# An echocardiographic study of right ventricular function and pulmonary systolic pressure in patients treated with anthracyclines

## TL;DR

This study examines how anthracycline chemotherapy affects right and left heart function in breast cancer patients, finding subtle changes in right heart parameters.

## Contribution

The study provides new insights into anthracycline-induced cardiotoxicity effects on right ventricular function, previously understudied.

## Key findings

- Anthracycline therapy caused modest decreases in right ventricular tricuspid annular plane systolic excursion (TAPSE) and TAPSE/sPAP ratio.
- Left ventricular ejection fraction decreased significantly after treatment, but no patients met criteria for cardiac dysfunction.
- Serum troponin I levels increased significantly following anthracycline treatment.

## Abstract

Anthracycline-based chemotherapy agents are widely used and are highly effective, particularly for breast cancer treatment. Although the cardiotoxic effects of anthracyclines on left ventricular (LV) function are well established, their impact on right ventricular (RV) function has not been sufficiently investigated. This study aimed to evaluate the effects of anthracycline therapy on RV function and to compare them with LV function to determine the potential cardiotoxic effects on both ventricles.

This single-center retrospective cohort study included 38 female patients with breast cancer who were treated with anthracyclines between January 2021 and June 2023. Echocardiographic parameters and cardiac biomarkers were evaluated at baseline and at 6-month follow-up visit. LV ejection fraction (LVEF) was calculated using the Teichholz method due to the retrospective design. RV function was assessed by tricuspid annular plane systolic excursion (TAPSE), systolic pulmonary artery pressure (sPAP), and the TAPSE/sPAP ratio. Cancer therapy–related cardiac dysfunction (CTRCD) was defined according to current European Society of Cardiology criteria. Serum troponin I and pro–brain natriuretic peptide levels were recorded. Paired comparisons were performed using the paired-samples t-test.

Following anthracycline therapy, LV end-systolic diameter increased (2.76 ± 0.24 cm vs. 3.03 ± 0.29 cm, P < 0.001), and LVEF decreased (67.3% ± 3.6% vs. 62.2% ± 4.5%, P < 0.001). No patient fulfilled the guideline-defined criteria for CTRCD. Early diastolic transmitral flow velocity (E wave) and mitral annular early diastolic velocity (e′) were reduced (E: 0.63 ± 0.16 m/sec vs. 0.52 ± 0.12 m/sec, P < 0.001; e′: 0.09 ± 0.03 m/sec vs. 0.07 ± 0.02 m/sec, P = 0.001). TAPSE decreased (2.28 ± 0.36 cm vs. 2.16 ± 0.27 cm, P = 0.047), and systolic pulmonary artery pressure showed a nonsignificant upward trend after treatment (P = 0.052). The TAPSE/sPAP ratio declined (1.11 ± 0.47 vs. 0.86 ± 0.20, P < 0.001), and pulmonary artery diameter increased (19.9 ± 2.0 mm vs. 21.3 ± 2.6 mm, P = 0.008). Serum troponin I levels increased significantly (4.84 ± 1.25 ng/L vs. 11.93 ± 4.91 ng/L, P < 0.001).

Anthracycline therapy may be associated with modest changes in both LV and RV parameters. Reductions in TAPSE and the TAPSE/sPAP ratio, together with a nonsignificant upward trend in systolic pulmonary artery pressure, may reflect subtle alterations in RV–pulmonary arterial interactions rather than overt RV dysfunction. Routine evaluation of RV function, alongside LV assessment, may provide additional insights during cardiotoxicity monitoring in anthracycline-treated patients. These findings should be interpreted cautiously and confirmed in larger prospective studies.