Case report; Disease activity marker; Disease relapse; High-sensitivity cardiac troponin; Isolated cardiac sarcoidosis.

Figure 1

Electrocardiogram at the initial visit. The initial electrocardiography reveals a third-degree atrioventricular block with a junctional escape rhythm, QTc prolongation, and frequent non-sustained polymorphic ventricular tachycardia that were consistent with torsade de pointes.

Figure 2

Cardiac magnetic resonance imaging. Late gadolinium enhancement images in the short-axis (A) and long-axis four-chamber (B) and two-chamber views (C) illustrate multifocal and extensive areas of transmural hyper-enhancement (arrowheads), which indicated non-ischaemic aetiologies.

Figure 3

Whole-body ¹⁸F-fluorodeoxyglucose positron emission tomography/computed tomography at baseline (coronal sections). Fluorodeoxyglucose positron emission tomography reveals increased ¹⁸F-fluorodeoxyglucose uptake in the septal and inferior walls of the left ventricle (arrowheads). No extracardiac abnormal ¹⁸F-fluorodeoxyglucose uptake was observed, consistent with isolated cardiac sarcoidosis.

Figure 4

The association of immunosuppressive therapy with high-sensitivity cardiac troponin I and brain natriuretic peptide concentrations in cardiac sarcoidosis. The high-sensitivity cardiac troponin I concentration dropped sharply after the introduction of glucocorticoid therapy. However, the high-sensitivity cardiac troponin I concentration increased when prednisolone therapy was tapered to a maintenance dose, even before elevation of BNP levels and worsening of symptoms. The high-sensitivity cardiac troponin I concentration re-declined after the intensification of glucocorticoid therapy.

Figure 5

Serial ¹⁸F-fluorodeoxyglucose positron emission tomography/computed tomography illustrates the changes in active inflammation of cardiac sarcoidosis. Fluorodeoxyglucose uptake was evident in the septal and inferior walls of the left ventricle (arrowheads) before the initiation of glucocorticoid therapy (A). ¹⁸F-fluorodeoxyglucose uptake vanished after initiation of glucocorticoid therapy (B). However, de novo¹⁸F-fluorodeoxyglucose uptake was confirmed in the apex of the heart (arrowheads) after reduction of the prednisolone dose to 5 mg/day (C).