Abstract
Purpose: It is well known that anticancer drugs used for treating breast cancer can cause cardiac toxicity, and less is known about vascular toxicity. The aim of this study was to assess subclinical vascular effects of anthracyclines and trastuzumab (TRZ) in women treated for breast cancer.Methods: We enrolled 133 female patients with breast cancer undergoing adjuvant treatment with anthracycline-containing chemotherapy (CT) followed by taxane (paclitaxel/docetaxel) + TRZ. Patients underwent a standard echocardiography including measurement of left ventricular ejection fraction and global longitudinal strain at baseline and at follow-up. Vascular toxicity was evaluated by measuring brachial blood pressure (BP) and arterial stiffness indices (pulse wave velocity and Beta stiffness index) at T0 (baseline), T1 (3 months), T2 (6 months), and T3 (12 months).Results: Arterial stiffness indices were significantly increased at T1 in patients treated with anthracycline-containing CT (PWV 5.5 m/s IQR 5.15–6.4 at T0 vs. PWV 6.7 m/s IQR 5.6–7.2 at T1, p < 0.05; Beta index PWV 6.7 IQR 5.25–6.65 at T0, PWV 8.35 IQR 6.5–10.15 at T1, p < 0.05) but not at T2 and T3, when treatment with anthracyclines was stopped and patients were under treatment with taxane and TRZ. Blood pressure values did not significantly change during follow-up.Conclusion: Changes in arterial stiffness parameters occur early after starting treatment with anthracyclines, and they seem to be reversible if anthracycline treatment is stopped. These changes are not influenced by blood pressure values modifications. Therefore, in breast cancer women, anthracyclines seem to cause early reversible subclinical vascular injury.
Highlights
Cardiotoxic effects of anthracyclines and their mechanism have been extensively studied (Zhang et al, 2012)
We found a significant increase at T1, as well as a decrease with a return to basal values at T2 and T3
We found a statistically significant increase in pulse wave velocity (PWV) at T1 (T0: 5.5 m/s interquartile range (IQR) 5.15–6.4 vs. T1: 6.7 m/s IQR 5.6–7.2, p < 0.05); variation was not significant at T2 (5.75 m/s IQR 5.2–6.7) and T3 (5.7 IQR 5.15–6.6; Figure 1)
Summary
Cardiotoxic effects of anthracyclines and their mechanism have been extensively studied (Zhang et al, 2012). Some studies revealed structural arterial remodeling, increased arterial stiffness, and endothelial dysfunction after anthracyclines therapy in patients with hematologic malignancies (Mozos et al, 2017). A significant increase in aortic stiffness was found very soon, within 4 months of anthracycline therapy initiation, in a study including patients with lymphoma or leukemia, regardless of age, sex, diabetes, hypertension, hyperlipidemia, or coadministration of other cytostatics. In survivors of childhood cancer, who completed anthracyclines therapy for a malignant disorder, aortic PWV was significantly higher compared to age- and sex-matched healthy controls (Herceg-Cavrak et al, 2011). The aim of this study was to assess vascular toxicity induced by anthracyclines and other anticancer drugs in breast cancer women, measuring arterial stiffness. We assessed myocardial deformation indices at echocardiogram to detect an early cardiac dysfunction
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