Bio-identical estrogen combined with spironolactone or bio-identical progesterone has actually shown to be cardioprotective, increase protection against heart disease and reduce blood pressure. The bad rap on hormones and heart disease is due to the use of some progestins (a modified version of progesterone) and non bio-identical forms of estrogens that have a strong/negative effect on coagulation and blood pressure.
Here, just a few studies:
Cardiovasc Res. 2006 Mar 1;69(4):777-80.
"There is an abundance of scientific evidence for the protective effect of estrogen against atherosclerosis, such as short-term vasodilating effects as well as long-term vascular protective and anti-atherosclerotic effects [2]. Epidemiological evidence shows that pre-menopausal women have a reduced risk for mortality from cardiovascular diseases [3] and that women are at a lower risk for the development of heart failure [4] and have enhanced cognitive function and reduced neurodegeneration associated with Alzheimer's disease and stroke [5]. Further proof for the protective effect of female gender is the fact that post-menopausal women have a similar or even increased risk for cardiovascular disease compared to men [3] and have an increased risk for adverse outcome after myocardial infarction and acute coronary syndromes, despite similar treatment with thrombolysis and percutaneous interventions [6]. It was therefore postulated that estrogen replacement would be beneficial in preventing cardiovascular diseases in post-menopausal females."
"The cardioprotective effect of estrogen is further supported by the findings that ovariectomy caused a loss of cardioprotection, which was regained by chronic estrogen replacement therapy."
"The vascular protective effects of estrogen and their mechanisms are thus fairly well-established."
Ann Clin Res. 1983;15 Suppl 38:1-121.
"Estradiol-17 beta substitution decreased the systolic and diastolic blood pressure in normotensive, hypertensive and borderline hypertensive postmenopausal women. The blood pressure of the hypertensive subjects decreased on average more than the blood pressure of the normotensive subjects."
"Irrespective of the pretreatment blood pressure levels, heart rate decreased during estradiol-17 beta substitution"
"Estradiol-17 beta substitution caused an increase in the blood volume in all groups of postmenopausal women"
"Cardiac output increased in the normotensive test subjects but decreased in the hypertensive and borderline hypertensive subjects"
With oral 17-beta estradiol.
Maturitas. 2008 Jul-Aug;60(3-4):185-201.
"Non-orally administered estrogens, minimizing the hepatic induction of clotting factors and others proteins associated with the first-pass effect, are associated with potential advantages on the cardiovascular system. In particular, the risk of developing deep vein thrombosis or pulmonary thromboembolism is negligible in comparison to that associated with oral estrogens. In addition, recent indications suggest potential advantages for blood pressure control with non-oral estrogens. To the same extent, a growing literature suggests that the progestins used in association with estrogens may not be equivalent. Recent evidence indeed shows that natural progesterone displays a favorable action on the vessels and on the brain, while this might not be true for some synthetic progestins."
Oral estrogen refers to non bio-identical forms, usually.
Horm Mol Biol Clin Investig. 2014 May;18(2):89-103.
"The cardiovascular protection observed in females has been attributed to the beneficial effects of estrogen on endothelial function."
"estrogen alone or combined with progesterone has been associated with decreased blood pressure"
"Estrogens physiologically stimulate the release of endothelium-derived vasodilator factors and inhibit the renin-angiotensin system."
Rev Prat. 1993 Dec 15;43(20):2631-7.
"This favourable effect of estrogens is completed by other mechanisms which modify platelet aggregation, prostacyclin/thromboxane equilibrium, endothelin, etc., and which improve arterial wall morphology and vasoactive reactions. Some synthetic progestogens, given with oestrogens for endometrium control, may compromise these spectacular vascular benefits, but this is not the case with natural progesterone."
"there is no known theoretical risk when oestradiol is given parenterally, which in France is the favoured method. This type of replacement therapy with oestradiol should be more often prescribed to subjects with atherogenic hyperlipidaemia, arterial hypertension or ischaemic coronary disease: not only it is not contraindicated, but it should soon become an indication."
Int J Pharm Compd. 2013 Jan-Feb;17(1):74-85
"Administration of compounded transdermal bioidentical hormone therapy in doses targeted to physiologic reference ranges administered in a daily dose significantly relieved menopausal symptoms in peri/postmenopausal women. Cardiovascular biomarkers, inflammatory factors, immune signaling factors, and health outcomes were favorably impacted, despite very high life stress, and home and work strain in study subjects. The therapy did not adversely alter the net prothrombotic potential, and there were no associated adverse events. This model of care warrants consideration as an effective and safe clinical therapy for peri/postmenopausal women especially in populations with high perceived stress and a history of stressful life events prior to, or during the menopausal transition."
Lancet. 1993 Jul 17;342(8864):133-6.
"Acute administration of oestradiol-17 beta therefore has a beneficial effect on myocardial ischaemia in women with coronary artery disease. This effect may be due to a direct coronary-relaxing effect, to peripheral vasodilation, or to a combination of these mechanisms. Oestradiol-17 beta may prove to be a useful adjunct to the treatment of angina in postmenopausal women with coronary heart disease."
J Am Osteopath Assoc. 2011 Mar;111(3):153-64.
"17β-Estradiol is FDA approved for menopausal symptoms, may have cardioprotective effects"
Hypertension. 1999 May;33(5):1190-4.
"Fifteen healthy postmenopausal women were studied in each of 3 conditions: on placebo, after 8 weeks of transdermal estradiol (...) twice per week, and again 2 weeks after addition of intravaginal progesterone"
"Levels of estrogen and progesterone similar to those in premenopausal women were achieved. On estradiol, nocturnal systolic BP (110+/-3 mm Hg), diastolic BP (63+/-2 mm Hg), and mean BP (77+/-2 mm Hg) fell significantly (P<0.02) compared with placebo systolic BP (116+/-2 mm Hg), diastolic BP (68+/-2 mm Hg), and mean BP (82+/-2 mm Hg). Daytime BP followed the same trend but was significantly lower only for mean BP. There was no activation of the RAAS. The addition of progesterone resulted in no further fall in BP but a significant activation of the RAAS. Thus, contrary to what is often assumed, administration of estradiol with or without progesterone not only did not raise BP but rather substantially lowered BP. This BP-lowering effect may be responsible for the lower incidence of hypertension in premenopausal than in postmenopausal women."
BMJ. 2012 Oct 9; 345
"In this randomised trial including 1006 women we found a significantly decreased risk of the composite endpoint of death, heart failure, or myocardial infarction when hormone replacement therapy was started early in postmenopause. The beneficial effect occurred in the 10 years randomisation phase and was maintained for an additional six years of non-randomised follow-up. The trend for all components of the endpoint was in the same direction (figs 3 to 6) and this finding was not associated with an increased risk of cancer, stroke, deep vein thrombosis, or pulmonary embolism. Thus this study implies that hormone therapy started in recently menopausal women and continued for a prolonged duration does not increase or provoke adverse cardiovascular events such as mortality, stroke, heart failure, or myocardial infarction."
"In human aortic endothelial cells 17-β-estradiol is superior to conjugated equine oestrogen in increasing the production of nitric oxide, partially because of a higher ability to activate the production of endothelial nitric oxide synthase.23"
In this study, oral 17-beta estradiol was used.
Obstet Gynecol. 2015 Mar;125(3):605-10.
"In transgender women, estrogen therapy, with or without antiandrogen therapy, was associated with lower BP."
"Transgender women were treated with estrogens. Fourteen (88%) were given sublingual micronized 17-beta estradiol (...) twice daily. One subject was given (...) estradiol via transdermal patch, and one subject received estradiol valerate (...) intramuscular every 2 weeks. All but one transgender woman (who wished to retain erectile function) were administered spironolactone"
"All transgender women had estradiol levels at least in the physiologic female – range at 6 months, with 3/16 (19%) having supraphysiologic levels > 1000pg/dl (including the one transgender woman using intramuscular estradiol valerate)."
"Transgender women (persons assigned male at birth, but who identify as females and who use estrogens with or without an anti-androgen to develop female secondary sex characteristics) had normal median baseline and 6 month body mass index (24.8 kg/m2 (IQR=4.3) and 23 kg/m2 (IQR=4.5) respectively). Both systolic and diastolic median blood pressures in this group dropped significantly from baseline to 6 months (130.5 mmHg (IQR 11.5) to 120.5 mmHg (IQR 15.5) p=.006; 78 mmHg (IQR 21) to 67 mmHg (IQR 12), p=.001 respectively)."
J Lipid Res. 2006 Feb;47(2):349-55.
"This prospective pilot study of 18 men with androgen-independent prostate cancer receiving ADT measured effects of TDE on lipid and inflammatory CVD risk factors before and after 8 weeks of TDE (...). During treatment, estradiol levels rose 17-fold; total cholesterol, LDL cholesterol, and apolipoprotein B levels decreased. HDL2 cholesterol increased, with no changes in triglyceride or VLDL cholesterol levels. Dense LDL cholesterol decreased and LDL buoyancy increased in association with a decrease in HL activity. Highly sensitive C-reactive protein levels and other inflammatory markers did not worsen. Compared with ADT, short-term TDE therapy of prostate cancer improves lipid levels without deterioration of CVD-associated inflammatory markers and may, on longer-term follow-up, improve CVD and mortality rates."
TDE = transdermal estradiol
ADT = androgen deprivation therapy
CLIMACTERIC 2005;8(Suppl 1):3–63
"In women with supraphysiological estradiol levels during treatment with implants, no adverse effects on lipid metabolism, but a reduction in LDL cholesterol and fasting insulin were observed."
Br J Obstet Gynaecol. 1990 Oct;97(10):917-21.
"Supraphysiological oestradiol levels are an uncommon consequence of oestradiol implants occurring most frequently in women with a history of depression or surgical castration. These high serum oestradiol levels were not associated with any deleterious effects and may be necessary for the control of symptoms in specific women"
"The mean serum oestradiol level of the 1388 women attending the clinic in 1988 was 767 pmol/l (range 78-2925 pmol/l), 66% had serum oestradiol levels <1000 pmol/l and 3% (38 women) had levels >1750 pmol/l (Fig 1)."
"The 15 women with PMS had a mean serum oestradiol of 2209 pmol/l (range 1760-2820 pmol/l). Their mean age at the start of treatment was 40 years (range 34-54) and the mean duration of therapy was 5.5 years (range 1-12)."
"The 23 menopausal women had a mean serum oestradiol of 2015 pmol/l (range 1785-2925 pmol/l). Their mean age was 46 years (range 29-58) and the mean duration of therapy was 4.5 years (range 1-10)."
