真鍋 治

PURPOSE: Cardiac sarcoidosis (CS) is a potentially life-threatening condition, and 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET) is highly sensitive for detecting myocardial inflammation. However, corticosteroid therapy may alter myocardial metabolism, complicating the interpretation of FDG PET. This study aimed to evaluate the impact of corticosteroid therapy on physiological myocardial FDG uptake and assess the utility of fasting plasma glucose (FPG) and free fatty acids (FFA) in distinguishing physiological from pathological uptake. MATERIALS AND METHODS: We retrospectively analyzed FDG PET/CT scans of 40 CS patients who underwent paired scans before and after corticosteroid therapy, following prolonged fasting (> 18 h). The frequency of physiological myocardial FDG uptake was compared, and FPG and FFA levels were assessed as predictors using receiver operating characteristic (ROC) analysis. Exploratory analyses were also performed to assess metabolic changes across different levels of corticosteroid exposure. RESULTS: Physiological myocardial FDG uptake significantly increased after corticosteroid therapy (from 2.5% to 15%, P = 0.048). Post-treatment FFA levels were significantly lower, while FPG levels were higher. An FFA cutoff of 615 µEq/L predicted physiological uptake with 100% sensitivity and 83.6% specificity (AUC = 0.96, P < 0.001), whereas FPG showed poor discrimination (AUC = 0.43, P = 0.83). Patients with physiological uptake had significantly lower FFA levels; FPG did not differ between groups. In analyses stratified by corticosteroid dose, physiological uptake was less frequently observed at lower dose levels, accompanied by relatively preserved metabolic parameters. CONCLUSION: Corticosteroid therapy increases physiological myocardial FDG uptake in CS patients, likely due to reduced FFA levels and altered metabolism. FFA may serve as a useful marker for distinguishing physiological FDG uptake from abnormal uptake, supporting more accurate PET interpretation during corticosteroid therapy.

Cardiac amyloidosis, characterized by extracellular deposition of amyloid fibrils within the myocardium, is an increasingly recognized cause of heart failure. With the advent of disease-modifying therapies, imaging has become central to diagnosis, subtype differentiation, prognostication, and treatment monitoring. This review provides a comprehensive update on multimodality imaging in cardiac amyloidosis, emphasizing its clinical utility across the disease continuum. Echocardiography, technetium-labeled bone scintigraphy, amyloid-specific positron emission tomography, cardiac magnetic resonance, and cardiac computed tomography each contribute uniquely to detecting amyloid burden and assessing cardiac function. In addition to outlining a practical diagnostic approach, we highlight emerging imaging biomarkers for monitoring treatment response and predicting clinical outcomes. The integration of these modalities into clinical practice enhances diagnostic accuracy, enables individualized risk stratification, and supports optimized, evidence-based care for patients with cardiac amyloidosis.

Cardiac sarcoidosis (CS) poses significant diagnostic and therapeutic challenges due to its heterogeneous clinical manifestations and the limitations of conventional diagnostic approaches. Advances in imaging modalities, particularly cardiac magnetic resonance imaging (CMR) and ¹⁸F-fluorodeoxyglucose positron emission tomography (FDG-PET), have revolutionized the evaluation and management of this complex condition. CMR, with its superior spatial resolution and advanced techniques such as late gadolinium enhancement, T1/T2 mapping, and extracellular volume quantification, offers unparalleled insights into myocardial structure and fibrosis. These techniques not only enhance diagnostic accuracy but also provide critical information on disease activity and treatment response. Among these, T2 mapping has emerged as a valuable marker for active inflammation, with high values reliably indicating acute disease states. FDG-PET serves as a complementary modality by detecting active granulomatous inflammation and guiding immunosuppressive therapy. The synergistic integration of CMR and FDG-PET provides a comprehensive approach to diagnosing and monitoring CS, enabling the identification of subclinical disease and the optimization of therapeutic strategies. Furthermore, the incorporation of quantitative biomarkers, such as strain metrics and T2 values, promises to refine disease assessment and management. These advancements have the potential to transform the paradigm of CS care, ultimately improving patient outcomes.