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Echocardiographic changes in right ventricular function in breast cancer patients receiving anthracycline-based chemotherapy at low cardiotoxic risk

Aug 2026 · European Heart Journal, Supplement · 0 citations

TL;DR

A significant decline in right ventricular function is demonstrated during anthracycline-based cardiotoxic therapy and persisting up to one year after treatment completion, even in patients with low cardiotoxic risk, despite changes being subclinical and largely within normal ranges.

Abstract

In advanced stage breast cancer, conventional chemotherapy is one of the most commonly used therapeutic options; however, it is associated with a potential risk of cardiotoxicity. Although the cardiotoxic effects of anthracyclines on the left ventricular function have been well studied, alterations of the right ventricle continue to be controversial. The assessment of conventional echocardiographic parameters remains the first-line imaging approach for evaluating and monitoring longitudinal right ventricular function. The purpose of this study was to evaluate the early effects of anthracycline-based chemotherapy on right ventricular function in newly diagnosed breast cancer patients at low risk for cardiotoxicity. This prospective study included 31 newly diagnosed breast cancer patients at low risk for cardiotoxicity who were treated with anthracycline-based chemotherapy. Baseline cardiovascular risk assessment was conducted according to established evidence-based risk stratification proformas for anthracycline cardiotoxicity. All patients received four cycles of chemotherapy. Transthoracic echocardiography was performed prior to anthracycline initiation, after the fourth (last) cycle, and 12 months after treatment completion. Variables included right heart parameters such as right ventricular (RV) end-diastolic and outflow tract dimensions, tricuspid annular plane systolic excursion (TAPSE), RV fractional area change (FAC%), Tissue Doppler systolic RV velocity (RVs’) and systolic pulmonary artery pressure. Right ventricular (RV) outflow tract dimensions increased by the end of the treatment protocol and persisted up to one year; however, statistical significance was observed only at the end of follow-up (III) compared with both baseline (I) and end-of-treatment (II) values (27,97±4,48 vs. 30,42±2,27, III vs. I (>) p=0,005; III vs. II (>) p=0,0001). RV end-diastolic dimensions although increasing, showed no significant change during follow-up. TAPSE and RVs′ demonstrated a significant reduction, with statistical significance evident at the end of follow-up compared with both baseline and end-of-treatment values. (22,42±2,80 vs. 21,19±2,04, III vs. I (<) p=0,029, III vs. II (<) p=0,028 and 14,00±1,69 vs. 13,03±1,37, III vs. I (<) p=0,002; III vs. II (<) p=0,001 respectively). No significant changes were observed in RV FAC% or systolic pulmonary artery pressure during treatment or at one-year follow-up. Although right ventricular dysfunction is not considered in the universal definition of cardiotoxicity, the right heart may undergo significant deteriorations. Our analysis demonstrated a significant decline in right ventricular function during anthracycline-based cardiotoxic therapy and persisting up to one year after treatment completion, even in patients with low cardiotoxic risk, despite changes being subclinical and largely within normal ranges.

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