Elsevier

American Heart Journal

Volume 142, Issue 4, October 2001, Pages 641-647
American Heart Journal

Secondary Prevention and Rehabilitation
Short-term oral estrogen replacement therapy does not augment endothelium-independent myocardial perfusion in postmenopausal women,☆☆

https://doi.org/10.1067/mhj.2001.118111Get rights and content

Abstract

Objectives The purpose of this study was to determine the effect of usual-dose estrogen replacement therapy (ERT) on myocardial perfusion and myocardial perfusion reserve (MPR) (evoked by an endothelium-independent vasodilator) in healthy postmenopausal women. Postmenopausal women have a decreased myocardial perfusion reserve compared with younger women. Estrogen infusions are known to enhance endothelium-dependent vasodilation of the epicardial coronary arteries in postmenopausal women, but whether ERT also enhances endothelium-independent myocardial perfusion and perfusion reserve is unclear. Methods In 24 healthy postmenopausal women who were not taking ERT, myocardial perfusion at rest, perfusion during the infusion of adenosine (a primarily endothelium-independent vasodilator), and MPR were determined by positron-emission tomography (PET) and oxygen 15–labeled water. The women were then randomly assigned in a double-blind fashion to receive either 0.625 mg of oral conjugated estrogens (Premarin) or placebo per day for 4 to 6 weeks, after which they underwent a repeat cardiac PET study. Results There was no statistical difference between those assigned to ERT and those assigned to placebo in the measurement of myocardial perfusion at rest (1.21 ± 0.31 vs 1.16 ± 0.18 mL/g/min, respectively) in response to adenosine (2.66 ± 0.96 vs 3.3 ± 0.45 mL/g/min) or MPR (2.24 ± 0.83 vs 2.88 ± 0.64 mL/g/min) after 4 to 6 weeks of oral ERT. There was also no difference between the groups in any of the myocardial perfusion measurements after correction for the rate-pressure product. Conclusions Short-term oral ERT does not affect myocardial perfusion at rest in response to adenosine or MPR in healthy postmenopausal women. Thus potential beneficial effects of ERT on vasomotor function may be limited to enhancement of endothelium-dependent vasodilative mechanisms affecting conduit vessels. (Am Heart J 2001;142:641-7.)

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.

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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.

    ☆☆

    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]

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