Abstract: BACKGROUND: The study with monoclonal antimyosin antibody-111In has proved to be useful in the detection of the myocardial damage present in different processes. There is active myocardial damage and specific antimyosin uptake in myocarditis, as both experimental and clinical trials have shown. In experimental models the evolution of myocardial damage has been studied, where a parallelism between the histological changes of the myocardial damage and the evolution on the antimyosin uptake has been found. In clinical myocarditis it is difficult to do an histological follow up of the inflammatory process, and therefore the evolution of myocardial damage present in myocarditis is unknown. The antimyosin antibody images allow a non-invasive study of this evolution. OBJECTIVES: a) to study with monoclonal antimyosin antibody-111In, the myocardial damage present regarding the disease evolution in children with suspected clinical diagnosis of myocarditis; b) to evaluate the evolution of the active myocardial damage reflected on the changes on the monoclonal antimyosin antibody-111In uptake. METHODS: A study with monoclonal antimyosin antibody-111In was carried out on 43 children, 16 males and 27 females with a median age of 39 months (SD 48 m; range: 2-167) with suspected diagnosis of acute myocarditis defined as the presence of congestive cardiac failure or severe ventricular arrhythmia with less than 12 months of evolution. The image evaluation was done visually and through the heart to lung ratio. Twenty of these patients were also followed up with antimyosin antibody scan for a period of 19 +/- 9 months, and 3.8 +/- 1.7 studies were performed on them in this time. RESULTS: The prevalence of positive myocardial uptake was 83.72%. There is a negative correlation (r = -0.352; p < 0.02) between the evolution time of the process and the heart to lung ratio: patients studied before two months, have a higher heart to lung ratio and greater prevalence of positive studies than those studied later (heart to lung ratio 2.09 vs 1.74; p = 0.013; 90% vs 69.2%). Of the patients followed up with antimyosin antibody scans, 6 showed a clinical relapse which increased their heart to lung ratio. The other 14 showed an progressive decrease of the heart to lung ratio reaching normality in 14 +/- 6 months. CONCLUSIONS: a) the uptake intensity of monoclonal antimyosin antibody-111In, as a reflection of the myocardial damage, depends on the disease evolution time, as in the first two months is when the major damage happens; b) the uptake intensity slowly decreases, tending to normality around the 14th month, although this evolution may be altered by the appearance of relapses.
