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Role of Noninvasive Antimyosin Imaging in Infants and Children with Clinically Suspected Myocarditis

María Eugenia Rioja Martin, MD, PhD1, Jose Luis Moya-Mur, MD, PhD2, Manuel Casanova, MD, PhD3, Angel Crespo-Diez, MD1, Enrique Asin-Cardiel, MD, PhD2, Jose Manuel Castro-Beiras, MD, PhD1, Luis Diez-Jimenez, MD, PhD1, Manel Ballester, MD, PhD4, Ignasi Carrio, MD, PhD4 and Jagat Narula, MD, PhD5

1 Department of Nuclear Medicine, Hospital Ramón y Cajal, Madrid, Spain
2 Cardiac Unit, Hospital Ramón y Cajal, Madrid, Spain
3 Pediatric Cardiac Unit, Hospital Ramón y Cajal, Madrid, Spain
4 Hospital Sant Pau, Barcelona, Spain
5 Hahnemann University Hospital, Philadelphia, Pennsylvania



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FIGURE 1. (A) Absence of myocardial antimyosin uptake (HLR = 1.4) in a scan with normal findings. (B) Moderate myocardial antimyosin uptake (HLR = 1.8) in a patient with myocarditis. (C) Intense myocardial antimyosin uptake (HLR = 2.5) in a patient with biopsy-verified myocarditis. (D) Right ventricular endomyocardial biopsy demonstrating a central focus of necrotic myocytes surrounded by lymphomononuclear cell infiltrate (arrows) diagnostic of myocarditis (hematoxylin and eosin, x200).

 


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FIGURE 2. (A) Distribution of myocardial antimyosin uptake by the interval between the onset of symptoms and scintigraphy. The intensity of antimyosin uptake is presented as heart-to-lung uptake ratio, and the abnormal antimyosin result is defined by the dashed horizontal line at HLR > 1.58. A relatively higher HLR was observed in patients evaluated within 2 mo of illness (dashed vertical line). (B) Histologic findings from 22 patients who underwent endomyocardial biopsy, and comparison with intensity of antimyosin uptake and interval from onset of symptoms. The myocarditis is represented by {blacksquare} and borderline myocarditis by {blacktriangleup}; nondiagnostic biopsy is shown as {circ}. All patients with an HLR > 2 had histologic evidence of myocardial inflammation.

 


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FIGURE 3. Kaplan–Meier curves for survival outcome (survival/heart transplantation) based on the intensity of antimyosin uptake in all patients (A), in patients evaluated within the first 2 mo of onset of illness (B), and in patients evaluated later (C).

 


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FIGURE 4. Schematic representation of clinical outcomes (death/heart transplantation [OHT], persistent left ventricular dysfunction, and complete recovery) based on the dichotomous distribution by intensity of antimyosin uptake and interval between onset of illness and scintigraphy.

 


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FIGURE 5. Evolution of myocardial damage in children with myocarditis as represented by the intensity of serial antimyosin scans. The graphs show data from individual patients (left) and the evolution of mean HLR with ±1 SD (right). Data are represented for all patients (top), patients who showed complete resolution of antimyosin uptake (middle), and patients who continued with persistent antimyosin uptake over time (bottom). The persistence of antimyosin uptake was associated with poor clinical outcomes and resolution with left ventricular functional recovery.

 





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