Left ventricular systolic and diastolic function after anthracycline chemotherapy in childhood

Background: In childhood, late cardiotoxicity is characterized by inappropriately thin wall and consequent increased end‐systolic wall stress, but the associations of impaired left ventricular geometry and function occurring under these circumstances need further investigation. Hypothesis: The purpose of this study was to assess anthracycline late effects on the relationships occurring between increased end‐systolic stress (ESS) and changes in both M‐mode systolic measurements (i.e., endocardial and midwall fractional shortening) and Doppler diastolic indices in the pediatric age. Methods: The population consisted of 101 children treated with anthracyclines for at least 12 months and 91 healthy children. Using M‐mode echocardiography, end‐systolic wall stress was calculated as index of afterload, and endocardial and midwall fractional shortening as systolic indices. Doppler transmitral measurements were made as diastolic indices. Results: Patients treated with anthracyclines showed significantly lower relative wall thickness and left ventricular mass index, greater end‐systolic wall stress, reduced endocardial and midwall fractional shortening and peak E/A ratio, prolonged deceleration, and isovolumic relaxation times. Direct relationships were found between end‐systolic wall stress and both endocardial and midwall shortening. The use of midwall shortening in the relation showed a greater, but not significant increase (from 3 to 6%) in the proportion of patients with depressed systolic function than did endocardial shortening. In the anthracycline group, end‐systolic wall stress was also inversely related to relative wall thickness and directly to isovolumic relaxation time. Conclusions: In childhood, reduced myocardial thickness and increased afterload explain much of systolic and diastolic dysfunction of late anthracycline toxicity. Midwall fractional shortening does not seem to add useful information for identifying subsets of children more prone to the development of heart failure.