Cardiac toxicity of anthracyclines in infants

The cardiac acute (immediate) or chronic (delayed) toxicity in infants, due to anthracyclines appears to be with the same clinical records as in adult. In exchange, the tardy sequels or the delayed toxicity in infants are known more recently. They are related to the anatomic injuries due to the anthracyclines administrated in childhood. The goal of this work is to evaluate in the infants afflicted with a hemopathy or a solid tumor, the tardy cardiac complications induced by an efficient treatment entailing the healing. A population of 41 infants (18 G, 23 B, 15± years) for which the delay between the treatment cessation and the follow-up being > 4 years, was explored both by gamma-cardiac-angiography (GCA) and echocardiography (EC). A GCA at effort was achieved in 31/41 infants. At rest, 15 infants of 41 (36%) presented: n = 5 (12%), an alteration of the systolic function and n = 10 (24%), an alteration of isolate diastolic function. Among the 5 infants having a systolic dysfunction, 2 presented a chronic toxicity in treatment of dilated cardiomyopathy; 7 and 10 years after the cessation of treatment by anthracyclines, a global hypokinesia of left ventricle (LV) still persisted. Other 3 patients indign of cardiac dysfunction at the treatment cessation, presented a diminution of the ejection fraction of LV at GCA and not at EC (n = 2), and a diminution of the cutting factor of EC and not by GCA (n = 1). Ten other infants showed only a diastolic dysfunction by GCA. The evolution of the LV ejection fraction at effort was normal in all the cases. For our population the delay between the cessation of anthracyclines and the follow-up was 8 ± 2 years. In conclusion, in our study (n = 41, delay = 8 years, total cumulated dose: daunorubicin = 279 mg/m2, or doxorubicin = 247 mg/m2), the incidence of tardy sequels is 0% in terms of clinic cardiac insufficiency, 7% if only the systolic criterion is retained and 32% if both systolic and diastolic criteria are retained. The question remains whether the alteration of filling of LV is a early sign of cardiac insufficiency