The objective of this study was to evaluate the effect of tamoxifen on the plasma concentration of NT-pro-B-type natriuretic peptide (NT-proBNP) in women undergoing chemotherapy for breast cancer and to correlate changes in NT-proBNP with the left ventricular ejection fraction (LVEF). Over a period of 12 months, we followed 60 women with a diagnosis of breast cancer. The patients were separated into a group that received only chemotherapy (n=23), a group that received chemotherapy + tamoxifen (n=21), and a group that received only tamoxifen (n=16). Plasma levels of NT-proBNP were assessed at 0 (T0), 6 (T6), and 12 (T12) months of treatment, and echocardiography data were assessed at T0 and T12. Plasma NT-proBNP levels were increased in the chemotherapy-only group at T6 and T12, whereas elevated NT-proBNP levels were only found at T6 in the chemotherapy + tamoxifen group. At T12, the chemotherapy + tamoxifen group exhibited a significant reduction in the peptide to levels similar to the group that received tamoxifen alone. The chemotherapy-only group exhibited a significant decrease in LVEF at T12, whereas the chemotherapy + tamoxifen and tamoxifen-only groups maintained levels similar to those at the beginning of treatment. Treatment with tamoxifen for 6 months after chemotherapy significantly reduced the plasma levels of NT-proBNP and did not change LVEF in women with breast cancer.

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.

To evaluate the effects of exercise training (ET) on cardiac dysfunction and ventricular remodeling in ovariectomized (OVX) rats subjected to myocardial infarction (MI) and the possible mechanisms involved. OVX Wistar rats were subjected to MI or Sham surgery and divided in Control, OVX+SHAMSED, OVX+SHAMET, OVX+MISED and OVX+MIET groups. ET was performed on a treadmill (5x/wk, 60 min/day, 8 weeks). Cardiac function was assessed by ventricular catheterization and DHE fluorescence was evaluated to analyze oxidative stress. Collagen deposition, myocyte hypertrophy and infarct size was assessed by histology. Catalase, SOD‐2, Gp91phox and AT1 receptor (AT1R) expression were evaluated by western blotting. MI‐trained rats had significantly increased in +dP/dt and decreased left ventricular end‐diastolic pressure compared with MI‐sedentary rats. Moreover, oxidative stress and collagen deposition was reduced, as was myocyte hypertrophy. There were a reduction in AT1R and gp91phox expression and an increase in catalase expression. Therefore, ET improves the functional cardiac parameters and attenuates cardiac remodeling associated with a reduction in oxidative stress in OVX rats subjected to MI. Thus, ET may be an important therapeutic target for the prevention of heart failure in postmenopausal women affected by MI.

Effects of swimming training and estrogen therapy on the vascular reactivity of hypertensive ovariectomized rats: role of renin angiotensin system Glaucia R Abreu, Nazare S Bissoli, Ana Ligia R Carvalho, Erick Roberto C Gonçalves, Patrick W Endlich: Health Science Center, Federal University of Espirito Santo, Brazil Several studies showed up regulation of Renin Angiotensin System (RAS) after menopause and the ability of physical training in reduces cardiovascular risk factors. The aim of this study was to analyze the effects of swimming training (eight weeks) and estrogen therapy (5 mg of 17β‐Estradiol, s.c.) on vascular reactivity and the expression of RAS of aorta rings in ovariectomized spontaneously hypertensive rats (SHR). The groups were divided: Sham (S), Ovariectomized (OVX), ovariectomized (OTE2), ovariectomized+swimming ON) and ovariectomized treated with E2 plus swimming (OE2+N). The systolic blood pressure was measured after the animals were sacrificed and blood was collected to measure Angiotensin II plasma levels by radioimmunoassay. Aorta reactivity we evaluated in response to Ang II and Angiotensin‐(1‐7) and RAS proteins expression were made by Western Blotting method. Both exercise and E2 increased Ang II plasma levels. However, the systolic blood pressure was attenuated by treatments. The OVX group showed increase in the constrictor response to Ang II and decrease dilatator response to Ang (1‐7), that was reverted by swimming training or E2 therapy associated to swimming. Moreover, ON and OE2+N groups showed increase in the AT2 and Mas receptor expression. On the other hand, the ON showed increase in the superoxide dismutase (SOD) anti‐oxidant enzyme and only the groups treated with E2 showed increase on eNOS expression. Then both swimming training and E2 treatment may play a non‐additive, role in the cardioprotection and the chronic physical exercise can be a feasible alternative in relation to estrogen therapy in post‐menopausal women. Grant Funding Source: Capes;CNPq

The increase in deaths from cardiovascular disease in women submitted to antineoplastic treatments for breast cancer is a fact observed in many work and is most often associated with cardiotoxic effects of chemotherapy. It is believed that the cardiotoxicity of chemotherapeutic agents is associated with increased oxidative stress in the body, although not well understood. The detection of this damage underlies the aims of this present study to assess the effects of treatments against breast cancer on biomarkers of cardiac injury and oxidative stress. Thirty women divided according to the therapeutic protocol in women treated only with hormone therapy with tamoxifen (Tam group, n = 10), women treated only with chemotherapy (chemo group, n = 10), and women treated with chemotherapy and then with hormone therapy with tamoxifen (Chemo+Tam group, n = 10) were monitored for one year. Blood samples was collected before initiation of treatment, six, and twelve months after for analysis of cardiac troponin I (cTnI), advanced oxidation protein products (AOPP) and plasma activity of the antioxidant enzyme glutathione peroxidase (GPx). At the end of research we observed that women in the Chemo group showed increased levels of cTnI and AOPP and lower plasma activity of GPx when compared to women groups Tam and Chemo + Tam. These data reinforce the involvement hypothesis of oxidative stress in cardiovascular diseases in a chronic period after end of chemotherapy and highlighted a cardioprotective effect of hormone therapy with tamoxifen.