The value of left ventricular global longitudinal strain assessed by three-dimensional strain imaging in the early detection of anthracycline-mediated cardiotoxicity

Abstract

Introduction: Anthracyclines are important anticancer drugs, but their use is limited by acute and chronic cardiotoxicity. Current approaches to surveillance are often inadequate to detect myocardial disease. Strain imaging might detect earlier myocardial dysfunction. Speckle analysis of three-dimensional (3D) echocardiography improves information about left ventricular (LV) segmental and global deformation by avoiding the loss of speckles seen in monoplane bidimensional-strain analysis. We assessed whether early 3D-strain analysis could predict later anthracycline-induced cardiotoxicity. Methods: Echocardiography, troponin T (TnT) and N-terminal pro-brain natriuretic peptide were used to evaluate 59 patients (age 51 ± 10 years) before, and at 12 and 36 weeks after anthracycline treatment. LV global longitudinal strain (3DGLS), global radial strain (3DGRS) and global circumferential strain (3DGCS) were determined using 3D-strain imaging before and after 12 weeks of chemotherapy. Percentage changes from baseline to 12 weeks after initiation of chemotherapy (Δ) were calculated for all parameters analysed. Results: During the follow-up period, eight patients (13.5%) developed cardiotoxicity. At 12 weeks after the initiation of chemotherapy, isovolumic relaxation time, 3DGLS, 3DGCS and 3DGRS had deteriorated and troponin was elevated (all p<0.05), before any decrease in LV ejection fraction. Cumulative anthracycline dose at 12 weeks, ΔLVEF, Δ3DGLS and ΔTnT were predictors of the later development of cardiotoxicity on univariate logistic regression. By multiple logistic regression, Δ3DGLS emerged as the only independent predictor of later cardiotoxicity (Odds ratio 1.09, p=0.04). Conclusions: Anthracycline therapy induced early deterioration of 3DGLS, 3DGCS and 3DGRS. Δ3DGLS seems to be a good predictor of the future development of anthracycline-induced cardiotoxicity.