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JACC CardioOncol ; 2(1): 13-22, 2020 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-34396205

RESUMEN

OBJECTIVES: The purpose of this study was to assess the associations between 3-dimensional echocardiography (3DE)-derived changes in right ventricular (RV) volumes and strains with subsequent RV cardiotoxicity in patients treated with anthracyclines. BACKGROUND: Although early detection and prediction of left ventricular (LV) dysfunction has been widely studied in patients receiving anthracyclines, little is known about the early changes in RV size and function in this population. METHODS: A total of 74 patients with diffuse large B-cell lymphoma who received 6 cycles of anthracycline-based treatment were enrolled. Echocardiography was performed at baseline or before chemotherapy (pre-chemotherapy) (T0); after 2 cycles (T1); after 4 cycles (T2); and at the end of 6 cycles of chemotherapy (T3). Right ventricular end-diastolic volume (RVEDV), end-systolic volume (RVESV), ejection fraction (RVEF), longitudinal free wall strain (RVLFS), and longitudinal septal strain (RVLSS) were quantified by 3DE. RV cardiotoxicity was defined as a relative reduction of >10% in 3D RVEF or a relative reduction of >5% to a value of <45%. Volume status was assessed by inferior vena cava diameter (IVCD) and the estimated right atrial pressure (RAP). RESULTS: Twenty-seven patients developed cardiotoxicity after 6 cycles of chemotherapy (T3). Compared to baseline, increases in 3D RVEDV (58.5 ± 7.7 ml vs. 64.2 ± 7.0 ml; p < 0.001) and RVESV (27.8 ± 4.2 ml vs. 31.3 ± 4.2 ml; p < 0.001) were observed by the end of the fourth cycle of chemotherapy (T2). 3D RVLFS (-27.3 ± 3.1% vs. -24.2 ± 2.6%; p < 0.001) was also decreased at T2 compared to baseline. Statistically significant declines in 3D RVLSS (-26.1 ± 2.5% vs. -22.9 ± 2.7%; p < 0.001) and RVEF (54.0 ± 2.8% vs. 49.8 ± 2.4%; p < 0.001) were only observed at T3. A relative decrease in RVLFS of >12.4% (sensitivity, 78.6%; specificity, 82.6%; area under the curve (AUC), 0.80; p < 0.001); and a relative increase in RVESV of >13.2% (sensitivity, 71.4%; specificity, 71.7%; AUC, 0.76; p ï¼œ0.001) from baseline to T2 predicted subsequent RV cardiotoxicity at T3. IVCD and RAP did not change significantly over time. CONCLUSIONS: 3DE-derived measurements of RV strain and volume were associated with subsequent changes in RVEF. With further study, RVLFS and RVESV could potentially be used to predict subsequent declines in RVEF with anthracyclines.

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