Hormone therapy with tamoxifen reduces plasma levels of NT-B-type natriuretic peptide but does not change ventricular ejection fraction after chemotherapy in women with breast cancer

Silva, F.B.; Romero, Walckiria Garcia; Carvalho, Ana Ligia; Borgo, Mariana Veronez; Amorim, Maria Helena Costa; Gouvêa, Sônia Alves; Abreu, Gláucia Rodrigues de

doi:10.1590/1414-431x20144189

Cited by 8 publications

(11 citation statements)

References 28 publications

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“…In the present study, patients with breast cancer who were positive for ER or HER2 may have additionally received tamoxifen and Herceptin treatment. Previous studies have suggested that tamoxifen has a protective effect on cardiac function (31), whereas Herceptin treatment may be cardiotoxic (32). However, there was no such evidence of either tamoxifen-mediated cardiac protection or Herceptin-mediated cardiotoxicity in the study, in agreement with other previous studies (33,34).…”

Section: Discussionsupporting

confidence: 91%

BNP as a marker for early prediction of anthracycline‑induced cardiotoxicity in patients with breast cancer

Zhao

Chen

et al. 2019

Oncol Lett

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Anthracycline chemotherapy serves an important role in treating patients with breast cancer but is associated with cardiotoxicity. Although brain natriuretic peptide (BNP) is not the ideal marker for detecting the presence of diseases of the heart, several studies have demonstrated the predictive utility of BNP in the diagnosis of anthracycline-induced cardiotoxicity (AIC). The aim of the present study was to evaluate the role of BNP as a marker for the early prediction of AIC in patients with breast cancer. In the present study, a total of 149 patients with breast cancer who received anthracycline therapy were evaluated. The levels of BNP and echocardiography were detected during the anthracycline-based chemotherapy and patients were followed up after chemotherapy to determine the cardiotoxicity-free survival times. In the patients who received chemotherapy, an increase in the levels of BNP was observed. The concentration of BNP was significantly higher in the cardiotoxicity group during anthracycline chemotherapy (P=0.022) compared with the non-cardiotoxicity group and it was an independent predictor of cardiotoxicity (P=0.028). The optimal diagnostic threshold of BNP after the last anthracycline chemotherapy treatment was 107.9 pg/ml, the diagnostic sensitivity was 0.538, the specificity was 0.794, the Youden index was 0.332, the positive predictive value was 0.583 and the negative predictive value was 0.762. Based on the BNP threshold, a log-rank test was performed and it was determined that the cardiotoxicity-free survival rate of the group with higher levels of BNP was always lower compared with the group with lower levels of BNP. BNP elevation was associated with cardiotoxicity during the anthracycline chemotherapy. Detecting BNP after the final treatment of anthracycline chemotherapy may contribute to the early detection of cardiotoxicity.

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Section: Discussionsupporting

confidence: 91%

BNP as a marker for early prediction of anthracycline‑induced cardiotoxicity in patients with breast cancer

Zhao

Chen

et al. 2019

Oncol Lett

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“…These data suggested that fenofibrate had a minor effect on the increase in adiponectin in DOX-triggered cardiotoxicity. In addition, a previous study reported that the level of pro-BNP was increased by chemotherapy 44 . In our study, DOX-induced increases in circulating BNP and pro-BNP were also attenuated by fenofibrate, and this effect was abolished by L-NAME.…”

Section: Discussionmentioning

confidence: 96%

Fenofibrate attenuates doxorubicin-induced cardiac dysfunction in mice via activating the eNOS/EPC pathway

Huang

Yin

Chen

et al. 2021

Sci Rep

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Endothelial progenitor cells (EPCs) improve endothelial impairment, which in turn restores endothelial function in patients with heart failure (HF). In the present study, we tested whether fenofibrate, with its anti-inflammatory and vasoprotective effects, could improve myocardial function by activating EPCs through the eNOS pathway in a doxorubicin (DOX)-induced cardiomyopathy mouse model. Wild-type mice were divided into 4 groups and treated with vehicle, DOX + saline, DOX + fenofibrate, and DOX + fenofibrate + L-NAME (N(ω)-nitro-L-arginine methyl ester). DOX-induced cardiac atrophy, myocardial dysfunction, the number of circulating EPCs and tissue inflammation were analyzed. Mice in the DOX + fenofibrate group had more circulating EPCs than those in the DOX + saline group (2% versus 0.5% of total events, respectively) after 4 weeks of treatment with fenofibrate. In addition, the inhibition of eNOS by L-NAME in vivo further abolished the fenofibrate-induced suppression of DOX-induced cardiotoxic effects. Protein assays revealed that, after DOX treatment, the differential expression of MMP-2 (matrix metalloproteinase-2), MMP-9 (matrix metalloproteinase-9), TNF-α (tumor necrosis factor-α), and NT-pro-BNP (N-terminal pro-B-type natriuretic peptide) between saline- and DOX-treated mice was involved in the progression of HF. Mechanistically, fenofibrate promotes Akt/eNOS and VEGF (vascular endothelial growth factor), which results in the activation of EPC pathways, thereby ameliorating DOX-induced cardiac toxicity.

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“…In this case, the data were significantly higher than those for patients receiving tamoxifen. [ 19 ] These findings encourage the possibility that such subclinical changes are predictive of cardiac damage in the future.…”

Section: Discussionmentioning

confidence: 83%

Effects of treatment with chemotherapy and/or tamoxifen on the biomarkers of cardiac injury and oxidative stress in women with breast cancer

Silva¹,

Romero

Carvalho³

et al. 2017

Medicine

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There has been an increase in deaths from cardiovascular diseases following breast cancer therapy. Evidence has shown that this outcome is, in part, associated with cardiotoxicity induced by the chemotherapeutic drugs and the increase in oxidative stress. The aim of this study was to evaluate the effects of chemotherapy and hormone therapy with tamoxifen on the biomarkers of cardiac injury and oxidative stress in women with breast cancer.Thirty women were followed-up for 1 year and were divided into 3 groups according to the treatment protocol: women treated only with tamoxifen and clinical follow up for 12 months (Tam, n = 10); women treated only with chemotherapy for 6 months with clinical follow up for an additional 6-month period (Chemo, n = 10); and women who received chemotherapy for 6 months followed by a 6-month period only with tamoxifen therapy and clinical follow up (Chemo + Tam, n = 10). Analysis of the blood levels of cardiac troponin I (cTnI), advanced oxidation protein products (AOPP) and the activity of the plasmatic isoform of the antioxidant enzyme glutathione peroxidase (GPx) was performed before treatment (T0) and at 6 (T6) and 12 (T12) months after treatment.The Chemo group showed higher levels of cTnI (0.065 ± 0.006 ng/mL, P < .05) and AOPP (4.99 ± 0.84 μmol/L, P < .05) and reduced GPx activity (24.4 ± 1.1 nM/min/mL, P < .05) at T12 than the Tam group (cTnI: 0.031 ± 0.001 ng/mL; AOPP: 1.40 ± 0.10 μmol/L; GPx: 28.0 ± 0.7 nM/min/mL) and Chemo + Tam group (cTnI: 0.037 ± 0.002 ng/mL; AOPP: 2.53 ± 0.30 μmol/L; GPx: 29.5 ± 1.0 nM/min/mL).These data support the hypothesis that long-term oxidative stress after chemotherapy may have an impact on cardiovascular diseases and that tamoxifen has cardioprotective effects.

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Hormone therapy with tamoxifen reduces plasma levels of NT-B-type natriuretic peptide but does not change ventricular ejection fraction after chemotherapy in women with breast cancer

Cited by 8 publications

References 28 publications

BNP as a marker for early prediction of anthracycline‑induced cardiotoxicity in patients with breast cancer

BNP as a marker for early prediction of anthracycline‑induced cardiotoxicity in patients with breast cancer

Fenofibrate attenuates doxorubicin-induced cardiac dysfunction in mice via activating the eNOS/EPC pathway

Effects of treatment with chemotherapy and/or tamoxifen on the biomarkers of cardiac injury and oxidative stress in women with breast cancer

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