Silvia Goldmeier1, Kátia De Angelis2, Karina Rabello Casali1, César Vilodre3, Fernanda Consolim-Colombo4, Adriane Belló Klein5, Rodrigo Plentz6, Polimara Spritzer7, Maria-Cláudia Irigoyen8. 1. Instituto de Cardiologia do Rio Grande do Sul/Fundação Universitária de Cardiologia (IC/FUC) Porto Alegre, Brazil. 2. Universidade Nove de Julho (UNINOVE) São Paulo, Brazil. 3. Division of Endocrinology, Gynecological Endocrinology Unit, Hospital de Clínicas de Porto Alegre (HCPA) Porto Alegre, Brazil. 4. Hypertension Unit, Heart Institute (InCor), Medical School of University of Sao Paulo Sao Paulo, Brazil. 5. Department of Physiology, Universidade Federal do Rio Grande do Sul (UFRGS) Porto Alegre, Brazil. 6. Department of Physiotherapy, Universidade Federal de Ciências da Saúde de Porto Alegre (UFCSPA) Porto Alegre, Brazil. 7. Division of Endocrinology, Gynecological Endocrinology Unit, Hospital de Clínicas de Porto Alegre (HCPA) Porto Alegre, Brazil ; Department of Physiology, Universidade Federal do Rio Grande do Sul (UFRGS) Porto Alegre, Brazil. 8. Instituto de Cardiologia do Rio Grande do Sul/Fundação Universitária de Cardiologia (IC/FUC) Porto Alegre, Brazil ; Hypertension Unit, Heart Institute (InCor), Medical School of University of Sao Paulo Sao Paulo, Brazil.
Abstract
OBJECTIVE: Women with primary ovarian insufficiency (POI) present an increased risk for cardiovascular disease. In this study we tested the hypothesis that POI in women under hormone therapy (HT) are associated with vascular vasodilatation attenuation and cardiovascular autonomic dysfunction and these impairments are related to changes in systemic antioxidant enzymes. Furthermore, the possibility that ovarian hormone deprivation can induce such changes and that HT cannot reverse all of those impairments was examined in an experimental model of POI. METHODS: Fifteen control and 17 patients with primary ovarian insufficiency receiving HT were included in the study. To test the systemic and cardiac consequences of ovarian hormone deprivation, ovariectomy was induced in young female rats that were submitted or not to HT. Spectral analysis of RR interval and blood pressure signals were performed and oxidative stress parameters were determined. RESULTS: POI women under HT have increased mean arterial pressure (94±10 vs. 86±5 mmHg) despite normal endothelial and autonomic modulation of vasculature. Additionally, they presented impaired baroreflex sensitivity (3.9±1.38 vs. 7.15±3.62 ms/mmHg) and reduced heart rate variability (2310±1173 vs. 3754±1921 ms(2)). Similar results obtained in ovariectomized female rats were accompanied by an increased lipoperoxidation (7433±1010 vs. 6180±289 cps/mg protein) and decreased antioxidant enzymes in cardiac tissue. As it was observed in women, the HT in animals did not restore hemodynamic and autonomic dysfunctions. CONCLUSION: These data provide clinical and experimental evidence that long term HT may not restore all cardiovascular risk factors associated with ovarian hormone deprivation.
OBJECTIVE:Women with primary ovarian insufficiency (POI) present an increased risk for cardiovascular disease. In this study we tested the hypothesis that POI in women under hormone therapy (HT) are associated with vascular vasodilatation attenuation and cardiovascular autonomic dysfunction and these impairments are related to changes in systemic antioxidant enzymes. Furthermore, the possibility that ovarian hormone deprivation can induce such changes and that HT cannot reverse all of those impairments was examined in an experimental model of POI. METHODS: Fifteen control and 17 patients with primary ovarian insufficiency receiving HT were included in the study. To test the systemic and cardiac consequences of ovarian hormone deprivation, ovariectomy was induced in young female rats that were submitted or not to HT. Spectral analysis of RR interval and blood pressure signals were performed and oxidative stress parameters were determined. RESULTS: POI women under HT have increased mean arterial pressure (94±10 vs. 86±5 mmHg) despite normal endothelial and autonomic modulation of vasculature. Additionally, they presented impaired baroreflex sensitivity (3.9±1.38 vs. 7.15±3.62 ms/mmHg) and reduced heart rate variability (2310±1173 vs. 3754±1921 ms(2)). Similar results obtained in ovariectomized female rats were accompanied by an increased lipoperoxidation (7433±1010 vs. 6180±289 cps/mg protein) and decreased antioxidant enzymes in cardiac tissue. As it was observed in women, the HT in animals did not restore hemodynamic and autonomic dysfunctions. CONCLUSION: These data provide clinical and experimental evidence that long term HT may not restore all cardiovascular risk factors associated with ovarian hormone deprivation.
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