Secondary Prevention and RehabilitationShort-term oral estrogen replacement therapy does not augment endothelium-independent myocardial perfusion in postmenopausal women☆,☆☆
Section snippets
Subjects: Enrollment criteria and screening procedures
A total of 40 postmenopausal women were screened to enroll 24 healthy women who met the inclusion criteria; all 24 completed the study. All women were from the St Louis metropolitan area. They were considered postmenopausal if they had not had a menses for ≥12 months, if they had undergone a bilateral oophorectomy, or if they had a follicle-stimulating hormone level >30 IU/L. None of the participants had taken any hormone replacement therapy, tamoxifen, raloxifene, or soy protein supplement
Results
The baseline clinical characteristics of the study subjects are listed in Table IA.At the time of entry into the study only SBP and DBP were statistically slightly higher in the group randomized to receive ERT. Table IB shows the medications that some of the subjects were on at the time of the study.
The hemodynamic characteristics of the subjects at rest in the PET suite after adenosine and before and after randomization are listed in Table II.There were no significant differences between the 2
Discussion
Our findings suggest that usual-dose oral ERT does not enhance endothelium-independent vasodilation and does not significantly increase rest myocardial perfusion or perfusion reserve. In the current study MPR remained in the 2 to 3 range, which is consistent with that of previous studies of older subjects but which is well below what is considered “normal” MPR in younger women (3.5 to 4.25).13, 14 Therefore, if ERT has salutary effects in humans on myocardial perfusion, this is likely to occur
Acknowledgements
We thank L. Michelle Vaughn, RN, Nathan Potts, Gary Hoffman, and Linda Willey for their assistance in data collection; Beth Engeszer and Benico Barzilai, MD, for their editorial assistance; Ava Ysaguirre and Carol Williams for their secretarial assistance; and Katherine Vehe, PharmD, for her assistance with the double-blind protocol.
References (35)
- et al.
Estrogen replacement therapy and coronary heart disease: a quantitative assessment of the epidemiologic evidence
Prev Med
(1991) - et al.
Effect of conjugated estrogen on peripheral flow-mediated vasodilation in postmenopausal women
Am J Cardiol
(1998) - et al.
Oestrogen and inhibition of oxidation of low-density lipoprotein in postmenopausal women
Lancet
(1994) - et al.
Noninvasive quantitation of myocardial blood flow in human subjects with oxygen-15–labeled water and positron emission tomography
J Am Coll Cardiol
(1989) - et al.
Individual and combined effects of estrogen/progestin therapy and lovastatin on lipids and flow-mediated vasodilation in postmenopausal women with coronary artery disease
J Am Coll Cardiol
(1999) - et al.
Serum lipids, lipoprotein, and apolipoproteins during postmenopausal estrogen replacement therapy combined with either 19-nortestosterone derivatives of 17-hydroxyprogesterone derivatives
Am J Med
(1991) - et al.
Effect of combined 17β-estradiol and vitamin E on low-density lipoprotein oxidation in postmenopausal women
Am J Cardiol
(1995) - et al.
Oestrogen and inhibition of oxidation of low-density lipoprotein in postmenopausal women
Lancet
(1994) - et al.
Estrogen replacement therapy and exercise performance in postmenopausal women with coronary artery disease
Am J Cardiol
(1997) - et al.
Hormone therapy to prevent disease and prolong life in postmenopausal women
Ann Intern Med
(1992)
Menopause and the risk of cardiovascular disease: the Framingham Study
Ann Intern Med
Estrogen use and all-cause mortality: preliminary results from the Lipid Research Clinics Program follow-up study
JAMA
Estrogen and blood vessel wall
Curr Opin Cardiol
Pulsatility index in internal carotid artery in relation to transdermal oestradiol and time since menopause
Lancet
Ethinyl estradiol acutely attenuates abnormal coronary vasomotor responses to acetylcholine in postmenopausal women
Circulation
Endothelial-dependent coronary vasomotor responsiveness in postmenopausal women with and without estrogen replacement therapy
Am J Cardiol
Effects of physiological levels of estrogen on coronary vasomotor function in postmenopausal women
Circulation
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2010, Nutrition, Metabolism and Cardiovascular DiseasesCitation Excerpt :Glucose metabolism may also be decreased because of substrate competition due to a greater fatty acid delivery to the myocardium. Hormone replacement treatment, i.e., a model to address the postulated actions of estrogens on the heart, did not influence resting myocardial perfusion and coronary flow reserve [26,27]. A trend towards higher myocardial use of fatty acids was retrospectively noted in women taking estrogens as compared with untreated women [21].
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2007, Journal of Nuclear CardiologyCitation Excerpt :If this holds true in future clinical studies, then the assessment of coronary circulatory function by PET imaging could be a promising and unique tool to successfully guide preventive medical therapy in the development or progression of the CAD process. In this regard, long-term estrogen replacement in postmenopausal women without traditional coronary risk factors may improve endothelium-related MBF responses to CPT, whereas no such effect was observed with short-term administration75,123,124 or in postmenopausal women with traditional coronary risk factors.75 In addition, β-hydroxymethylglutaryl–coenzyme A reductase inhibitors (simvastatin) beneficially altered the lipid profile in hypercholesterolemic patients, which was accompanied by a significant increase in dipyridamole-stimulated mean hyperemic MBF from 1.82 ± 0.36 mL · g−1 · min−1 at baseline to 2.38 ± 0.58 mL · g−1 · min−1 at follow-up, as measured with N-13 ammonia and PET.119
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Supported by grants from the American Heart Association, Missouri Affiliate, the American Society of Nuclear Cardiology/Amersham Award, and the Missouri Valley Chapter of the Society of Nuclear Medicine. Adenosine was provided by Fujisawa USA, Inc, and the Premarin and placebo were provided by Wyeth-Ayersy Laboratories.
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Reprint requests: Linda R. Peterson, MD, FACC, Washington University School of Medicine, Cardiovascular Division, 660 S Euclid Ave, Campus Box 8086, St Louis, MO 63110. E-mail: [email protected]