Anthracycline therapy in children with ALL significantly reduced left atrial conduit strain at end diastole (-25.8 vs -36.6, p=0.028), indicating early subclinical diastolic dysfunction.
Cohort (n=25)
Does anthracycline therapy impair left atrial strain and diastolic function in children treated for acute lymphoblastic leukemia?
In children treated for ALL, early anthracycline-induced subclinical diastolic dysfunction can be detected by left atrial strain before conventional echocardiographic parameters become abnormal.
Tasa de eventos absoluta: -25.8% vs -36.6%
valor p: p=0.028
Abstract Background Anthracyclines are very efficient in acute lymphoblastic leukemia (ALL) treatment resulting in promising survival rates. Anthracycline related cardiotoxicity has been detected by the diastolic and systolic cardiac impairment in the follow-up of adult oncological patients and childhood cancer survivors. The data for children on echocardiographic detection of early anthracycline induced diastolic dysfunction is lacking. Purpose We aim to present preliminary results of the study on left ventricle diastolic function evaluation among children treated for acute lymphoblastic leukemia before initiation of anthracycline treatment and after induction and intensification of the therapy. Methods For this prospective study, consecutive pediatric patients diagnosed with ALL were enrolled. Transthoracic echocardiography was conducted following diagnosis and prior to the initiation of anthracycline therapy (first assessment), and after the completion of induction and intensification therapy (second assessment)(fig 1). All studies were performed on the same echocardiographic machine and were obtained from at least 2 cardiac cycles. The echocardiography included conventional 2D diastolic function assessment with tissue doppler imaging and the left atrial (LA) strain. Interobserver reliability of the data was assessed by two echocardiographers. Results The preliminary study group included 25 children (13 females, 12 males) aged between 1-16 years (mean age 5,8±3,7years). All of the children were diagnosed with ALL type C and were treated with the same treatment protocol. Mean dosage of anthracycline equivalent was 107,4±45 mg/m2(min. 26.4 - max 216.0 mg/m2), 7 children received 120 mg/m2 and 1 child 200mg/m2 of anthracycline equivalent. Mean time between the first and second assessment was 214±42 days(~7 months). Diastolic left ventricle function assessed by the E/A ratio, deceleration time, tissue Doppler and left atrial volume index (LAVI) was not significantly different between the first and the second assessment (table 1). However, the LA conduit strain at end diastole (LAScd ED)(-36.6 ± 16.0 vs -25.8 ± 12.0, p=0.028) as well as at atrial contraction(LAScd AC)(-33.4 ± 14.1 vs -23.1 ± 10.9, p=0.016) were significantly reduced after the anthracycline therapy. Other left atrial strain parameters including LA strain during reservoir at end diastole(LASr ED) and at atrial contraction(LASr AC), in the contraction phase at end diastole(LASct ED) and at atrial contraction(LASct AC) did not differ significantly between the assessments. The systolic function of the left ventricle were within norms at both measurements(table 1). Conclusions Early anthracycline induced LV diastolic dysfunction may not be detectable by the conventional echocardiographic methods in children treated for ALL. Subclinical dysfunction may be identified by close echocardiographic monitoring with the left atrial strain.
Haponiuk-Skwarlińska et al. (Thu,) conducted a cohort in Acute lymphoblastic leukemia (ALL) (n=25). Anthracycline therapy vs. Baseline (prior to therapy) was evaluated on Left atrial conduit strain at end diastole (LAScd ED) (p=0.028). Anthracycline therapy in children with ALL significantly reduced left atrial conduit strain at end diastole (-25.8 vs -36.6, p=0.028), indicating early subclinical diastolic dysfunction.