Ida Gregersen1, Else Høibraaten2, Kirsten B Holven3, Lene Løvdahl4, Thor Ueland4, Marie-Christine Mowinckel5, Tuva Børresdatter Dahl6, Pål Aukrust7, Bente Halvorsen4, Per Morten Sandset8. 1. Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Institute of Clinical Medicine, University of Oslo, Oslo, Norway. Electronic address: ida.gregersen@rr-research.no. 2. Department of Haematology, Oslo University Hospital, Oslo, Norway. 3. Department of Nutrition, Institute for Basic Medical Sciences, University of Oslo, Oslo, Norway; National Advisory Unit on Familial Hypercholesterolemia, Department of Endocrinology, Morbid Obesity and Preventive Medicine, Oslo University, Oslo, Norway. 4. Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Institute of Clinical Medicine, University of Oslo, Oslo, Norway. 5. Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Department of Haematology, Oslo University Hospital, Oslo, Norway. 6. Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Department of Microbiology, Oslo University Hospital HF, Rikshospitalet and University of Oslo, NO-0424 Oslo, Norway. 7. Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Section of Clinical Immunology and Infectious Diseases, Oslo University Hospital Rikshospitalet, Oslo, Norway. 8. Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Department of Haematology, Oslo University Hospital, Oslo, Norway.
Abstract
BACKGROUND:Women develop cardiovascular disease (CVD) approximately 7-10 years later than men, but progress with similar risk after menopause. Recent studies suggest that hormone replacement therapy (HRT) is cardioprotective when initiated early after menopause, but the mechanisms involved are still unclear. OBJECTIVE: In the current study, we aimed to examine the effects of HRT treatment on the plasma atherogenicity in postmenopausal women. We studied the total lipid profile in blood samples collected in a randomized, double-blinded, placebo controlled clinical trial of women with a history of venous thrombosis (VT), the EVTET study. METHODS:One-hundred and forty postmenopausal women <70 years were included in EVTET and randomized either to active treatment (one tablet of 2 mg estradiol and 1 mg norethisterone acetate daily) (n = 71) or placebo (n = 69). Blood samples were taken at baseline and after 3 months and subjected to routine assessment of hemostatic factors and lipids. RESULTS: Our study show that HRT compared to placebo significantly reduced plasma levels of Lp(a), ApoA1, ApoB, total cholesterol (TC), HDL-C, LDL-C, TC/HDL-C and LDL-C/HDL-C ratio at 3 months. No effect was observed on ApoB/ApoA1 ratio or triglycerides. The change in Lp(a) was significantly and inversely correlated with the change in estradiol (r = -0.32; P = 0.001) and positively correlated to the change in lipids, tissue factor pathway inhibitor activity and antigen, protein C and fibrinogen (r between 0.26 and 0.45, p < 0.01). CONCLUSION: In sum, this study confirms a strong effect of HRT on atherogenic lipids with a large reduction in the pro-thrombotic Lp(a), suggesting an overall favorable effect on thrombogenicity after HRT replacement therapy in post-menopausal women at risk of VT.
RCT Entities:
BACKGROUND:Women develop cardiovascular disease (CVD) approximately 7-10 years later than men, but progress with similar risk after menopause. Recent studies suggest that hormone replacement therapy (HRT) is cardioprotective when initiated early after menopause, but the mechanisms involved are still unclear. OBJECTIVE: In the current study, we aimed to examine the effects of HRT treatment on the plasma atherogenicity in postmenopausal women. We studied the total lipid profile in blood samples collected in a randomized, double-blinded, placebo controlled clinical trial of women with a history of venous thrombosis (VT), the EVTET study. METHODS: One-hundred and forty postmenopausal women <70 years were included in EVTET and randomized either to active treatment (one tablet of 2 mg estradiol and 1 mg norethisterone acetate daily) (n = 71) or placebo (n = 69). Blood samples were taken at baseline and after 3 months and subjected to routine assessment of hemostatic factors and lipids. RESULTS: Our study show that HRT compared to placebo significantly reduced plasma levels of Lp(a), ApoA1, ApoB, total cholesterol (TC), HDL-C, LDL-C, TC/HDL-C and LDL-C/HDL-C ratio at 3 months. No effect was observed on ApoB/ApoA1 ratio or triglycerides. The change in Lp(a) was significantly and inversely correlated with the change in estradiol (r = -0.32; P = 0.001) and positively correlated to the change in lipids, tissue factor pathway inhibitor activity and antigen, protein C and fibrinogen (r between 0.26 and 0.45, p < 0.01). CONCLUSION: In sum, this study confirms a strong effect of HRT on atherogenic lipids with a large reduction in the pro-thrombotic Lp(a), suggesting an overall favorable effect on thrombogenicity after HRT replacement therapy in post-menopausal women at risk of VT.
Authors: David Šuran; Helena Blažun Vošner; Jernej Završnik; Peter Kokol; Andreja Sinkovič; Vojko Kanič; Marko Kokol; Franjo Naji; Tadej Završnik Journal: Front Public Health Date: 2022-07-05
Authors: Sabine Elisabeth Segerer; Stephan Georg Segerer; Carl-Joachim Partsch; Wolfgang Becker; Frank Nawroth Journal: Front Endocrinol (Lausanne) Date: 2020-12-14 Impact factor: 5.555